Goat Medicine and Surgery

Goat Medicine and
Surgery
Goat Medicine and
Surgery
DAVID HARWOOD BVETMED FRCVS
Chairman Goat Veterinary Society
Honorary Veterinary Surgeon, British Goat Society
Visiting Reader in Veterinary Field Pathology, Department of Pathology and Infectious Diseases
School of Veterinary Medicine, University of Surrey
Guildford, UK
Formerly Veterinary Investigation Officer, Animal and Plant Health Agency, UK
KARIN MUELLER MVSC DCHP DIPECBHM MRCVS

RCVS and European Diplomate & Specialist in Cattle/Bovine Health
Senior Lecturer Animal Husbandry & Reproduction
Institute of Veterinary Science, University of Liverpool
Liverpool, UK
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742
© 2018 by Taylor & Francis Group, LLC

CRC Press is an imprint of Taylor & Francis Group, an Informa business
No claim to original U.S. Government works
Printed on acid-free paper
International Standard Book Number-13: 978-1-4987-4863-6 (Hardback)
This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been
made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liabil-
ity for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this
book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the
publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care profession-
als and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s
medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances
in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader
is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’
printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this
book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately
it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat
patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in
this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright
material has not been acknowledged please write and let us know so we may rectify in any future reprint.
Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any
form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming,
and recording, or in any information storage or retrieval system, without written permission from the publishers.
For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.
com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-
profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy
license by the CCC, a separate system of payment has been arranged.
Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and
explanation without intent to infringe.
Library of Congress Cataloging‑in‑Publication Data
Names: Harwood, David, BVM, author. | Mueller, Karin, author.

Title: Goat medicine and surgery / David Harwood and Karin Mueller.
Description: Boca Raton : CRC Press, [2018]
Identifiers: LCCN 2017034019 (print) | LCCN 2017035549 (ebook) | ISBN
9781315152233 (Master eBook) | ISBN 9781498748636 (hardback : alk. paper)
Subjects: LCSH: Goats--Diseases. | MESH: Goat Diseases
Classification: LCC SF968 (ebook) | LCC SF968 .H27 2018 (print) | NLM SF 968
| DDC 636.3/90896--dc23
LC record available at https://lccn.loc.gov/2017034019
Visit the Taylor & Francis Web site at

http://www.taylorandfrancis.com
and the CRC Press Web site at

http://www.crcpress.com
CONTENTS
v
Preface xix
Abbreviations xxi
CHAPTER 1 INTRODUCTION 1
EVOLUTION 1
GOAT BREEDS AND THEIR PURPOSES 3
GENOMICS 3
BEHAVIOUR 4
NUTRITION 7
ENVIRONMENT 11
Housing 11
Fencing 12
Tethering 12
HANDLING 12
PHYSIOLOGY AND BODY FEATURES 13
Lactation 13
Horns 13
Coat 13
Wattles 14
Weight 14
Longevity 14
HISTORY TAKING AND CLINICAL EXAMINATION 14
Farm related history of interest 14
For the individual animal, history of interest 14
Basic clinical examination 14
ADMINISTERING MEDICATION 15
Oral administration 15
Subcutaneous injection 16
Intramuscular injection 16
Intravenous injection and catheterisation 17
Intraperitoneal injection 18
Subconjunctival injection 18
ROUTINE PROCEDURES AND HEALTH PLANNING 18
BIOSECURITY 18
LEGISLATION 20
vi C on t e n t s
CHAPTER 2 REPRODUCTIVE SYSTEM 21

THE DOE 21
NORMAL STRUCTURE AND FUNCTION 21
FERTILITY 21
FECUNDITY 22
OESTROUS CYCLE AND SIGNS OF OESTRUS 22
CONTROL OF OESTRUS 23
Out-of-season breeding 23
Synchronisation during the breeding season 23
OVARIAN DISORDERS 24
Anoestrus 24
Cystic ovarian disease 25
BREEDING 25
Natural service 25
Artificial insemination 26
Embryo transfer 27
Pregnancy diagnosis 28
Misalliance 28
UTERINE DISORDERS 28
Anatomical abnormalities – congenital 28
Anatomical abnormalities – acquired 29
Endometritis 30
Uterine neoplasia 31
HERD INFERTILITY PROBLEM 32
INFECTIOUS DISEASES 32
Caprine herpesvirus 1 32
EMBRYONIC LOSS AND ABORTION 33
ABORTION 34
Common infectious causes of abortion 35
Toxoplasmosis 35
Chlamydiosis (syns. enzootic abortion, ovine enzootic abortion) 36
Q fever 38
Brucellosis 39
Listeriosis 40
Less common infectious causes of abortion 41
Salmonellosis 41
Neosporosis 42
Tick-borne fever 42
Arbovirus infections 42
Campylobacter infection 42
Leptospirosis 43
Border disease virus/bovine viral diarrhoea virus (BDV/BVDV) 43
Caprine herpesvirus 43
Rift Valley fever 43
Maceration – non-specific 43
C on t e n t s vii
Non-infectious causes of abortion 43

Pharmacological products 43
Toxicity 44
Vitamin/mineral deficiencies 44
Malnutrition/pregnancy toxaemia 44
Habitual abortion in Angora goats 44
Mummification – non-specific 44
THE BUCK 45
OUT-OF-SEASON BREEDING 45
Indications 45
Technique 45
EXAMINATION FOR BREEDING SOUNDNESS 45
Indications 45
Aetiology 46
History 47
Physical examination 47
Genital tract examination 47
Semen evaluation 47
TESTICULAR AND EPIDIDYMAL ABNORMALITIES 49
Testicular hypoplasia 49
Testicular degeneration or atrophy 49
Orchitis and epididymitis 50
Cryptorchism (syn. retained gonad) 51
ACCESSORY SEX GLAND DISORDERS 52
PENIS AND PREPUCE ABNORMALITIES 52
Penile deviation 52
Penile trauma 53
Phimosis and paraphimosis 54
Balanoposthitis 54
Neoplasia of the male reproductive tract 55
CASTRATION 56
VASECTOMY 57
TEMPORARY SUPPRESSION OF FERTILITY 59
OTHER MALE DISORDERS 59
Gynaecomastia 59
Venereal disease 59
CHAPTER 3 PREGNANCY AND PARTURITION 61

PREGNANCY 61
Pregnancy diagnosis 61
PREPARTUM PROBLEMS 63
Hypocalcaemia and pregnancy toxaemia 63
Mummification, maceration and fetal maldevelopment 63
Pseudopregnancy (syns. cloudburst, hydrometra) 63
viii C on t e n t s
Hydrops uteri 64
Vaginal and cervical prolapse 65
Rupture or herniation of the uterus 66
Induction of parturition 67
Ante-natal preparation 67
PARTURITION 67
Normal parturition 67
Dystocia 68
Failure of cervical dilation (syn. ringwomb) 70
Uterine torsion 71
Caesarean section 72
Fetotomy 75
POST-PARTURIENT PROBLEMS 77
Haemorrhage 77
Laceration of the cervix 77
Laceration of the vagina 78
Recto-vaginal fistula 78
Vaginal prolapse – post-parturient 79
Uterine rupture 79
Uterine prolapse 79
Retained fetal membranes 81
Metritis 82
Necrotic vaginitis 84
Bladder eversion or herniation 84
CHAPTER 4 NEONATOLOGY 85
INTRODUCTION 85
WEAK NEWBORN KIDS 85
Congenital abnormalities 85
Genetic abnormalities 85
Developmental insult abnormalities 85
Mineral shortfall abnormalities 86
Known heritable abnormalities 86
RESPIRATION 86
Normal adaptation 86
Asphyxia 86
CARDIAC FUNCTION AND CIRCULATION 88
Absent heartbeat 88
Cardiovascular defects 88
THERMOREGULATION 89
Hypothermia 89
C on t e n t s ix
IMMUNE SYSTEM 90
Failure of passive transfer 91
Neonatal septicaemia (syn. sepsis) 93
GASTROINTESTINAL TRACT 95
Hypoglycaemia 95
Meconium retention 96
Atresia ani, recti or coli 96
Cleft palate (syn. palatoschisis) 97
URINARY FUNCTION 97
Urine retention 97
MUSCULOSKELETAL FUNCTION 98
Contracted tendons 98
Flexor tendon laxity 99
Arthrogryposis 99
White muscle disease 100
METABOLIC DISORDERS 100
Neonatal acidosis 100
Floppy-kid syndrome 100
Beta-mannosidosis 101
Iodine deficiency (congenital hyperplastic goitre) 101
NEUROLOGICAL FUNCTION 101
Congenital central nervous system abnormalities 102
Congenital swayback 102
MISCELLANEOUS 102
Neonatal maladjustment syndrome 102
Prematurity 103
Low birth weights 103
Sticky kid disease 104
ARTIFICIAL REARING 104
Fostering 104
Supplementing 104
Routine artificial rearing 105
CHAPTER 5 DIGESTIVE TRACT AND ABDOMEN 109

CLINICAL EXAMINATION OF THE DIGESTIVE SYSTEM 109
Oral and dental examination 109
Abdominal examination 109
Ancillary diagnostics 111
x C on t e n t s
NON-INFECTIOUS DISEASES OF THE DIGESTIVE TRACT AND ABDOMEN 114

Dental problems 114
Normal structure and function 114
Mandibular brachygnathia and prognathia (syns. underbite/overbite) 115
Dental disease 115
Oral problems (excluding dental) 118
Neoplasia 118
Drenching/bolus gun injury 119
Tongue lesions 120
Oesophageal problems 120
Megaoesophagus 120
Obstruction (syn. choke) 121
Forestomach problems 121
Rumen tympany (syn. bloat) 121
Rumen acidosis (syn. carbohydrate overload) 122
Traumatic reticuloperitonitis 124
Surgery of the rumen 124
Trocarisation 124
Rumen fistula 124
Rumenotomy 124
Abomasal problems 125
Abomasal emptying defect (syns. pyloric stenosis,
abomasal impaction, distal vagal indigestion) 125
Abomasal displacement 126
Abomasal ulceration 127
Abomasitis (syn. abomasal bloat) 128
Intestinal problems 130
Intussusception 130
Torsion of the mesentery or mesenteric root 131
Intestinal obstruction 132
Rectal prolapse 132
Exploratory laparotomy 134
Liver and pancreas problems 136
Liver abscessation 136
Hepatic lipidosis (syn. fatty liver necrosis) 136
Ovine white liver disease 136
Metastatic tumours 136
Pancreatic disorders 136
Umbilical disorders 137
Umbilical hernia 137
C on t e n t s xi
Umbilical infections 138

Patent urachus 139
Umbilical surgery 139
INFECTIOUS DISEASES OF THE DIGESTIVE SYSTEM AND ABDOMEN 142
Rotavirus 142
Cryptosporidiosis 142
Coccidiosis 144
Escherichia coli 146
Salmonellosis 147
Yersiniosis 148
Clostridium perfringens (syn. enterotoxaemia) 149
Johne’s disease (syn. paratuberculosis) 151
Parasitic gastroenteritis 153
Liver fluke (syns. fascioliasis, fasciolosis) 159
Small liver fluke (syn. lancet fluke) 160
Tapeworms (cestodes) 160
Metacestode disease 161
Peste des petits ruminants (syn. goat plague) 161
Bluetongue 163
Miscellaneous conditions 163
CHAPTER 6 RESPIRATORY SYSTEM 165

CLINICAL EXAMINATION OF THE RESPIRATORY SYSTEM 165
General aspects 165
Specific observations 165
TREATMENT PRINCIPLES 167
Tracheotomy 167
NON-INFECTIOUS DISEASES OF THE RESPIRATORY SYSTEM 169
Conditions affecting the nasal passages and sinuses 169
Laryngeal problems 169
Aspiration pneumonia 170
Pleural effusion 170
Pneumothorax 171
Toxicities 171
Neoplasia 172
INFECTIOUS DISEASES OF THE RESPIRATORY SYSTEM 172
Contagious caprine pleuropneumonia 172
Pasteurellosis 173
Parasitic pneumonia 174
MISCELLANEOUS CONDITIONS 176
Other Mycoplasma organisms 176
Peste des petits ruminants (syn. goat plague) 176
Caprine arthritis encephalitis 176
xii C on t e n t s
Caseous lymphadenitis 176

Tuberculosis 176
Fungal pneumonia/allergic pneumonitis 176
Vena cava thrombosis 177
CHAPTER 7 CARDIOVASCULAR DISEASE AND DISORDERS OF

THE HAEMATOPOIETIC SYSTEM 179
CLINICAL EXAMINATION OF THE CARDIOVASCULAR SYSTEM 179
Clinical assessment 179
Ancillary diagnosis 180
Blood sampling and basic in-house analysis 180
CARDIOVASCULAR DISEASE 181
Septal defects 181
Endocarditis 182
Pericarditis 183
Cardiomyopathies 184
Other conditions 185
DISORDERS OF BLOOD VESSELS 185
Venous thrombosis 185
Caudal vena cava thrombosis 186
Other vascular abnormalities 187
DISORDERS OF THE HAEMATOPOIETIC SYSTEM 187
Anaemia 187
Milk goitre/thymic enlargement 189
Neoplasia of lymph nodes or thymus 190
Swelling disease 191
Babesiosis 193
CHAPTER 8 NERVOUS SYSTEM DISORDERS 195

CLINICAL EXAMINATION OF THE NERVOUS SYSTEM 195
Consciousness, alertness and behaviour 195
Reflexes, upper motor neurons and lower motor neurons 195
Vestibular syndrome 197
Spinal lesions 197
Peripheral nerves 197
Specific assessment considerations 198
Cerebrospinal fluid collection and analysis 199
Imaging and further diagnostics 201
NON-INFECTIOUS DISEASES 201
Central nervous system 201
Disbudding injury 201
Acquired storage disease 201
C on t e n t s xiii
Inherited central nervous system disorders 202

Swayback (syn. enzootic ataxia) 202
Polioencephalomalacia (syn. cerebrocortical necrosis) 202
Floppy kid syndrome 204
Peripheral nervous system 204
Peripheral nerve paralysis 204
Listerial encephalitis 206
Bacterial meningitis/encephalitis 208
Tetanus 209
Enterotoxaemia 210
Scrapie and bovine spongiform encephalopathy 210
Rabies 212
Aujeszky’s disease (syn. pseudorabies) 212
Louping ill 213
Coenurosis (syn. gid) 213
Cerebrospinal nematodiasis (syn. meningeal worm) 214
CHAPTER 9 MUSCULOSKELETAL DISEASE INCLUDING FOOT DISORDERS 215

CLINICAL EXAMINATION OF THE MUSCULOSKELETAL SYSTEM 215
Ancillary diagnosis 216
Nutritional muscular dystrophy/white muscle disease 217
Rickets 217
Osteodystrophy of mature bone 218
Fractures 219
Bone sequestrum 221
Joint dislocation 223
Tendon injuries 223
Cartilage disorders 224
Bacterial arthritis (syn. joint ill) 227
Mycoplasma arthritis 228
Clostridial myositis 229
Arbovirus infection (Akabane, Schmallenberg) 229
FOOT DISORDERS 229
Laminitis 229
Scald and footrot 230
Treponeme-associated foot disease 232
Overgrown claws 233
Routine foot trimming 233
White line disease 234
xiv C on t e n t s
Pedal joint abscess 235

Foreign bodies and foot lameness 235
Foot and mouth disease 235
CHAPTER 10 URINARY TRACT DISEASE 237

CLINICAL EXAMINATION OF THE URINARY TRACT 237
Urethral obstruction caused by urolithiasis 240
Urethrotomy and urethrostomy 242
Tube cystotomy 243
Renal insufficiency and failure 244
Toxic nephrosis 245
Neoplasia 245
Cystitis and pyelonephritis 245
CHAPTER 11 SKIN DISEASES 249

CLINICAL EXAMINATION OF THE SKIN AND INTEGUMENT 249
NON-INFECTIOUS SKIN DISEASES 250
Pemphigus foliaceus 250
Zinc deficiency (zinc-responsive dermatosis) 250
Pygmy goat syndrome (syn. seborrhoeic dermatitis) 251
Photosensitisation 252
Physical and toxic causes 253
Fibre break or loss 253
Hypotrichosis 253
INFECTIOUS SKIN DISEASES (PARASITIC) 253
Chorioptic mange 253
Sarcoptic mange 255
Demodectic mange 256
Psoroptic mange 257
Lice 257
Ticks 258
Flies 258
Insect bite reactions 260
Besnoitiosis 260
INFECTIOUS SKIN DISEASES (VIRAL/BACTERIAL/FUNGAL) 260
Contagious pustular dermatitis (syns. orf, contagious ecthyma) 260
Goat pox 262
C on t e n t s xv
Bluetongue 263
Peste des petitis ruminants 263
Foot and mouth disease 263
Aujeszky’s disease (syn. pseudorabies) 263
Staphylococcal dermatitis/folliculitis 263
Malassezia 264
Mycotic dermatitis (syns. dermatophilosis, streptothricosis) 264
Ringworm (syn. dermatophytosis) 265
CUTANEOUS SWELLINGS 265
Morel’s disease 265
Lymphoma 265
Neoplasia 265
Thymus enlargement 266
Haematoma 266
Injection site abscesses 266
SURGERY OF SKIN ADNEXA 267
Disbudding 267
Dehorning 267
CHAPTER 12 MAMMARY GLAND DISORDERS 271

CLINICAL EXAMINATION OF THE UDDER 271
Sampling for culture 272
Ultrasonography 272
Trauma 272
Neoplasia 272
Enlarged pendulous udder 272
Maiden milkers 272
Post-partum agalactia 273
Induction of lactation 273
Contagious agalactia 274
Mastitis 275
Udder impetigo (syn. staphylococcal folliculitis of the udder) 281
SURGERY OF THE MAMMARY GLAND 281
Supernumerary teat removal 281
Teat surgery 282
Mastectomy 283
CHAPTER 13 SENSORY ORGAN DISEASE 285

THE EYE 285
xvi C on t e n t s
CLINICAL EXAMINATION OF THE EYE 285

Further diagnostics 286
FIRST AID FOR OCULAR TRAUMA 287
NON-INFECTIOUS DISEASE 287
Entropion 287
Foreign bodies 288
Corneal ulceration and stromal abscessation 289
Neoplasia 290
INFECTIOUS DISEASE 291
Infectious keratoconjunctivitis (syn. pink eye) 291
Uveitis and iritis 293
OCULAR SURGERY 293
Tarsorrhaphy 293
Third eyelid flap 293
Conjunctival pedicle flap 294
Enucleation 294
SYSTEMIC DISEASES AFFECTING THE EYE 295
THE EAR 295
CLINICAL EXAMINATION OF THE EAR 295
NON-INFECTIOUS DISEASE 295
Ear lacerations 295
Tagging injuries 296
Aural haematoma 296
INFECTIOUS DISEASE 297
Otitis 297
Ear tip necrosis 298
CHAPTER 14 METABOLIC DISORDERS 299

Hypocalcaemia (syns. milk fever, eclampsia, parturient paresis) 299
Hypomagnesaemia (syns. grass tetany, grass staggers) 300
Pregnancy toxaemia 301
Lactational ketosis (syn. acetonaemia) and fatty liver complex 303
Metabolic acidosis 304
Floppy kid syndrome 304
Swelling disease in Angora goats 304
CHAPTER 15 TRACE ELEMENT AND VITAMIN DISORDERS 305

TRACE ELEMENTS 305
Copper deficiency 306
Selenium/tocopherol (vitamin E) deficiency
(syns. nutritional muscular dystrophy, white muscle disease) 308
Cobalt deficiency 309
Iodine deficiency 310
Zinc deficiency 311
C on t e n t s xvii
VITAMINS 311
Retinol (vitamin A) deficiency 311
Thiamine (vitamin B1) deficiency 311
Cyanocobalamin (vitamin B12) deficiency 312
Calciferol (vitamin D) deficiency 312
Tocopherol (vitamin E) deficiency 312
CHAPTER 16 POISONING AND TOXICITIES 313

INTRODUCTION 313
GENERAL APPROACH 313
COMMON POISONS AND TOXINS 314
Genus Rhododendron 314
Yew 315
Other plants, trees and shrubs potentially toxic to goats 316
Oxalate poisoning 316
Nitrate poisoning 317
Copper poisoning 318
Urea poisoning 319
Mycotoxins 319
Water source poisons 321
CHAPTER 17 EXOTIC AND EMERGING DISEASES 323

INTRODUCTION 323
Foot and mouth disease (aphthous fever) 323
Bluetongue 326
Tuberculosis 328
Anthrax 329
New and emerging diseases 330
CHAPTER 18 ANAESTHESIA, FLUID THERAPY, EUTHANASIA 333

SEDATION 333
General principles 333
Sedatives 333
Reversal 334
GENERAL ANAESTHESIA 334
Preoperative starvation 334
Preoperative assessment 334
Intraoperative support 334
Hypothermia 334
Induction 335
Inhalation anaesthesia 335
Injection anaesthesia 335
xviii C on t e n t s
Monitoring 336
Recovery 336
LOCAL AND REGIONAL BLOCKS 336
Drugs 337
Specific blocks 337
ANALGESIA 341
Opioids 341
Non-steroidal anti-inflammatory drugs 342
Corticosteroids 342
NMDA receptor antagonists 342
FLUID THERAPY 342
Assessing hydration status 342
Fluid rates 343
Route of administration 343
Choice of fluids 343
EUTHANASIA 344
Lethal injection 344
Free-bullet firearms 344
Captive bolt 345
Conditionally acceptable methods 345
Emergency on-farm slaughter of neonatal kids 345
Unacceptable methods 346
CHAPTER 19 POST-MORTEM EXAMINATION AND SAMPLING 347

INTRODUCTION 347
HISTORY 347
HEALTH AND SAFETY 348
PREPARATION 348
POST-MORTEM EXAMINATION APPROACH 348
SAMPLING PROTOCOLS 351
Bacteriology 351
Histopathology 351
Aborted goat kids 352
APPENDICES 353
1 LABORATORY REFERENCE INTERVALS 353
2 CONVERSION FACTORS 355
3 FURTHER READING 356
INDEX 357
PREFACE
xix
One of the main objectives in writing Goat Medicine and The book is richly illustrated with over 450 images.
Surgery was to bring together in a single text all the Expansions for abbreviations used in the text are
medical and surgical considerations when faced with a listed on page xxi.
goat health or welfare problem, be it a single emergency Anaesthetic procedures and surgical and other
procedure or a long-standing herd problem. The book interventions are dealt with in a structured format
begins by providing the reader with some background and, where possible, within the relevant chapter.
information on goat evolution, behaviour, nutrition Miscellaneous procedures such as fluid therapy,
and basic physiology, and is then divided into a series euthanasia and post-mortem examination are also
of chapters dealing with individual conditions based on covered.
body systems including reproduction. Although written by two UK based authors, the
Each chapter highlights relevant aspects of the book provides a comprehensive overview of goat
specific clinical examination, giving guidance on health and welfare and the diseases and conditions
baseline clinical and physiological parameters and to which they are susceptible around the world. It
the ancillary diagnostic tools that may be available, will be a useful addition to the library of veterinar-
such as relevant laboratory tests and ultrasonogra- ians, undergraduate students and anyone interested
phy or radiography. Each condition is then described in understanding and improving goat health.
in a consistent format, covering its aetiology, patho-
physiology, presenting signs, diagnosis, differen- David Harwood
tial diagnosis, treatment, management and control. Karin Mueller
ABBREVIATIONS
xxi
ACDP Advisory Committee on Dangerous CT computed tomography

Pathogens CV cardiovascular
AI artificial insemination DJD degenerative joint disease
ALD angular limb deformity DGGE denaturing gradient gel electrophoresis
ALP alkaline phosphatase DM dry matter (diet)
AST aspartate transaminase/aspartate EAE enzootic abortion of ewes (see OEA)
aminotransferase EBV estimated breeding value
BAER brainstem auditory evoked response ECF extracellular fluid
BD border disease eCG equine chorionic gonadotropin
BDV border disease virus ECG electrocardiography
BHB beta-hydroxybutyrate EDTA ethylenediamine tetra-acetic acid
BCS body condition score EEJ electroejaculation
BPD biparietal diameter EHEC enterohaemorrhagic E. coli
bpm beats per minute (heart); breaths per ELISA enzyme-linked immunosorbent assay
minute (lungs) EMG electromyography
BSE bovine spongiform encephalopathy EPEC enteropathogenic E. coli
BTV bluetongue virus epg eggs per gram
BVD bovine viral diarrhoea ET embryo transfer; endotracheal (tube).
BVDV bovine viral diarrhoea virus ETEC enterotoxigenic E. coli
CAE caprine arthritis encephalitis EU European Union
CAEV caprine arthritis encephalitis virus FB foreign body
CCN cerebrocortical necrosis (see PEM) FEC faecal egg count
CCPP contagious caprine pleuropneumonia FMD foot and mouth disease
CIDR controlled internal drug release FSH follicle stimulating hormone
(intravaginal progesterone releasing GA general anaesthesia
device) gGT gamma-glutamyl transferase (liver
CK creatinine kinase (measure of muscle function test)
pathology) GI gastrointestinal
CL corpus luteum GLDH glutamate dehydrogenase (liver
CLA caseous lymphadenitis function test)
CMT California mastitis test GnRH gonadotropin-releasing hormone
CNS central nervous system GSH-Px glutathione peroxidase (a selenium
COD cystic ovarian disease dependent enzyme)
CODD contagious ovine digital dermatitis Hb haemoglobin
CP crude protein hCG human chorionic gonadotropin
CPD contagious pustular dermatitis (orf) HCl hydrochloride
CpHV-1 caprine herpesvirus 1 Hct haematocrit
CRI constant rate infusion IFAT indirect fluorescent antibody test
CRT capillary refill time Ig immunoglobulin (IgA, IgE, IgG, IgM)
CSF cerebrospinal fluid IKC infectious keratoconjunctivitis
xxii A bbr e v i at ions
i/m intramuscular OIE World Organisation for Animal Health

IOP intraocular pressure (formerly Office International des
i/p intraperitoneal Epizooties)
i/v intravenous OWLD ovine white liver disease
ISR injection site reaction PAGE polyacrilamide gel electrophoresis
IU International unit PCR polymerase chain reaction
IVRA intravenous regional anaesthesia PCV packed cell volume
KOH potassium hydroxide PDA patent ductus arteriosus
L1 first-stage larvae – also L2, L3 PDS polydioxanone
(nematode life cycle) PEM polioencephalomalacia (see CCN)
LDH lactate dehydrogenase PGE parasitic gastroenteritis
LH luteinising hormone PGF2α prostaglandin-F 2 alpha
LMN lower motor neurone PME post-mortem examination
MAP Mycobacterium paratuberculosis subsp. PMI point of maximum intensity
paratuberculosis PO2 partial pressure of oxygen
MCH mean corpuscular haemoglobin PPR Peste des petits ruminants
MCHC mean corpuscular haemoglobin PPV positive pressure ventilation
concentration PrP prion protein
MCV mean corpuscular volume PSP phenolsulphonphthalein
mEq milliequivalent RAMALT rectoanal mucosa-associated lymphoid
MGA megestrol acetate tissue
MHz megahertz RFM retained fetal membranes
MJ ME megajoules of metabolisable energy SAP serum alkaline phosphatase
ML macrocyclic lactone (includes the SARA subacute ruminal acidosis
avermectins and the milbemycins) s/c subcutaneous
MRI magnetic resonance imaging SCC somatic cell count; squamous cell
MTB Mycobacterium tuberculosis carcinoma
MV maedi visna (sheep) SDH sorbitol dehydrogenase (liver enzyme)
MZN modified Ziehl–Neelsen SICCT single intradermal comparative cervical
NaCl sodium chloride test
NaHCO3 sodium bicarbonate SRLV small ruminant lentivirus
NDF neutral detergent fibre (in diet) T3 triiodothyronine
NEB negative energy balance T4 thyroxine
NO2 nitrogen dioxide TB tuberculosis
NSAID non-steroidal anti-inflammatory TBC total bacterial count
drug TLC ‘tender loving care’
NTEC necrotoxigenic E. coli TMR total mixed ration
OC osteochondrosis TP total protein
OD outer diameter (tubing); optical density TSE transmissible spongiform
(laboratory test results) encephalopathy.
OEA ovine enzootic abortion (see EAE) WBCC white blood cell count
Off-cascade Relating to use of drugs. The UK UHT ultra-high temperature (usually
veterinary prescription cascade can not referring to high temperature
be applied to such drugs processing of e.g. milk)
Off-licence Relating to use of drugs. Such drugs UK United Kingdom
are licensed in food producing animals, UMN upper motor neurone
but for any of: a different species, US/USA United States of America
another indication, another route of UV ultraviolet
administration, another dose rate ZN Ziehl–Neelsen
CHAPTER 1
INTRODUCTION
1
EVOLUTION •• Provision of shelter from predators and the

environment.
Goats are one of the earliest examples of a domes- •• Provision of food.
ticated animal. Around 12,000 to 14,000 years ago,
our Neolithic ancestors began the process of domes- From a domestication perspective, goats are with-
tication of the arable crops and livestock resources out doubt the best example of a multipurpose spe-
available to them at that time. It is this process that cies, providing the following benefits for those who
underpins what we recognise today as our modern have domesticated them:
agricultural and farming practices. Approximately
40 distinct livestock species have been domesticated, •• Milk.
but only six species are currently found on all con- •• Meat.
tinents, namely goats, cattle, sheep, pigs, horses and •• Skins to keep warm, for carrying water (and
donkeys. wine), as flotation devices for crossing water.
Archaeological records can give us some indi- •• Fibre for clothing.
cation of timescales, with the goat exhibiting the •• Dried faeces for fuel.
earliest signs of domestication around 10,000 years •• Transport through pulling small carts.
BP. BP is the abbreviation for the archaeological •• Goat kid skin used as parchment.
term ‘before present’, which is based on the year
1950 when carbon dating first became widely avail- As a result of domestication and a much closer
able. For comparison, these same records show contact between our ancestors and the species they
sheep domestication at 8,500 years BP and cattle began to ‘keep’, it is hardly surprising that goats
at 7,000 years BP. All figures refer to the earliest began to feature in many other aspects of their lives,
archaeological evidence of domestication based on and goats have regularly been referred to in the arts,
the circumstances in which such evidence was found. mythology, the bible and common folklore.
The oldest goat remains indicative of domestication Following this early domestication, goats today
were found in Iran, but the process appears to have are one of the most widely kept domestic animals
fanned out from there to the near and middle east worldwide, mainly as a result of the relative ease
and the northern Indian subcontinent. with which they can be kept and the obvious ben-
Records suggest that modern goats have all efits provided to those who keep them. In 2011, it
evolved from the wild Bezoar goat (or Bezoar Ibex) was estimated that there were more than 924 mil-
of the Zagros Mountains in Iran and Iraq, a species lion live goats around the globe, according to the
still found in the region today. UN Food and Agriculture Organization. The larg-
The key elements to domestication include: est population is in China, with an estimated 149
million goats making up around 16% of the total
•• Breeding in captivity with control of the world goat population. India follows with approxi-
breeding cycle. mately 125.7 million and Pakistan with 56.7 million,
•• Modification to make them more useful/ followed by Bangladesh, Nigeria, Sudan, Ethiopia,
productive. Iran, Mongolia and Indonesia. According to 2012
2 Chapter 1
data there are just over 2.6 million goats in the USA, milk for their own consumption. This practice began
heavily concentrated in the south west, particularly to decline towards the end of the 18th century with
in Texas. Australia reports between 3 and 4 million the Enclosure Movement, which effectively began to
goats, of which only around 0.4 m illion are farmed, place what was formerly common land into private
the remainder being referred to as range or ‘free ownership. The availability of common land then
living’ goats. Within Europe, Greece has the largest declined as it was fenced off and farmed. From the late
population of around 5 million, followed by Spain 19th century through to around 1940, goat keeping
(3 million) and France (1 million). The UK has a was mainly confined to rural families and those with
relatively small population of around 100,000. poorly paid jobs such as miners and railwaymen. Due
The evolution of goat keeping will vary from to the need for food and the effects of food ration-
country to country. In the UK, for example, many ing during the Second World War, goat keeping did
families kept one or more ‘house goats’, to produce enter a period of growth, but there was then a gradual
decline after the war ended. The British Goat Society
(holding the pedigree goat herd books) was founded
in 1879, and with the exception of the Hereford cattle
herd book is the oldest such record in the UK.
Modern goat keeping gives us a full spectrum of
activity from nomadic tribes moving from location
to location with their animals, to the range keep-
ing activities in Australia, to units fattening goat
kids for meat and to intensive goat dairy production
systems in which several thousand goats are housed
and milked through highly automated parlours.
Alongside these production systems are those in
which goats are kept in small numbers as a hobby,
as pets and at public attractions where their docile
and inquisitive behaviour make them popular with
Fig. 1.1 Nomadic goats in India. all ages (Figs. 1.1–1.3).
Fig. 1.2 Goats in Norway. Fig. 1.3 Intensive dairy goat farming in the UK.
Note the high stocking rate and raised feeding table.
I n t roduc t ion 3
This background information gives the reader

an insight into the wide range of environmental,
management and socio-economic factors that have
an influence on goat health and welfare worldwide,
each of which needs to be considered when arriving
Hip joint
at a diagnosis and formulating therapeutic and pro-
phylactic regimes.
Stifle joint
GOAT BREEDS AND THEIR PURPOSES
The goat is a member of the family Bovidae and is

closely related to the sheep, as both are in the goat-
antelope subfamily Caprinae. Goats (genus Capra)
have 60 chromosomes and sheep (genus Ovis)
have 54. Goats and sheep can very rarely breed with
Fig. 1.4 The distinct face marking of Toggenburgs
each other, and although most offspring will be
is similar to that of the British Alpine, but their base
stillborn, there are a number of reports of offspring
colour is grey to grey–brown. This image also shows
surviving with a chromosome count of 57. Such off-
restraint by a neck collar. The dotted line outlines
spring are often referred to colloquially as a ‘geep’.
the quadriceps muscle (suitable for intramuscular
It is estimated that there are now over 300 dis-
injections).
tinct breeds of goat kept worldwide, many having
been bred selectively to enhance a particular trait
to increase productivity, quality or survivability. As Goat meat is consumed by around 75% of the
an example, the Saanen and its derivatives comprise world’s population. In countries such as the UK and
the most popular dairy breed. Other dairy breeds USA, the majority of goat meat has traditionally been
include the Toggenburg (Fig. 1.4) and its deriva- eaten by some ethnic communities only, but there is
tives, the British Alpine and the Anglo-Nubian. increasing evidence of a wider developing demand
The most popular fibre breed is the Angora, which for goat meat. Gourmet wholesale and retail markets
produces mohair. Cashmere is not a breed of goat (many of which are internet based) and local restau-
but describes the soft underhair that grows as an rants are beginning to stock goat meat, leading to
insulating layer, and goats are farmed commercially new goat meat units, both specialist and those rear-
for this. One of the most popular meat breeds is the ing male kids surplus to the dairy sector (Fig. 1.5).
Boer goat, originating from South Africa and bred Part of this increasing popularity is the goat’s rep-
specifically for carcass conformation and meat yield. utation as a healthy meat alternative in comparison
Pygmy goats are commonly kept as pets in the UK with other red meats. It is low in fat, cholesterol, cal-
because of their small size. The breed originates orific energy and saturated fat (50% lower in c alories
from West Africa and they are more accurately than beef and around 30% lower in saturated fat
described as West African Dwarf goats. than chicken; Table 1.1).
There will be local variation in terminology used,
but in broad terms, female goats are referred to as GENOMICS
‘does’ or ‘nannies’, entire males as ‘bucks’ or ‘bil-
lies’, and their offspring are ‘kids’. Castrated males The goat genome was the first reference genome for
are ‘wethers’. Meat for human consumption from small ruminant animals to be defined. This has led to
younger animals is called kid or cabrito (Spanish), an increased interest in harnessing these techniques
and from older animals is simply known as goat meat to improve goat health and productivity, focussing
or, sometimes, is called chevon. on identifying desirable and undesirable traits.
4 Chapter 1
Table 1.1 Composition of meat of various species (per 85 g [3 oz] roasted meat).
CALORIES FAT (G) SATURATED FAT (G) PROTEIN (G) IRON (G)
Goat 122 2.58 0.79 23 3.2
Beef 245 16.0 6.8 23 2.0
Pork 310 24.0 8.7 21 2.7
Lamb 235 16.0 7.3 22 1.4
Chicken 120 3.5 1.1 21 1.5
Source: United States Department of Agriculture.
It is important to ensure that top performing

goats have high functional fitness. By using confor-
mation assessment and scoring of relevant physical
attributes (such as legs, feet, udders and teat confor-
mation), EBVs can be developed. Combining these
with production trait EBVs should ensure that high
productivity is achieved without compromising
overall robustness.
Accelerating the rates of response to selection can
be achieved by improving the accuracy of selection,
reducing the generation interval (keeping younger,
more productive animals with a higher genetic merit
than the previous generation) and only selecting the
very best animals for breeding.
This is an evolving process, and it will become
more widely available and technologically advanced.
BEHAVIOUR
Goat behaviour can be interesting, unusual and at

times frustrating. Domestication has had an impact
on what could be described as a goat’s natural behav-
iour when running wild, although the constant
objective for any goat keeper should be to not inhibit
Fig. 1.5 Goat carcases recently slaughtered and such behaviour in any way that could compromise
dressed. overall goat health and welfare.
Goats develop strong bonds with each other, par-
Using commercial milk production as an exam- ticularly with siblings and other family members,
ple, it is recognised that there are considerable dif- and as a result, separation can have a negative impact
ferences between the performances of daughters on welfare. When kept in increasing numbers, they
from different sires in their milk yield, milk quality, will develop close groups each with their own strong
conformation, disease resistance, live weight, feed hierarchical structure, with regular confrontations
intake and other traits. By selecting goats that are (head to head butting, Fig. 1.6) to establish domi-
genetically more productive by using, for example, nance by both males and females. For this reason,
estimated breeding values (EBVs) as an aid to selec- it is inadvisable to keep goats with horns and goats
tion, cumulative benefits can be realised. that have been dehorned/disbudded or are naturally
I n t roduc t ion 5
Fig. 1.6 Goats head to head butting. This may be Fig. 1.7 A goat browsing through the fence.
playful or used to establish dominance.
switches, electric cables, gate fasteners). They can
polled together, to avoid potentially harmful con- stand on their hind legs, reaching up to 2 metres
frontations. It follows, therefore, that goat groups above the ground, therefore any building, paddock
need to remain fairly static where possible – constant or yard should be constructed in such a way that it
movements and regrouping can be unnerving and is not simply stock-proof but ‘goat proof’; they are
lead to reduced milk yields, and may even predispose masters of escape (Fig. 1.7).
to illness. Goats should be moved in pairs or small Goats are good climbers and extremely agile,
groups (e.g. after kidding) so that they integrate into clambering into and over obstacles that are of inter-
the herd faster and face significantly fewer interac- est, including trees. This natural behaviour, although
tions than if they were introduced individually. to be encouraged, can also lead to misadventure as
Separating goats from the herd should be avoided goats can get caught up in fencing, netting or other
whenever possible. If isolation is necessary, then as material with broken limbs a possible sequela, par-
much as is practicable, locate the isolated goat in ticularly in young kids, and strangulation at any age
a pen nearby or adjacent to the herd or provide it if an inquisitive head gets caught (Fig. 1.8).
with a companion. Keeping small groups of animals This inquisitive and gregarious behaviour
together when handling for veterinary procedures should be fostered at all times, avoiding barren
such as blood sampling will mean that they remain
much calmer and easier to handle.
Goats also appear to develop an affinity for own-
ers, and are often unnerved by changes in owner and
environment.
There may be subtle breed differences in behav-
iour. In the UK, for example, British Alpine, British
Toggenburg and Saanen goats appear to be more laid
back and are not easily unnerved, whereas Anglo-
Nubian and Golden Guernsey goats are more easily
unsettled, although as ever there will be individual
exceptions.
Goats are gregarious animals, can become e asily
bored and will constantly look for stimuli, hence
their apparent desire to investigate anything in their Fig. 1.8 A goat’s inquisitive nature can result in its
environment by licking and chewing (including light head becoming trapped.
6 Chapter 1
environments and instead providing environmental when something is wrong. Knowing your stock is
enrichment. The following can be very simple fix- vitally important.
tures for goats to climb onto: There are three reasons why a normally quiet,
placid goat may start bleating, and particularly bleat-
•• Mounds of earth, or a large stone (Fig. 1.9a). ing more constantly:
•• An old trailer (Fig. 1.9b).
•• Straw bales (Fig. 1.9c). 1 When they are hungry or thirsty. This is usually
•• Large plastic drums open at one end to roll around. alleviated by giving food or water, with a quick
return to normal behaviour.
Places to hide in or under are also important; 2 During the breeding season, particularly when
goats have evolved as prey species and as such will a doe is on heat, or during the latter part of
seek out a place of safety if frightened. pregnancy as kidding approaches.
When considering the individual goat as a clini- 3 Finally, when a goat is sick or in pain and, as
cian, it is useful to bear in mind that they are usu- with the human voice, the volume and pitch
ally very quiet individuals, and it is not often that will change depending on the intensity of
you will hear a goat vocalising for no reason. A goat pain or discomfort. Conversely, as the animal
starting to vocalise more is often a sign that some- deteriorates the sound will be of a lower
thing is wrong. In contrast, some goats make gentle intensity in a goat that is feeling really miserable.
noises when they are content and become quieter
Goats seem to have a relatively low pain thresh-
old when compared with other farm animals such as
cattle. They do not tolerate ill-health very well, and
a diligent owner will be aware of this and the need
to give plenty of TLC (‘tender loving care’) to any
sick goat to ensure it continues to feed, is warm and
comfortable, and maintains an interest in life.
In the wild, a pregnant doe will separate herself
away from the main herd and attempt to hide as
kidding becomes imminent. She may attempt this
behaviour when confined, even attempting to build
a nest in which to hide the kid after it is born. One
consequence of this behaviour is the rapid inges-
(a) tion of placenta and any other products of kidding
(b) (c)
Figs. 1.9 Environmental enrichment. (a) Encouraging safe climbing (top). (b) Making hay feeding fun (left).
One disadvantage is potential faecal contamination of feed. (c) Playing with a straw bale (right).
I n t roduc t ion 7
or abortion to conceal the birth; this can be partic- from around the tree base, and given the opportu-
ularly frustrating when investigating the causes of nity will also climb up into trees to continue their
abortion. More information on kidding and care of search for feed. When kept in confinement, goats
the neonate can be found in the relevant chapters. are often very wasteful of their feed, as they sort
In summary, there are certain behaviours the goat through and discard even good quality forage. They
needs or wants to perform. Allowing these can pro- are extremely fussy about the quality of their feed,
mote welfare, denying them can lead to stress, bore- readily refusing to eat spoiled or contaminated feed.
dom and frustration. Secondly, physical and mental Their preferred pasture sward height is similar to
health can be expressed in behaviour. Understanding cattle (i.e. 7–8 cm).
behavioural needs and assessing behavioural activi- The exact nature of the diet fed will vary between
ties displayed can help prevent and solve health geographical regions dependent on what is avail-
problems on the farm. able, but should consist of a source of forage (most
commonly hay; Figs. 1.11, 1.12) for maintenance,
NUTRITION balanced where necessary to allow for pregnancy,
lactation and growth by additional compound, con-
Many generic aspects of the nutrition and feeding centrate or cereal feed. Both grass and maize silage
of goats are similar to other farmed species. Because (often as part of a total mixed ration [TMR]) are
they are ruminants, the principles of rumen function widely fed to commercial herds and, as with other
(and dysfunction) should be understood. Weight for ruminant species, good silage making and subse-
weight, a dairy goat will produce considerably more quent storage are key factors, partly to ensure a good
milk than the equivalent dairy cow, but it will only palatable and nutritious product, but also to reduce
achieve this potential if it is fed properly, with a daily the risk of high levels of Listeria organisms, to which
intake of an adequate quantity of feed of the correct goats are very susceptible (Figs. 1.13, 1.14).
nutritional value and in a form that the goat will eat. It is important to ensure that all goats can feed
Goats have evolved into very efficient brows- together when providing any feedstuff in which
ing animals (versus cattle and sheep who are graz- individual component parts are still visible (such as
ers). They will readily eat grass, thistles and other a course mix). If there is insufficient trough space
weeds, hedgerow and leaves and branches from over- available for all goats to feed simultaneously (rec-
hanging trees, often standing on their hind legs to ommended linear space is 0.75–0.95 metres per
achieve this (Fig. 1.10). When other sources of feed adult goat), then the dominant goats can selectively
(‘browse’) are in short supply, they will eat the bark consume the best bits, leaving the poorer quality
Fig. 1.10 Browsing and feeding behaviour extends to Fig. 1.11 Feeding dried lucerne (syn. alfalfa) in
weeds and even thistles. Norway.
8 Chapter 1
Fig. 1.12 Big-bale haylage in Iceland. Fig. 1.13 Feeding a total mixed ration, based on
maize silage, on a commercial dairy unit in the UK.
translates to about 8.5 MJ of ME for a 50 kg goat and

10.5 MJ of ME for a 70 kg goat. For animals at pas-
ture, an additional 20–25% is allowed for increased
activity levels. An additional 6 MJ of ME/day above
maintenance is added in the last 2 months of preg-
nancy. Lactation requires 4.4 MJ of ME/kg of milk
produced (at 3.5% fat).
To fulfil baseline dietary protein requirements,
a maintenance ration should have 11% crude pro-
tein (CP) (averaged across the entire ration), and
for lactation or growth 14% CP. Rumen unde-
gradable protein should be increased for lactation
(e.g. soya bean meal).
Monitoring body condition and balancing this
Fig. 1.14 A maize silage clamp. Aside from good condition to the nutritional demands of the goat and
techniques during harvest, ensiling and storage, good the available feedstuff is important. Goats are often
face management is important. described as looking thin when compared with sheep
and cattle. They have evolved essentially as tropical
constituents for subordinate goats. Feeding a com- and subtropical animals and, as such, have only mini-
mercial pellet or other well milled product will mal subcutaneous fat, their body fat stores being laid
overcome this problem. Overfeeding is common in down internally, particularly in the abdominal cav-
goats, especially when fed titbits. ity and omentum (Fig. 1.15). Due to the variation
As with any ruminant feeding programme, it is in rumen fill, body weights are less reliable in rumi-
important to ensure that any dietary change is made nants, hence the widespread use of condition scoring
gradually to allow the rumen microflora to adjust (Fig. 1.16). The lack of subcutaneous lumbar fat in
and mitigate against any potential dietary disorders goats, however, makes the procedure less reliable than
such as rumen acidosis, bloat or enterotoxaemia. in cattle and sheep, and a second assessment should be
Baseline energy requirements are: 0.44 MJ of made by palpation of the fat pad overlying the ster-
ME (megajoules of metabolisable energy)/kg body num – this is convex in goats in good condition and
weight 0.75 for maintenance in the housed goat, which progressively concave in thinner goats (Fig. 1.17).
I n t roduc t ion 9
Score 1 Score 2
Score 3
Score 5
Score 4
Fig. 1.15 Goat fat storage site – abdominal cavity. Fig. 1.16 Schematic illustration of the lumbar area
for different body condition scores (in cross-section;
muscles shaded pink, bone shaded nude, fat deposits
shaded light blue).
Score 1 Score 2
Score 3
Score 4 Score 5
Fig. 1.17 Schematic illustration of the fat deposits Fig. 1.18 Satisfactory water provision with multiple,
(shaded grey) overlying the sternum (shaded largely clean drinking points. Automatic drinkers,
turquoise) and ribcage (shaded pink). such as these, must be checked regularly for full
functionality. Note: Positioning water points at the
In a commercial herd, it would be advisable to
back of the bedded area should be avoided, as wet and
condition score all or a proportion of goats at:
poached bedding invariably results.
•• Drying off.
•• Last 2 weeks of gestation.
•• 6 weeks into lactation. Water must be easily accessible, and also be kept
•• Turnout onto pasture (if grazing). clean and free from extraneous debris, or goats will
•• Beginning of breeding season. refuse to drink (Figs. 1.18–1.20). A goat may drink
up to 18 litres of water (4 gallons) each day, depend-
Suggested target condition scores (on a scale of
ing on climate and ambient temperature, type of diet
1 to 5 with 1 = thin):
fed and milk yield. A lactating goat requires 1.4 litres
•• Kidding: 3.0–3.5. (0.3 gallons) of water per 1 kg (2.2 lb) milk produced.
•• Service: 3.0–3.5. At least 10% of the goats in a group must be able to
•• During pregnancy: 3.0. drink at the same time.
10 Chapter 1
Fig. 1.19 Poor water provision. The water is dirty Fig. 1.20 A water bowser, here self-made using an
and access is partially obstructed by a board. Also, intermediate bulk container on a trailer, provides a
being placed in the bedded area means that the trough satisfactory way to get water to paddocks. The bowser,
is unlikely to be emptied and cleaned regularly. as well as the trough, should be cleaned regularly
(e.g. with dilute bleach). Natural water sources for
Problems related to vitamin or mineral disorders grazing animals are suboptimal. Water quality in
do occur in goats, but when outdoors their natural stagnant bodies such as ponds is often poor, and
browsing activities do seem to result in fewer defi- rivers or streams may carry pathogens from upstream
ciencies than might be expected when compared with livestock farms.
other ruminants (specific disorders are discussed in
Chapter 15). A well balanced diet (with known nutri-
tional values) is key to preventing deficiencies or
toxicity, with problems more likely to occur when
feeding forage alone, home mixed rations or by rely-
ing too heavily on ad-libitum mineral blocks or free
access mineral, where individual intakes will be vari-
able and haphazard.
It is important to remember some fundamen-
tal principles related to the safe storage and use
of any composite feed or feed constituents, which
can pose a potential risk to goat health if they are
not followed. Owners and stock-keepers should be
encouraged to:
Fig. 1.21 Good feed safety on a small-holding:
•• Obtain feed from safe and reliable sources.
concentrates are stored in bins with secure lids, and the
•• Store feed securely to prevent access (where
buckets are turned upside down after feeding to reduce
possible) by rodents and wild birds in particular
the risk of contamination and attraction of wildlife.
(Fig. 1.21).
•• Recognise unexpected changes in colour, odour,
texture or appearance. •• Ensure that feed labels are kept and notes made
•• Know where in any rearing or production of dietary constituents contained therein.
system there may be a potential for unacceptable •• Ensure that all those involved in feeding goats
feed risks to occur (e.g. change in dietary have clear and concise feeding instructions
constituents or feeding programmes). (Fig. 1.22).
I n t roduc t ion 11
Fig. 1.22 Simple, but effective feed board for the Fig. 1.23 A horizontal board provides protection
kidding period, showing number of animals per pen from down draughts in a goatling pen.
and whether supplementary feed has been given on a
particular day (dates along the top).
The target is to provide air changes (stale air out;
fresh air in) of at least 30 m3/hr during the winter,
ENVIRONMENT and 120–150 m3/hr throughout the summer. For the
majority of time (around 95%) in the UK, air speed
Housing is above 1 m/sec, which allows suitable ventilation
The ideal housing environment for goats is very provided there is sufficient air inlet and outlet. For
similar to that required for other livestock. It should the remaining 5% of time, ventilation is reliant on
provide as a bare minimum: the ‘stack effect’ (i.e. warm air rises and is vented
from the apex of the roof and in doing so pulls fresh
•• Adequate ventilation free of draughts (Fig. 1.23). air into the building). If the outlet is insufficient or
•• Temperatures not exceeding upper or lower the inlet area is too small or compromised by sur-
critical levels in summer and winter. rounding buildings or other features such as trees,
•• Plenty of light, including artificial lighting for then natural ventilation will fail. This results in the
the hours of darkness to meet physiological air cooling and collapsing back on to the bedding
needs and allow inspection; however, an and goats. This stagnant air is damper, leading to
appropriate period of rest from lighting must be greater levels of dust particles, bacteria and viruses.
provided each day. Stack effect ventilation depends on heat generated
•• Enough room to be able to move around by the stock, temperature difference inside and out,
freely (minimum 2.0–2.5 m 2 floor space/goat; height difference inlet to outlet, and the inlet and
Fig. 1.3). outlet areas.
•• Good access to food and water (Figs 1.3, 1.18). Adequate air inlet can be provided by space
•• A dry bed to lie on. boarding, or Yorkshire boarding in very exposed
areas. Boarding is usually placed above a wall that is
Effective ventilation removes heat, water vapour, higher than head height to avoid potential draughts.
microorganisms, dust and gases. It distributes air An alternative to space boarding is the installa-
evenly and prevents draughts. These factors com- tion of curtain sides to the building, which allows
bine to reduce stress in housed goats, reduce the the amount of air admitted through the inlets to be
amount of bedding required, improve the environ- varied according to prevailing weather conditions.
ment leading to an improvement in productivity, and These curtains can be lifted and raised manually
potentially reduce respiratory problems. or automatically and provide greater environmental
12 Chapter 1
control. As a general rule of thumb, inlets should should be placed well out of reach. Door fasteners
amount to 50% of the surface area of the side of the need to be of a type they cannot open, and any sharp
building, bearing in mind that neighbouring build- or projecting objects should be removed or covered.
ings and trees can potentially disrupt airflow. Where possible there should be two openings to any
Suitable outlet ventilation can be provided by an building or section, to prevent any dominant goat
open ridge. Concern is often expressed about rain from blocking others entering or leaving.
and snow falling on to the floor below. If the area Some form of shelter should be available for goats
beneath is a feed table, then this is unlikely to be when outdoors, to offer shade and protect them from
a major issue – in reality very little rain does come inclement weather, in particular wetness and wind.
through an open ridge in adequately stocked build-
ings. An alternative ridge design is the protected Fencing
ridge, which still provides the correct area of air There is no such thing as a 100% goat proof fence.
outlet, but minimises the chance of rain coming Fences should be strongly constructed, prefer-
through. ably of a material that they cannot get their head
Goats are homoeothermic animals and need to caught in, and high enough that they cannot jump
maintain a constant body temperature of between over (minimum 1.2 metres [4 feet]). Goats will often
38.7° and 40.7°C. Correct building design and venti- stand with their hind legs on top of a fence to reach
lation take account of the goats’ thermoneutral zone overhanging branches, and if this is done repeatedly,
(i.e. the temperature range at which the animals then even a strong fence may sag or collapse in time.
operate most efficiently). The range of temperature Some goat keepers use electric fencing or electric
of the comfort zone does vary according to breed fence topping wire to good effect.
and their habitat of origin, and is influenced by lev-
els of body fat, thickness of coat and diet. However, Tethering
as a generalisation, most breeds found in the UK Goats are occasionally kept on tethers when out-
have a lower critical temperature of 0°C (i.e. a tem- doors, and specifically when kept in areas that are
perature below which they need to convert feed into difficult to fence around. It is important, however, to
heat and where they feel cold). In extreme cases tem- ensure that adequate care is provided at all times, as
peratures below the lower critical temperature can tethered goats are particularly vulnerable to attack by
lead to reduced feed intake, potentially resulting in dogs, to getting caught up in the tether, to knocking
nutritional disorders such as pregnancy toxaemia. over feed and water supplies out of reach, and to any
The upper critical temperature is around 30°C, at extremes of weather from which they cannot escape.
which temperature goats potentially become heat
stressed, although this figure will depend on breed HANDLING
type and local environmental factors such as average
daily ambient temperature and humidity. Heat stress Goats need to be handled to move them from one
in turn can lead to low-grade production problems location to another, for management procedures
through reduced feed intake, digestibility and rate such as medication or foot trimming, and for clinical
of passage through the gut, to more serious conse- procedures. Any such procedure should be under-
quences including death in extreme cases. taken in a manner that will keep stress levels to an
Relative humidity has an influence on the ther- absolute minimum.
moneutral zone. In winter, it can make the animal’s There are a number of generic factors to consider
coat wet, which reduces the insulating properties. In when handling ruminants:
summer, it reduces evaporation and limits heat loss.
Additionally, care should be taken to make the •• They have excellent peripheral vision.
building ‘goat proof’. As stated previously, goats are •• They prefer to move towards light and do not
inquisitive animals, so electric cables and switches like to enter dark buildings.
•• They have a natural herding instinct, and can PHYSIOLOGY AND BODY FEATURES
become distressed and agitated if they are
separated from the rest of their group. Baseline physiological information is provided at the
•• They like to follow a leader. beginning of each chapter.
•• If a handling procedure is stressful or
frightening, this unpleasant experience may well Lactation
make any future similar experience even more Goats will start lactogenesis at the end of pregnancy,
stressful, so get it right first time round. but unlike other ruminants some females can lactate
spontaneously (so called maiden milkers). Milk pro-
Additionally, goats’ natural inquisitiveness for duction will vary tremendously between breeds, and
anything they encounter, together with their friendly will also be dependent on nutritional input. Dairy
disposition, can ‘slow things up’. As with other rumi- breeds typically produce around 1,000 litres per lac-
nants, they will want to move as a group, but there tation, with some top females capable of 2,000 litres
are often complex mini or family groups that may per lactation. Lactation lengths are often extended
lead to increased hesitancy when driven. Their abil- to 365 days or longer. Milk composition is similar to
ity to escape should never be forgotten. Gates and cattle, although milk taints are occasionally reported
other barriers will need to be higher than those used as a problem (Table 1.2).
for sheep, and any potential escape hole or gap will be
explored. When stressed some goats will simply lie Horns
down and can become trampled and suffocated – for Most goat kids are born with the horn bud already
this reason, always keep groups to be handled small developing. Some kids can be born naturally polled,
and manageable. but in many dairy breeds, such as the Toggenburg,
Individual goats should be caught by firmly plac- Saanen and Alpine breeds of European descent, this
ing an arm around their neck or torso, or by grab- is linked genetically to an infertility trait. In these
bing at a collar or horns (Fig. 1.4). The latter should breeds the presence of horn buds is determined by
be a last resort, as goats resent being pulled by their a recessive gene. The polled trait is dominant, but
horns and it may encourage head-butting, even is linked to a recessive gene for infertility. A female
though it is tempting to use the horns as ‘handles’. goat that is homozygous for the polled gene develops
Once caught, tame goats will usually remain fairly into a sterile intersex.
calm, and can be trained to be haltered and lead
around. Struggling goats are best backed into cor- Coat
ners, and may be straddled for procedures such as The coat of all goats is formed basically of primary
drenching. follicles producing long coarse guard hairs, and sec-
Foot examination and trimming is best carried out ondary follicles producing undercoat or down. It
in the standing position, although there are handling is the secondary follicle in Angoras that has been
crates designed to hold goats firm if large numbers are selectively modified to produce mohair. In tropical
to be examined (see Fig. 9.22). Goats can be placed regions, the undercoat is minimal or absent, while
onto their haunches as with sheep but, unlike sheep,
they rarely become passive and will often continue to
Table 1.2 C
omparative average composition of
struggle; however, this approach may be useful when goat and cow milk.
examining the penis and prepuce of males.
Care should be taken at all times to protect the DRY MINERAL
handler from injury, particularly when working MATTER PROTEIN FAT LACTOSE MATTER
closely with horned goats where there is a potential Goat 12.1% 3.4% 3.8% 4.1% 0.8%
risk of injury to the face and eyes (safety goggles Cow 12.2% 3.2% 3.6% 4.7% 0.7%
should be considered).
14 Chapter 1
secondary follicle undercoat production is greatly •• Recent disease or management problems and
increased in colder climates. Cashmere is the fine changes, including seasonal changes and weather
downy undercoat of many goat breeds. events.
•• Local disease occurrences.
Wattles
Many goat breeds have ‘wattles’ found in the throat For the individual animal,
area (see Fig. 2.3, p. 22). They have no known func- history of interest
tion and consist of a central cartilage core, smooth Includes:
muscle, connective tissue, a blood and nerve supply,
and covering skin. •• Signalment: age, gender, breed, home-bred or
bought-in (and when), value.
Weight •• Specific concern or complaint of owner, and
With more than 300 distinct goat breeds worldwide, atypical behaviour noted (in particular feed
there is a wide variation in body weight, but as a intake).
rough guide approximate goat weights are: •• Others in the group or herd affected, including
other clinical signs that could be part of
Adult dairy Doe 55–105 kg (120–230 lb) the same picture (e.g. salmonellosis causing
Buck 75–120 kg (165–265 lb) abortion and diarrhoea). Where group problem,
Adult Angora Doe 33–55 kg (73–120 lb) morbidity and mortality, and timeline.
Buck 70–85 kg (155–187 lb) •• Production status of animal and interval to
last major event: for example, drying-off,
Adult Pygmy Doe 22–27 kg (48–60 lb)
parturition, weaning.
Buck 28–32 kg (62–70 lb) •• Production data for the animal: milk yield,
weight gains, reproductive events.
Longevity •• Gradual or sudden onset, and any potential
When kept as pets or companion animals, goats can triggering events.
live well into their teens and occasionally beyond •• Health history of this particular animal,
20 years of age. Such geriatric goats may need spe- including routine treatments: for example,
cial care. vaccination, anthelmintics, castration.
•• Environment of animal: housed or at pasture,
HISTORY TAKING AND and recent changes to this.
CLINICAL EXAMINATION •• Diet and any recent changes to this (deliberate or
accidental).
Relevant history is unique to each case; however, •• Treatments administered by farm for current
there are common important aspects to consider. problem, and response seen. Also taking into
consideration that recent treatments may mask
Farm related history of interest clinical signs.
Includes:
Basic clinical examination
•• Type and purpose of enterprise: meat, dairy, Specific ancillary diagnostics will be highlighted in
smallholding, pedigree, etc. the relevant chapters.
•• Closed or open. If closed, soundness of policy/ Observations of the environment, and the patient
risk of breaches. If open, buying-in policy. at a distance, are important and include:
•• Other species or enterprises managed
concurrently (for example, arable contractor or •• Animal’s environment: water availability and
farm shop). quality; feed types, availability and quality;
•• Routine preventive protocols. space allowance; bedding quantity and quality;
ventilation, draughts and unpleasant smells; skin lesions, masses or nodules, supramammary
ambient temperature; exposure to inclement lymph nodes.
weather; signs of disturbance (for example, •• Locomotor system: stance and gait, stride
breakages, animals rubbing against structures); length, weight-bearing, swellings, abnormal
undesirable components (waste products, angulation or sounds, foot horn integrity.
poisonous plants, injury risks, etc.). •• Neurological system: mental state and
•• Group behaviour and interactions: bullying, behaviour, ability to stand and rise, stance and
crowding, restlessness or agitation. gait, head position, skin sensation, reflexes.
•• Patient behaviour: proximity to group, stance
and gait, respiratory rate In the neonate, particular attention should be
paid to the presence of congenital defects.
The clinical examination itself may either address
body systems one at a time, or follow a ‘nose-to-tail’ ADMINISTERING MEDICATION
pattern. Aspects to observe include:
Oral administration
•• Vital signs: respiratory rate, heart rate, rectal For administration via tube, the orogastric route is
temperature, rumen rate. preferable over nasogastric administration. It is use-
•• Body condition score (BCS): in particular ful to indicate the distances to the larynx and ulti-
poor or emaciated. mate end-point (cervical oesophagus in preweaned
•• Mental state: the normal goat is alert, bright animals, rumen in weaned animals) on the tube with
and responsive to approaches. permanent marker.
•• Respiratory system: airflow through nostrils, In preweaned animals, drugs or fluids should be
nasal or ocular discharge, respiratory effort deposited into the cervical oesophagus (one-third
and pattern, coughing, response to palpation to one-half down the neck) to trigger the oesopha-
of larynx and trachea, superficial lymph nodes, geal groove reflex, resulting in channelling of the
adventitious sounds over trachea or thorax, medication into the abomasum. A lamb feeder tube
percussion of sinuses and thorax. (6 mm OD, 40 cm length) is suitable for kids up to
•• Cardiovascular system: mucous membrane about 4 weeks old, and a mouth gag is not neces-
colour, capillary refill time, surface temperature sary in this age group. The kid is held on the han-
of extremities, jugular filling and deflation dler’s lap with its back end towards the handler
and presence of jugular pulse, femoral and its chin supported by the non-dominant hand
pulse character, audibility of heart sounds, (Fig. 1.24). After stimulating the suckle reflex for
adventitious sounds, heart rate and rhythm, 30–60 seconds, the mouth is held open with a finger
hydration status. or thumb of the non-dominant hand. The tube is
•• Digestive system: oral mucosa integrity, passed over the tongue and, when reaching the lar-
dental health, abdominal shape, rumen fill and ynx, gentle pressure is maintained until swallowing
character of rumen contractions, borborygmi, occurs. Correct location is ascertained by observ-
percussion of abdomen, abdominal pain tests, ing fleece movement and palpating the tube in the
trans-abdominal palpation (depending on size oesophagus with the other hand.
and BCS), defecation and character of faeces, In adult goats, a foal-size stomach tube (9–11 mm
perineal staining. OD, minimum length 120 cm) is suitable, and the
•• Urogenital system: urination and character of inner tube of a bandage roll makes a useful mouth
urine, vulval discharge and/or staining of tail or gag to provide protection from the sharp molar
perineum. Transabdominal palpation of kidneys teeth (Fig. 1.25). The goat is reversed into a cor-
(depending on size and BCS). ner, and the handler stands astride over the ani-
•• Mammary system: colour, surface temperature, mal with their legs in front of the goat’s shoulder
pain, swelling or oedema, milk character, teat or (Fig. 1.26). The non-dominant hand holds the chin
16 Chapter 1
Fig. 1.24 Use of an oesophageal feeder (here shown Fig. 1.25 The inner tube of a bandage roll can
in a lamb). The kid is rested on the handler’s lap with be used effectively as a gag and protector to pass a
its back end towards the handler. The dominant right stomach tube in adults (here shown in an alpaca).
hand holds the chin and oesophageal tube. The left
hand is at the target level of insertion (halfway down
Correct location is confirmed by the presence of
the neck) and palpates the oesophagus for the tube.
rumen smell and the absence of coughing or expi-
ration through the tube.
Small approximate amounts of medication may be
administered using a catheter-tip syringe. Its nozzle
is inserted through the diastema, placed onto the
tongue and aimed towards the larynx. It is impor-
tant to hold the goat’s head only just above hori-
zontal and to administer slowly, to avoid accidental
inhalation (especially in recumbent patients).
Subcutaneous injection
Suitable sites include the proximal or distal neck
and the fleece-less area caudal to the elbow. The
escutcheon is useful for injecting goats in the par-
lour (Fig. 1.27).
Intramuscular injection
The quadriceps muscle is suitable for all ages of
Fig. 1.26 Standing astride over an animal with its goats, taking care to inject into the bulk of the mus-
back end in a corner, and the handler’s legs in front cle (thereby avoiding stifle joint, sciatic nerve, etc.;
of its shoulders provides good restraint for stomach see Fig. 1.4).
tubing and intravenous access (here shown in a calf). Neck muscles may also be used, particularly in
meat goats, thus avoiding a higher value cut of meat.
of the goat and the mouth gag. The tube is passed However, injections into the neck muscles should be
over the tongue and, once the larynx is reached, avoided in nursing kids, as inflammation secondary
gentle pressure is maintained until the animal to the injection may reduce suckling. The ligament
swallows. Moderate resistance may be encountered nuchae and spinal column must be avoided in this
as the tube passes the thoracic inlet and the cardia. region (Fig. 1.28).
Fig. 1.28 When using the neck for intramuscular

injections, the ligament nuchae and spinal column
Fig. 1.27 The escutcheon is readily accessible in
(shaded areas) must be avoided.
many parlours for subcutaneous injections.
The gluteal muscles may be used in well-

conditioned goats.
Intravenous injection
and catheterisation
The jugular, cephalic and saphenous veins are all
suitable in all ages and types of goat. The jugular
vein is accessed in the upper third of the neck to
reduce the risk of intra-arterial injection (Fig. 1.29).
This is particularly important when administer-
ing sedatives – inserting the needle off the syringe
allows confirmation that the vein has been entered
prior to injection. The mammary vein should only
ever be used for euthanasia.
Catheter placement is greatly aided by subcutane-
ous injection of 1–2 ml of local anaesthetic, followed
by a small stab incision through the skin with a scal-
pel blade. Jugular catheters should be at least 50 mm
Fig. 1.29 Intravenous injection into the jugular vein.

Note that the vein is entered in the upper third of the
neck. Blood sampling is often easiest if the goat’s head
and neck are held straight (rather than towards one side).
18 Chapter 1
Using the non-dominant hand, the kid is held

vertically by its front legs (hand placed near elbows),
with its back to the handler’s body (Fig. 1.31a). The
needle insertion point is one finger-width lateral and
caudal to the umbilicus (Fig. 1.31b). Long fleece
in this area is clipped, and disinfectant applied (for
example, povidone–iodine solution). The needle is
inserted at an angle of 30–45 degrees to the skin
(pointing towards the tail base) and advanced slowly
into the peritoneal cavity up to its hub. After aspira-
tion to check that no viscera have been entered, the
fluid is injected steadily.
Subconjunctival injection
The head of the animal is rotated to expose as much
sclera as possible. Using an episcleral vessel as ref-
erence point, topical anaesthetic is applied with
a cotton bud to the scleral conjunctiva. A 23–25
gauge needle is inserted under the conjunctiva and
advanced for a few millimetres parallel to the eye
ball (Fig. 1.32).
Fig. 1.30 An intravenous catheter held in place with ROUTINE PROCEDURES AND
sutures. Use of a T-port connector preserves catheter HEALTH PLANNING
hygiene.
The key to keeping goats healthy and productive,
long, to accommodate skin movement over the jugu- and ensuring that their welfare is not compromised,
lar grove. For adult goats, 16–20 gauge is suitable, is to develop a health plan, and reference to this will
for kids 20–22 gauge. Short-stay catheters are suit- be made throughout the book. Such a plan need not
able for a dwell time of up to 72 hours. For longer be complex, but should ensure that routine proce-
dwell times, a medium- or long-stay catheter is used. dures such as vaccination, worming, disbudding
Super glue is a convenient alternative to suturing and foot trimming are carried out in a structured
where the catheter remains in place for a few hours manner, and that other information is readily avail-
only (Fig. 1.30). able on disease recognition and management. Such
a plan is relevant no matter whether goats are kept
Needle sizes in large numbers commercially, or as two or more
Usually, a needle length of 2.5 cm (1 in) is suitable for goats kept as pets.
subcutaneous, intramuscular and intravenous injec- Individual procedures will be outlined in the
tions, both in adult goats and kids. For low viscosity relevant chapter.
drugs, 20 or 21 gauge needles are used; for more vis-
cous drugs or large volumes, 18 or 19 gauge. BIOSECURITY
Intraperitoneal injection Biosecurity is defined as ‘the prevention of disease-

Intraperitoneal injection of glucose may be employed causing agents entering or leaving any place
in hypothermic or hypoglycaemic neonates (see where farm animals are present (or have been pres-
Chapter 4). The recommended needle size is 18–20 ent recently)’. It involves a number of measures and
gauge, 2.5 cm (1 in) long. protocols designed to prevent disease-causing agents
Fig. 1.31 Intraperitoneal

injection. (a) The kid is
held by its front legs just
above the elbows, with its
back against the handler’s
body. (b) The needle is
inserted at a 30–45-degree
angle one finger-width
lateral and caudal to the
(a) (b) umbilicus.
from entering or leaving a property and being spread.

The word farm animal is emphasised in this para-
graph because of the number of infectious agents
shared with livestock species other than goats, and in
particular other ruminants such as sheep and cattle.
Good general hygiene and biosecurity is essential to:
•• Prevent the introduction of infectious diseases.

•• Protect the health of goats, other susceptible
animals in the vicinity and any humans in close
daily contact.
•• Reduce the risk of disease exposure to any
members of the public who visit goat premises.
This is particularly important if open days are
held, especially involving young children or
disease-vulnerable adults.
Fig. 1.32 For a subconjunctival injection (shown
here in a bovine), the head is rotated to expose the Farm animal diseases relevant to goats are mainly
sclera. After point application of topical anaesthetic, spread through:
the needle is inserted parallel with the eye ball. The
clinician’s thumb is on the lower eyelid and index •• Animals, people and machinery moving between
finger on the upper eyelid. and within holdings.
20 Chapter 1
•• Outside visitors to livestock holdings – people be considered if tuberculosis is a known local prob-
and vehicles. lem, and a quarantine anthelmintic treatment should
•• Introducing new animals (of any species). be given to avoid the risk of introducing anthelmin-
•• Contact with neighbours’ livestock over the tic resistant nematodes. Any vaccinations relevant to
fence or gate. the holding onto which they have been moved should
•• Shared farm equipment – a particular problem be administered, together with any other prophylac-
with hobby goat keepers. tic or therapeutic regime deemed necessary, based
•• Contamination by vermin and wild birds. on history and clinical and laboratory test results.
•• Goats drinking from contaminated rivers and
streams. LEGISLATION
New goats moving onto a unit should be kept Legislation relevant to the goat will vary widely
in quarantine for a minimum of 14 days, but ide- depending on where and how they are kept, and as
ally longer if possible. A building with a separate such any detailed description is beyond the remit of
airspace to the main goat accommodation is ideal this book. However, legislation will for the most part
(Fig. 1.33), as is a separate paddock outdoors, probe relevant to all goats, no matter why and how they
viding goats do not have nose to nose contact with are kept. In the UK, for example, all goats including
others in adjoining fields. They should not, how- those kept as pets are designated as farm animals,
ever, be kept in social isolation, but should always mainly because of their susceptibility to notifiable/
be within sight, sound and contact of at least one scheduled diseases such as foot and mouth disease
other goat for company. and the need for relevant authorities to be aware of
During this quarantine period, they should be their geographical location for possible disease con-
examined for any clinical evidence of infectious trol measures. Such legislation may include the
disease such as ectoparasites, footrot and caseous requirement to:
lymphadenitis (CLA). A blood sample should be
taken to assess, for example, the caprine arthritis •• Be kept on a registered holding.
encephalitis or CLA status. A tuberculin test should •• Ensure individual goat identification such as an
ear tag, electronic identification device, tattoo,
pastern or collar mark.
•• Keep a record of movements onto and off the
premises.
•• Maintain a medicines record of products
administered, and be aware of the required meat
and milk withhold times.
•• Be aware of any mandatory codes of goat
welfare.
•• Be aware of those notifiable or scheduled
diseases relevant to the country within which
the goats are kept.
•• Be aware of any relevant legislation covering
Fig. 1.33 This isolation pen was constructed in a minor procedures such as castration and
tractor shed. Wooden walls make disinfection more disbudding, and also of on-farm emergency
difficult, therefore should be avoided. euthanasia.
CHAPTER 2
REPRODUCTIVE SYSTEM
21
THE DOE
NORMAL STRUCTURE AND FUNCTION
The goat has a bicornual uterus, with a short uter-

ine body of about 30 mm, and curled-up horns
(Fig. 2.1). The endometrium is grey–pink in colour
(in older females sometimes brown–yellow) and
bears the typical caruncles (Fig. 2.2). Pigmentation
of the endometrium is rare in the doe.
The external cervical os lies close to the vagi-
nal floor, with a transverse mucosal fold in front of
it. The internal os is poorly developed. The cervi-
cal mucosa forms 5–8 circular folds (Fig. 2.2) and
contains cervical glands that are unique to the goat
and cat (in contrast, vestibular glands are absent in Fig. 2.1 Normal reproductive tract of a doe (vagina
the goat). at bottom, horns and ovaries at top of image).
The caprine ovary is oval to round, about
15 mm long and 10–18 mm high, weighs 1–2 g and
Ovary
is encased by the ovarian bursa. Twin ovulations Caruncle
may originate either from the same ovary or from Cervix
Body Vagina
both ovaries. Therefore, corpora lutea (CLs) from
the same oestrous cycle may be present in one or in
both ovaries.
The oviduct is 140–150 mm long.
FERTILITY
Fig. 2.2 Partially opened reproductive tract,
Goats are regarded as highly fertile, regularly showing the circular folds of the cervix and caruncles.
achieving >90% overall pregnancy rate. Puberty (Note: Endometrial pigmentation, as in this tract, is
starts at 5–10 months of age, when the goat has rare in the doe.)
reached about 45% of its mature body weight. Most
breeds are pubertal around 200–220 days (240 days
for the Angora). rate was 50% in Angora doelings <22 kg, compared
Nulliparous (maiden) animals should have with 90% when >27 kg. Doelings <27 kg showed a
achieved at least 60–65% of their expected mature conception rate of only 50%, compared with 80% if
body weight at the point of breeding. Fertility is >27 kg. Twin ovulations are rare in small maidens,
reduced in small maidens. For example, the ovulation yet reach 100% for females >45 kg.
22 Chapter 2
FECUNDITY polyoestrus breeders. In Northern Europe they are

typically in anoestrus between April and June, in
Litter size varies with genotype due to differences the transitory phase in July and August, with full
in kisspeptides, which are major upstream regulators ovarian activity between September and January to
of gonadotropin-releasing hormone (GnRH). There February.
is a positive correlation between prolificacy and the The oestrous cycle is 19–21 days long, with
presence of wattles (Fig. 2.3). behavioural oestrus lasting 24–36 hours and ovu-
lation taking place 24–36 hours after the start
OESTROUS CYCLE AND of oestrus. At the start and end of the breeding
SIGNS OF OESTRUS season, short oestrous cycles may occur. Equally,
ovulation may occur without oestrus behaviour.
Goat breeds originating from mid- to high lati- Puberty and onset of ovarian activity is linked
tudes (temperate regions) are short-day seasonal to body weight in the maiden female, and occurs
when she reaches 40–50% of her expected mature
body weight.
Signs of oestrus include flagging of the tail
(Fig. 2.4), bleating (which can be very vocal), vulval
hyperaemia and oedema, and frequent urination.
Occasionally, does will mount each other, but this
can also be a sign of dominance or hermaphrodit-
ism and, therefore, is not a reliable sign on its own.
The doe will show interest in the male (Fig. 2.5)
and, on farms without a buck, a ‘scent cloth’ (also
Fig. 2.3 Wattles, here in a British Alpine goat, are

associated with prolificacy.
Fig. 2.4 Two does showing tail flagging, a sign of Fig. 2.5 The doe (animal in the foreground)
oestrus. Frequent urination may also be seen. expresses interest in the buck when in oestrus
(and vice versa).
R e produc t i v e Sys t e m 23
known as ‘billy rag’) may be used to detect this. by up to 1.5 months. For earlier onset or higher
The buck’s reaction to the doe can also be used as response rates, a combination of lighting regime
an indicator of oestrus. Buck pens may be usefully mimicking long days and melatonin is required.
placed at the exit of the milking parlour to detect 4 Progesterone in combination with equine
receptive does. chorionic gonadotropin (eCG):
• Megestrol acetate (MGA), given orally at
CONTROL OF OESTRUS a total daily dose of 0.25 mg for 8–14 days,
either mixed into TMR or divided into two
Out-of-season breeding daily doses 12 hours apart.
Overview • Intravaginal progesterone-impregnanted
There are four main options for manipulating the sponges: for example, ones containing
breeding season. The total period of ovarian activity fluorogestone acetate (minimum dose
in such stimulated females is often shortened. Use of 20 mg [some authors prefer 40–45 mg]
progesterone typically results in the stimulated oes- for 11–18 days), or CIDR® Sheep and
trus plus one other, before anoestrus sets in again. Goat Devices (0.3 g progesterone) for
For natural service, sexual activity must be ensured 18–21 days. Two days before the device is
in the buck – if necessary by lighting regime stimu- removed, 400–800 IU of eCG are given.
lation. The doe:buck ratio is reduced to 5–10:1 for Prostaglandin-F 2 alpha (PGF2α) is not
synchronised does. necessary during the anoestrus period. Natural
mating or artificial insemination (AI) is carried
Technique out 40–48 hours after device removal (or
1 Artificial lighting: a change from exposure to 30 and 48 hours for double insemination).
long days (16–20 hours of light) to short days • 3 mg norgestomet as an ear implant (using
(8–12 hours) will induce ovarian activity. Long half of the available cattle implants) for
and short days are alternated every 60–90 11 days. Twenty-four hours prior to removal,
days to achieve the desired breeding period. PGF2α and 500 IU eCG are given. Oestrus
Alternatively, for spring mating does are exposed follows within 24 hours of implant removal.
to long days from mid-winter. Exposure to
7 hours of light during the day, plus one hour The dose rate of eCG depends on age (doelings
of light 16–17 hours after dawn is sufficient to receiving a lower dose) and gap to natural breeding
mimic a long day. Light intensity should be about season (the wider, the higher the dose). The higher
300 lux (equivalent to illumination in an office). dose rates may stimulate moderate superovulation,
2 Presence of male: exposure to a sexually active resulting in larger litters.
male (including vasectomised) before or after
the normal breeding period shortens and delays, Synchronisation during
respectively, the anoestrus period of does by the breeding season
around 1.5 months. In addition, the continuous Indication
presence of photostimulated males prevents Synchronisation can facilitate batch kidding or the use
seasonal anoestrus in the majority of does, and of AI, although pregnancy rates to AI are often lower
the introduction of such males can trigger ovarian than to natural service following synchronisation.
activity during the normal anoestrus period.
3 Melatonin: exposure to melatonin mimics a Technique
short day. It may be administered either in 1 Use of progesterone sponges or CIDR® Sheep
the early afternoon, orally or by i/m injection, and Goat Devices (as above) for 14–16 days.
or as a slow-release implant (e.g. Regulin®, 400 IU eCG plus PGF2α are either given
containing 18 mg melatonin). In Northern 2 days before or at the time of sponge removal.
European breeds, the season can be advanced Most animals are in oestrus 30 hours later,
24 Chapter 2
with single service or insemination at 40–48

hours, or double at 30 and 48 hours.
2 Two doses of 2.5 mg of PGF2α given 11 days
apart. Does may be bred to observed oestrus
after the first injection or at a fixed time after
the second injection (double insemination
recommended). In either case, mean interval to
oestrus is 44–50 hours after injection.
OVARIAN DISORDERS
Anoestrus
Nulligravid animals (maiden, doeling):
•• Prepubescent because of suboptimal growth

(see above).
•• Intersex:
• Overview. A recessive gene with incomplete
penetrance, and closely linked to the polled
gene, resulting in genetically female animals
(60 XX chromosome complement), of which
most are male hermaphrodites. Sterility in
males results from blocked epididymes.
Fig. 2.6 An enlarged clitoris (arrow) may be seen in
• Clinical presentation. Varying degrees of
intersex females.
phenotypic appearance, including abnormally
long (>3 cm) anogenital distance, and
an enlarged clitoris (Fig. 2.6) or penile
structure ventral to the anus in the female.
The vulva may appear normal. In the male,
a shortened penis, hypospadias (Fig. 2.7)
and testicular hypoplasia may be present.
Depending on the abnormalities present,
urine scalding may result.
• Diagnosis. If no outward signs, check vaginal
length in infertile or anoestrus doelings. Also
useful is ultrasonography of the reproductive
tract. Affected males are often aspermic.
•• Freemartinism (XX and XY chimera) is
relatively rare in goats.
•• Partial aplasia of reproductive tract unrelated to Fig. 2.7 Hypospadias may be present in intersex
intersex. males, shown here in a lamb lying in right lateral
recumbency.
Age-independent causes of anoestrus include:
•• Lactational anoestrus.
•• Season: breeding attempts out of season. •• Negative energy balance resulting in suboptimal
•• Pregnancy: unobserved mating, especially if luteinising hormone (LH) surge.
male kids weaned later than 4 months of age. •• Poor heat detection.
•• Failure to stand: not being in oestrus; fear of the Treatment/management/control

buck, especially in maiden animals. Options mirror those used in cows: PGF 2α for
•• Old age: ovarian activity will progressively wane luteal cysts and GnRH for follicular cysts, or intra-
from teen years onwards. vaginal progesterone for either type. It should be
noted that goats appear to be less responsive than
Cystic ovarian disease cows to treatment of COD. In valuable does, physi-
There is limited information on the prevalence or cal destruction via laparoscopy may be considered.
incidence of cystic ovarian disease (COD). One abat- For treating follicular cysts, the dose rates are:
toir study showed 12% of goats had COD.
•• 8–10 µg buserelin;
Clinical presentation •• 25–50 µg gonadorelin.
Luteal cysts typically result in anoestrus or pro-
longed inter-oestrus intervals. Follicular cysts may BREEDING
result in anoestrus, irregular inter-oestrus intervals
and, occasionally, nymphomania. Natural service
Male behaviour
Diagnosis The male’s reaction to a doe in oestrus consists of
Ovarian ultrasonography allows the most definitive sniffing her urine (Fig. 2.5), flehmen, striking with
diagnosis (Fig. 2.8). Milk or blood progesterone the front leg, tongue flicking and vocalisation (snort-
levels may be used to confirm the type of cyst (luteal ing- and clicking-like sounds). Copulation takes place
cysts resulting in high levels, and follicular cysts in in the standing position. Thrusting, often with simul-
low levels). taneous throwing back of the head, indicates ejacula-
tion. Sperm is deposited into the cranial vagina.
Technique
Hand mating is commonly employed, provid-
ing control over the mating process and allowing
accurate recording of breeding date and sire. The
AM-PM rule applies, meaning that a doe first seen
in oestrus in the morning is presented to the buck
in the evening and vice versa. Alternatively, the doe
may be bred every 12 hours until going out of oes-
trus. Sexual performance, including time to mount-
ing and ejaculation, is shortened in bucks that have
observed another male mating a doe.
For single-sire group mating, a doe:buck ratio
of 50:1 is acceptable for a mature buck. The ratio
is 10:1 for a yearling (or where does are syn-
chronised) and 25:1 for a 2-year-old male. After
6 weeks, the buck should be moved to a differ-
ent group of females to maintain sexual interest.
On farms with multiple buck–doe groups, fight-
ing along the fence line is avoided either by wide
alleyways between paddocks or, less effectively,
solid fence panels.
Fig. 2.8 Ultrasound image of a follicular cyst. Multiple sire groups afford the easiest manage-
Characteristic are the thin wall and anechoic fluid. ment. However, sire and breeding dates will be
26 Chapter 2
unknown, and dominance and fighting often lead technique, the presence of a teaser female appears
to suboptimal pregnancy rates (Fig. 2.9). Horned to increase sperm output. An insemination dose of
and polled bucks should not be mixed in the same 60–120 × 106 spermatozoa is common. Bucks may be
paddock. light-stimulated to allow collection throughout the
If raddles are used, the harness must be well- year.
fitting and the bucks checked regularly for harness- After dilution, fresh semen is kept at 30°C in tris-
induced trauma. buffer or ultra-high temperature (UHT) skimmed
milk, and used within 30 minutes of collection. For
Artificial insemination chilled semen, the sperm needs to be washed if egg
Overview yolk is used as buffer (to remove the phospholipase A
AI allows effective use of the best male genetics, enzyme from the seminal plasma). The semen is then
reduces biosecurity and disease risks and is inde- gradually cooled to 5°C and used within 24 hours of
pendent of the geographical proximity of the male collection. For cryopreservation, standard freezing
and female. Pregnancy rates between 40% and 60% methods are used as for other species, again washing
are achievable, in part influenced by type of semen the sperm if egg yolk is used.
(fresh, chilled or frozen-thawed) and insemination
method (transcervical or laparoscopic). In contrast Technique – insemination
to several other species, yearling females appear to For frozen-thawed semen, the AM-PM rule applies
have a lower pregnancy rate following AI than older (see above). Fresh and chilled semen have a longer
does. Pregnancy rates also decline by about 5% in survival time in the doe, making insemination tim-
does that have received several hormonal treatments ing in relation to ovulation less critical.
or where cryopreservation of the semen exceeds Suppliers’ guidelines on thawing frozen semen
9 years. Sexed semen is reported to achieve about a should be followed (Fig. 2.10). If not stipulated,
40% pregnancy rate, with 83% accuracy of gender semen is thawed at 35–37°C for at least 40 seconds.
of the kids. Chilled semen does not require warming prior to
use.
Technique – semen collection Insemination via laparoscopy has replaced lapa-
Semen is collected into an artificial vagina. Either rotomy, and allows precise placement of semen into
the buck is allowed to mount a female in oestrus, the horn ipsilateral to the corpus luteum (Fig. 2.11).
or they are trained to use a dummy. For the latter The fasted doe is either anaesthetised (e.g. with a
Fig. 2.9 Fighting between bucks is common in Fig. 2.10 After thawing an AI straw, all water must be
multiple sire groups. removed from its outside prior to insemination.
Fig. 2.12 A human sigmoidoscope with a ring light

source is invaluable for transvaginal procedures.
A head with a ring-shaped light is obtainable for
most ophthalmoscope base units (e.g. Welch Allyn,
Buckinghamshire, UK).
be variable, and costs may be deemed prohibitive by

the producer, with ET costing about ten times more
Fig. 2.11 Insemination via laparotomy. (Image than AI per kid produced. In addition, the repeated
courtesy Angelika von Heimendahl.) use of large molecule hormones carries a hypersensi-
tivity reaction risk.
xylazine–ketamine combination) or sedated followed
by local anaesthesia, and placed in dorsal recum- Technique
bency with the head tilted slightly downwards. The superovulation programme is best started after
Transcervical intrauterine insemination is often a natural or induced reference heat (= day 0). A pro-
more practical and yields acceptable, if up to 20% gesterone sponge is inserted on day 0 for 11 days.
lower, results. It may be used in does that have kid- A luteolytic dose of PGF2α is given on day 9. A total
ded at least once. Semen is deposited deep into the dose of 16–20 mg follicle stimulating hormone
cervix. A straight insemination pipette is warmed (FSH) is administered every 12 hours in a tapering
by vigorous rubbing. An air-bubble is drawn up dose from day 9 (e.g. 2 × 4 mg on day 9, 2 × 2 mg
into the syringe prior to filling with the semen on days 10 and 11; Fig. 2.13). FSH is preferred over
dose. Sedation and epidural anaesthesia are recom- eCG; however, with both hormones premature
mended. The doe’s hindquarters are lifted up high luteal regression may be observed leading to the loss
and the perineal area dry-wiped. Using a human of the embryos. The use of GnRH, LH, human cho-
sigmoidoscope with a ring-light source (Fig. 2.12), rionic gonadotropin (hCG) or flunixin meglumine
the external os is visualised and the pipette advanced after the onset of oestrus is variably successful in
into the cervix. The doe is kept in the elevated posi- reducing this risk.
tion for 1–2 minutes. Flushing is carried out 6–7 days after oestrus in
the anaesthetised or sedated (plus local anaesthetic)
Embryo transfer doe. Laparoscopy is the conventional method, but
Overview transcervical collection is also possible. For the lat-
Embryo transfer (ET) allows proliferation of geneti- ter, administration of PGF2α 8–16 hours prior to
cally superior females or expansion of small breed flushing makes catheterisation of the cervix easier
populations. Just as with AI, additional applications and results in good embryo recovery rates.
include biosecurity and disease control, and inter- For freezing, ethylene glycol is a suitable
country exchange. This technique is not as reliably cryopreservant.
developed in goats as in other species, although The recipient’s oestrus should be synchronised to
pregnancy rates of 50% have been achieved. The occur within 12 hours either side of the donor’s oes-
doe’s response to the hormonal programme can trus. Transfer is by laparoscopy.
28 Chapter 2
Fig. 2.14 Oviduct patency test. After placing phenol-

sulphonthalein (Phenol red) into the uterus, the dye
passes into the peritoneum via the oviduct, enters the
peritoneal circulation and is excreted via the kidneys.
Urine is collected every 5 minutes via a Foley catheter
(under epidural anaesthesia). Dye in the urine after 10
Fig. 2.13 Multiple follicles on an ovary after a minutes indicates both oviducts are patent; dye after
superovulation programme. 20 minutes indicates one oviduct is patent; no dye
after 30 minutes indicates both oviducts are blocked.
Pregnancy diagnosis Best performed 14 days after oestrus.
See Chapter 3.
Clinical presentation
Misalliance Nulligravid (maiden) females are affected. Disorders
Administering PGF2α up to day 90 after breeding affecting the uterus or oviduct (syns. fallopian tube,
will quite reliably induce abortion 42–76 hours later. salpinx) will lead to failure to conceive. Ovarian
There are no data on misalliance after day 90, but a aplasia or hypoplasia will present as anoestrus if
similar effect would be expected. bilateral or irregular oestrous cycles if unilateral.
Agitation during mating on either the maiden
UTERINE DISORDERS female’s or buck’s part may indicate a persistent
hymen.
Abattoir study-based prevalence of acquired repro-
ductive tract abnormalities (such as salpingitis or Diagnosis
endometritis) is reported in the region of 2%. To Transrectal ultrasonography is the best method to
reduce the number of potential differential diagno- detect uterine and ovarian abnormalities. Sedation
ses, it is useful to group disorders into congenital and the use of an epidural is recommended to reduce
versus acquired. the risk of trauma. A persistent hymen may be con-
firmed with the aid of a speculum (e.g. a human
Anatomical sigmoidoscope). An oviduct patency test may be
abnormalities – congenital necessary to rule out fallopian tube abnormalities
Overview (Fig. 2.14).
Abnormal embryological development of the female
reproductive tract may lead to incomplete perfora- Differential diagnosis
tion, canalisation, duplication or partial or complete Other causes of failure to conceive and irregularities
agenesis or aplasia. of the oestrous cycle, as discussed elsewhere.
Treatment/management/control
A thin, membrane-like persistent hymen may be
broken down with the aid of forceps and a vaginal
speculum. Removal of a thick, flesh-like hymen is
usually unsatisfactory and may result in substan-
tial haemorrhage. Doelings with unilateral ovarian
or oviduct abnormalities could, in theory, be bred
from, either with ultrasonographic monitoring of
activity on the normal ovary or using oocyte aspira-
tion and in-vitro fertilisation techniques. However,
a genetic base to the abnormalities must be consid-
ered, and such doelings are best removed from the
breeding pool.
Anatomical abnormalities – acquired

Overview
Primi- or multiparous does may acquire abnor-
malities such as scarring, incomplete vulval or
cervical seal (Fig. 2.15), rectovaginal fistula or
salpingitis.
Aetiology
Trauma may result from the mating process, partu- Fig. 2.15 Vulval sutures to address a prolapse have
rition or reproductive manipulations such as trans caused marked tissue trauma, inflammation and
rectal ultrasonography, vaginal examination and AI distortion, potentially leading to a poor vulval seal.
or ET techniques. Infectious aetiologies are also
common, typically involving opportunistic or com-
mensal pathogens.
Disorders of the vulva and perineum are obvious
on clinical examination. Vulval discharge, failure
to conceive, oestrous cycle abnormalities and signs
of abdominal discomfort (such as back arching,
tail lifting, squatting) should prompt examina-
tion of the reproductive tract. Frequent squatting
and straining may give the appearance of dysuria
(Fig. 2.16).
Diagnosis
Vaginal examination with the aid of a speculum Fig. 2.16 Abnormal urination behaviour can indicate
(e.g. human sigmoidoscope; Fig. 2.12) will reveal an acquired uterine tract abnormality.
abnormalities involving the vestibulum, vagina and
external cervical opening. Oviduct abnormalities Differential diagnosis
may be detectable on transrectal ultrasonography. For signs of abdominal discomfort, these include
Sedation and the use of an epidural are recom- disorders of the urinary or gastrointestinal tract that
mended for both methods. result in pain.
30 Chapter 2
Surgical correction of traumatic lesions may be con-
sidered. Surgery is either conducted within a few
hours of the trauma occurring or after several weeks
when healing by secondary intention has occurred
and tissues have remodelled. Incomplete seal of the
vulval lips may be addressed by Caslick surgery or
vulvoplasty. Where the Caslick technique is used,
mating must be supervised or AI used to avoid
trauma, and the seal opened surgically prior to par-
turition. Vaginal trauma leading to urine pooling
may be corrected by vaginoplasty.
Infectious lesions are treated with a course of
antimicrobials. Fig. 2.17 Dystocia is a risk factor for endometritis,
For both groups of lesions, anti-inflammatory as in this ewe that required a caesarean section.
drugs are strongly recommended, and the doe must
be sexually rested until complete resolution of the The doe is not systemically affected.
problem.
Diagnosis
Endometritis Excessive uterine fluid, typically echodense, is detected
Overview during ultrasonography (Fig. 2.18). Establishing the
Endometritis is mild to moderate inflammation presence of a corpus luteum is important for treatment
of the endometrium only, with or without infec- decisions. Vaginal examination using a speculum or
tion and without systemic effects. Clinically, the
term is often used to describe chronic endometritis
(i.e. beyond the normal puerperal period [i.e. present
after 14–21 days post partum]). Occurrence tends to
be occasional in the doe.
Aetiology
A variety of gram-positive and gram-negative
pathogens, including anaerobes, may be involved,
including Trueperella pyogenes, Fusobacter necrophorum,
Escherichia coli and Streptococcus spp. Occasionally,
fungal pathogens are involved.
Affected does often have a history of dystocia
(Fig. 2.17) or retained fetal membranes (RFM).
Mucopurulent to purulent vaginal discharge is
present, often noticed on the tail or hind legs, but Fig. 2.18 A mid-tone echogenicity of uterine
sometimes only apparent on vaginal examination or fluid suggests the presence of debris. This, together
during oestrus. Uterine involution is often delayed. with uterine horn enlargement, is a common
The cervix typically remains open; however, if it is finding in endometritis or pyometra (as in this
closed, the sub-form ‘pyometra’ results. Frequent image of a 10-year-old Pygmy goat). The outline
return to oestrus is common, but anoestrus or other of the uterus is indicated by the white diamonds.
irregular oestrous patterns also occur.
endoscope shows mucopurulent fluid exiting through Uterine neoplasia

the cervix. Overview
Definitive diagnosis requires either culture or No firm data on incidence or prevalence exist.
uterine biopsy. These are rarely performed in prac- As with most neoplasia, older does are more com-
tice, but should be considered in protracted cases. monly affected.
To obtain a sample for culture, a double-guarded
pipette is used to avoid contamination from the more Aetiology
caudal tract. A variety of tumours have been reported, including
adenocarcinoma, leiomyoma or leiomyosarcoma,
Differential diagnosis and lymphoma (Figs. 2.19, 2.20). These may affect
Uterine neoplasia frequently presents with vulval any part of the tubular reproductive tract and also
discharge (ultrasonography and biopsy are used to the broad ligament. Squamous cell carcinoma of the
confirm). The discharge present in metritis typi- vulval lips has occurred. Vaginal papillomas may be
cally has a haemorrhagic and malodorous element seen, which are typically benign.
to it and the doe is often systemically affected. It is
important to establish that the discharge originates Clinical presentation
in the uterus, not the urinary tract. Affected does often present because of chronic
vaginal discharge. Failure to conceive may also be
Treatment/management/control reported.
The aim of hormonal treatment is to exert oestro-
gen influence. This is achieved by a luteolytic dose
of PGF2α if a corpus luteum is present, or use of
exogenous oestrogen if available for veterinary use
(e.g. oestradiol benzoate).
Hormonal treatment may be combined with
antimicrobials, typically given systemically because
of the impracticality of intrauterine administra-
tion in the doe. Suitable groups include penicillins
(from week 5 post partum), tetracyclines (at mini-
mum 10 mg/kg) and cephalosporins. Not suitable
are trimethoprim–sulphonamide, aminoglycosides,
streptomycin and enrofloxacin, because of a com-
bination of presence of necrotic material, low oxy-
gen tension, acidic pH and presence of anaerobic
pathogens.
No goat-specific treatment studies of fungal
endometritis are available. In the mare, lufenuron
has been found useful.
Plasma and colostral whey intrauterine infusions
are being investigated in the cow.
The mainstays of control are avoidance of predis-
posing factors, such as dystocia, unhygienic inter-
vention and RFM, and, if they do occur, prompt
treatment. Routine post-partum administration Fig. 2.19 Reproductive tract neoplasia in a 9-year-
of PGF2α has shown ambiguous results in the cow. old Toggenburg doe presented for return to oestrus.
Immunosuppression (e.g. caused by endoparasitism) A follicular cyst and purulent vaginal discharge were
should be ruled out. present.
32 Chapter 2
•• Concurrent disease (e.g. endoparasite burden).

•• Nutritional deficits (possibly including
phosphorus, copper, selenium, iron).
•• Excessive stress levels (e.g. frequent re-grouping,
bullying).
•• AI technique (where used): poor storage, handling
and insemination technique, wrong timing.
•• Presence of venereal or abortive pathogens.
INFECTIOUS DISEASES
Caprine herpesvirus 1
Definition/overview
Fig. 2.20 Cervical tumour in an elderly doe. (Cervix Caprine herpesvirus 1 (CpHV-1) infection is associated
to the right, uterine horns to the left.) predominantly with a venereally transmitted vulvovagi-
nitis and balanoposthitis. The virus can also cause early
Diagnosis embryonic death or abortion and a fatal viraemia in new-
Ultrasonography combined with uterine biopsy is born kids. The condition has been reported in the USA,
most useful. Where treatment is attempted, a thor- Australia and New Zealand, but also more recently in a
ough clinical examination combined with thoracic number of European countries. Its presence has often
and abdominal ultrasonography and radiography is been confirmed only by serological surveys, with little
advisable to rule out metastasis. or no evidence of known clinical infection.
Differential diagnosis Aetiology

For vaginal discharge, endometritis. For failure to A DNA virus, one of a closely related group of alpha-
conceive, multiple differentials are possible, as dis- herpesviruses known to cause a spectrum of diseases
cussed elsewhere in this chapter. in ruminants (e.g. bovine herpesvirus 1 causing
infectious bovine rhinotracheitis infection in cattle).
Treatment/management/control Although cross-species infection with these viruses
Ovariohysterectomy may be attempted if metastasis can occur experimentally, natural cross infection is
is not present. This may be followed by chemother- uncommon.
apy, although very limited clinical experience exists
in the goat. Pathophysiology
Infection is acquired either via the intranasal route,
HERD INFERTILITY PROBLEM resulting in a viraemia and localisation in the geni-
tal tract, or the venereal route whereby infection
Areas to investigate include: appears to remain localised without systemic spread.
One of the features of herpesvirus infection is latent
•• Female to male ratio (max. 50:1, or 5–10:1 if infection and subsequent recrudescence of clinical
synchronised). disease, and this feature is recognised in goats with
•• Out-of-season breeding (where used): males not CpHV-1 infection. Recrudescence can occur during
sexually active. oestrus, potentially resulting in the rapid spread of
•• Oestrus detection rate and accuracy poor; wrong infection during the breeding season.
timing if hand-mating used.
•• No male contact provided. Clinical presentation
•• Negative energy balance and/or suboptimal Both males and females are susceptible to the geni-
body condition in does. tal form of the disease, which tends to occur as an
outbreak during the breeding season, rather than Differential diagnosis

in a sporadic form. Vulval lesions begin with swell- Other causes of vulvovaginitis and balanopos-
ing and congestion of the vulval lips; some does thitis (Fig 2.21), including some Mycoplasma and
may develop a vaginal discharge (there are usually Ureaplasma spp., and Corynebacterium renale in males.
no systemic signs). Over the next few days, small
shallow multiple erosions appear over the vulval Treatment/management/control
and vaginal mucosa, and the discharge becomes There is no treatment for the primary viral infec-
more copious and mucopurulent in appearance. tion, although topical or parenteral antibiotic may be
These lesions gradually develop superficial scabs useful if secondary bacterial infection has occurred.
before healing spontaneously, although recru- Most cases regress spontaneously. Any attempt to
descence often occurs during the next breeding eradicate disease must be based on a repeated test and
season. Infected males may be asymptomatic or cull policy, although this can be a slow process due to
develop hyperaemia and congestion of the penile latency and recrudescence of infection. Vaccines have
and preputial mucosa, followed by the emergence been developed and are available in some countries.
of small superficial erosions and a penile dis-
charge. In severe cases, males may be reluctant to EMBRYONIC LOSS AND ABORTION
serve. Infection via the intranasal route, resulting
in viraemia, may lead to early embryonic loss and Once implantation has taken place, there are a
abortion, otherwise the overall effect on reproduc- number of infectious and non-infectious insults
tive performance is minimal. Many infected goats that may challenge the viability of the developing
may remain completely asymptomatic. embryo and fetus, resulting in embryonic loss or
abortion.
Diagnosis Early embryonic losses may go unnoticed, merely
Diagnosis is based on the presenting clinical signs resulting in an apparent failure to conceive with
during the breeding season. Paired serology may give return to oestrus, or may be evident at scanning
further confirmation, although any test employed when one or more fluid-filled areas may be appar-
must be able to distinguish between CpHV-1 and ent in the uterus where implantation had originally
other alpha-herpesviruses. Definitive diagnosis is occurred.
based on a demonstration of the virus either in cell Infectious causes of early embryonic loss include:
culture or by means of other available tests such as
polymerase chain reaction (PCR). •• Toxoplasmosis: if a naive doe is exposed to heavy
field infection in early pregnancy.
•• Border disease virus (BDV).
•• Schmallenberg virus.
•• Caprine herpesvirus.
•• Tick-borne fever.
•• Any infectious agent causing pyrexia in
the critical early stages of implantation and
establishment of the developing embryo in the
uterine wall. Also subclinical endometritis.
Non-infectious causes of early embryonic loss

include:
•• Nutrition: goats will breed successfully in arid

Fig. 2.21 Balanoposthitis of unknown aetiology. areas even when nutritional input is very low,
(Image courtesy Yoav Alony-Gilboa.) and carry kids to full term. Overt starvation
34 Chapter 2
would need to be extreme to cause embryonic evidence of contact with sheep, particularly if preg-
or fetal loss. Specific vitamin and trace element nant/breeding, the ages of does affected and an esti-
deficiencies, imbalances and excesses have all mate of the current abortion rate. A good recording
been cited as causing embryonic loss in goats, system enables comparisons with previous years.
but any underlying mechanisms are poorly Clinical examination may identify relevant factors
understood, and any association is rarely proven. such as pyrexia or septicaemia, or any intercurrent
•• Genetic abnormalities affecting either the disease problem such as enterotoxaemia.
autosomes or the sex chromosomes. Material should be collected from aborting does
•• Failure of the maternal body to recognise the for laboratory examination – this includes:
presence of the embryo (interferon tau) or failure
of hormonal support (especially progesterone). •• Placenta.
•• Environmental stress such as extremes of •• Fetus.
temperature. •• Maternal blood sample.
•• Trauma, including AI of a pregnant doe and
forceful early pregnancy diagnosis. If fetuses cannot be sent directly to a laboratory,
•• Inadvertent use of PGF2α causing luteolysis. the following samples should be submitted:
•• Inadvertent overdose with a wide range of
pharmacological agents in early pregnancy has •• Aseptically collected fetal stomach content
been cited as leading to embryonic loss. (e.g. using a sterile vacutainer). In the absence
•• Sheep and goat hybrids: when run together, of free fluid, an aseptically taken swab.
inadvertent matings between sheep and goats •• Free abdominal or thoracic fluid.
may occur. If a male sheep fertilises a female •• Portion of placenta to include a cotyledon.
goat, then the resulting embryo rarely survives •• Maternal blood sample.
beyond the second month of pregnancy.
It may also be useful to collect fresh fetal spleen,
ABORTION brain and lung and store them in a freezer, together
with similar tissue in fixative, for submission for fur-
Ascertaining the cause of abortion in goats requires ther more specific testing after routine testing has
a thorough, well-structured investigation including been completed.
an assessment of the environment and any nutri- Blood samples can also be collected from other
tion and management factors, in addition to gath- goats at the same stage of pregnancy, which can be
ering material for laboratory examination. Many of retained as stored serum for serology pairing if any
the infectious causes of abortion in goats also cause does do subsequently abort. Material from more
abortion in sheep (and vice versa). than one aborting doe is gathered, if possible, to
At what stage intervention is necessary will reduce the chance of selecting an atypical sporadic
depend on the size of the unit and the number abortion case.
and timescale of losses. Occasional abortion is an Goats do present the investigating veterinary
inevitable risk of every pregnancy, often related to surgeon with a dilemma, however, as they are fas-
physiological or anatomical abnormalities of the tidious about clearing up any evidence that they
fetal–maternal unit. As abortions escalate in num- have either aborted or kidded. As such, the pla-
ber, and in particular if ‘abortion storms’ occur, the centa will often be consumed rapidly and may not
likelihood of a common underlying cause will rise, be easily obtainable for submission. It is the single
and an investigation becomes necessary. most useful specimen to collect, so its importance
History taking should include the current man- should be stressed to the owner or stock-keeper,
agement of the cohort, the diet fed and recent diet who should remain vigilant, swiftly harvesting any
changes, recent purchases or other introductions that may appear (and, most importantly, from rep-
to the group (including both goats and sheep), any resentative cases).
Management advice to minimise any further sub- the environment. Oocysts sporulate when voided
sequent spread of infection includes: within 1–5 days, depending on aeration and tem-
perature, and remain viable in the environment for
•• The rapid removal and safe disposal of any several months. It is suggested that cats generally
aborted material including fetus and placenta. develop immunity to T. gondii after the initial infec-
•• The removal and safe disposal of any tion, but may continue to shed if re-exposed.
contaminated bedding (e.g. by incineration). Goats become infected by eating forage, bedding,
•• The isolation of any goat that has aborted. cereals or concentrate contaminated by cat faeces
(Fig. 2.22). Cats nesting in amongst straw or hay
It is important to remember that many of the bales are considered a particular risk. If the goat is
infectious causes of abortion in goats are potential pregnant at first exposure, invasion of the fetus and
zoonoses, including Q fever (Coxiella burnetii) and placenta follows haematogenous spread. Exposure at
enzootic abortion (enzootic abortion of ewes [EAE]; any other time results in widespread tissue distribu-
Chlamydia psittaci), the latter organism presenting a tion and immunity. Immunity after exposure is usu-
particular risk to pregnant women. ally strong and protective, although there are reports
of repeat abortion in subsequent pregnancies.
Common infectious causes of abortion
Toxoplasmosis Infection in early pregnancy may result in fetal
Definition/overview loss, with no other clinical signs evident. Infection
Toxoplasmosis is an important cause of abortion in in later pregnancy may result in the death of one or
both goats and sheep and has a worldwide distribu- more developing fetuses, which may or may not be
tion. Although widespread tissue distribution of instantly voided. Therefore, kids of different sizes
oocysts may occur in a susceptible goat after inges- and of apparently differing gestational lengths can
tion, clinical disease other than abortion is rare. It is be encountered. It is also possible to have live healthy
a potentially zoonotic disease, with risk to humans kids born alongside smaller (often mummified) kids.
associated with the potential excretion of tachyzoites Infection in late pregnancy may also result in the
in the milk and the presence of tissue cysts in the birth of acutely infected, weak kids.
meat of recently infected goats, killed by pasteurisa-
tion and adequate cooking, respectively.
Aetiology
Toxoplasmosis is caused by the obligate intracellular
protozoal parasite Toxoplasma gondii, of the Family
Sarcocystidae, of which there are a number of rec-
ognised genotypes that are useful in epidemiological
surveys.
Pathophysiology
The cat (both wild and domestic) appears to be
the definitive host for this parasite, and becomes
infected by eating small rodents, undercooked meat
or aborted ruminant material. It can also become
infected congenitally from an infected dam. Oocysts Fig. 2.22 The control of cats on farm, and in
are first seen in the faeces at around 3 days after particular preventing their faecal contamination of
infection and may be released for as long as 20 days, feed, forage and bedding, is important in the control
when many million oocysts will have contaminated of T. gondii.
36 Chapter 2
Diagnosis T. gondii antibody can be widespread in goat popu-

Although not pathognomonic, the appearance of lations regardless of abortion rates, therefore single
aborted kids of differing sizes, including smaller maternal seropositive results from aborting dams
mummified kids, is highly suggestive of toxoplasmo- may give misleading results, although a seronegative
sis (Fig 2.23). The placental cotyledons may show result will probably rule out infection. Histological
small foci of necrosis (Fig 2.24), although anec- examination of brain and other organs, including
dotally these are less well pronounced than those placenta, may demonstrate non-specific necrosis,
described in aborted lambs. aided by specific immunohistochemistry.
Laboratory diagnosis may include demonstration
of antigen in placental material by indirect fluores- Differential diagnosis
cent antibody test (IFAT) or PCR, and the demon- Other potential causes of abortion.
stration of antibody in immunocompetent fetuses
voided in late pregnancy by IFAT (this requires Treatment/management/control
goat-specific antigen). Surveys have shown that (including prognosis)
Successful control is based predominantly on reduc-
ing environmental exposure to the infective oocyst.
The cat population should be managed where pos-
sible, and ideally all cats neutered, because pregnant
cats and young kittens can shed at higher levels and
entire tomcats are likely to roam between farms.
Where possible cats should be kept away from feed
stores, and feeds stored securely. Bales of hay or straw
Fig. 2.23 that show signs of cat faeces or of recent kittening
Aborted Boer activity should be discarded. Placental material and/
goat kids with or aborted fetuses should be made inaccessible to
toxoplasmosis cats.
confirmed. Toxoplasmosis vaccines are available in some
Note the small countries, most of which will have been licensed
mummified for use in sheep, with minimal data as to efficacy in
kid (and goats. Prophylaxis in the face of an abortion storm
absence of has also been suggested using, for example, iono-
placenta). phore preparations. In the UK, decoquinate (Deccox
6% premix) has a marketing authorisation for toxo-
plasmosis control in sheep at a dose rate of 2 mg/kg
daily in feed, and has been used off-licence and with
unvalidated results in goats. Care should be taken to
avoid overdosing.
Chlamydiosis (syns. enzootic

abortion, ovine enzootic abortion)
Definition/overview
Chlamydiosis, also referred to as EAE or OEA
(ovine enzootic abortion), is a worldwide cause of
abortion in ruminants, particularly sheep and goats,
between which infection can be readily transmitted.
Fig. 2.24 Toxoplasma infection. Note the focal Infection can also be linked occasionally to ocular
cotyledonary necrosis. and respiratory infections.
It is an important zoonotic pathogen, particularly membranes, often covered in a purulent exudate.

for pregnant women exposed to infective material Infection in late pregnancy can result in the birth
such as placenta, uterine fluids or kids from aborting of live kids that can be congenitally infected and
does. It is generally advised that during pregnancy themselves abort when first pregnant following a
women should not be involved in lambing or kidding period of latency.
or in the rearing of sick or ailing neonates.
Diagnosis
Aetiology The appearance of the placenta is not pathognomonic
The causative agent of chlamydiosis is Chlamydia and laboratory confirmation is required (Fig. 2.25).
abortus (previous nomenclature Chlamydophila abor- Staining impression smears prepared from the placen-
tus and Chlamydia psittaci), which is a gram-negative, tal surface using a modified Ziehl–Neelsen (MZN)
intracellular organism containing both DNA and technique will demonstrate intracellular acid-fast
RNA. inclusions, although these can be difficult to distin-
guish from Coxiella and Brucella spp. Some laborato-
Pathophysiology ries may use other staining methods (e.g. Giemsa).
The organism can be carried in the intestinal tract More specific PCR tests are now available to aid in
and potentially introduced to a clean unit by faecal confirming a diagnosis. In the absence of a placenta,
shedding, although the main route of transmission smears or PCR testing can also be undertaken on
between goats (or goats and sheep) is via the prod- fetal stomach content.
ucts of abortion and the oral route. Multiplication Serological testing of aborting does with a specific
occurs intracellularly in the gut wall, resulting in ELISA test gives further confirmatory evidence.
a septicaemic episode, which in turn leads to colo-
nisation of the fetus and placenta, with particularly Differential diagnosis
severe damage to the placental unit resulting in fetal Other potential causes of abortion.
death and expulsion.
Whereas in sheep abortion tends to occur in the Treatment/management/control
pregnancy following ingestion, it is recognised that The generic principle of isolating any goat that
goats can become infected while pregnant and abort aborts and removing the products of abortion
in that same pregnancy, thus leading to some quite promptly is significant in the control of this highly
dramatic ‘abortion storms’.
The role of the male is poorly understood in
goats - in rams cases of chlamydial orchitis have been
reported. The potential faecal carriage of infection
by a newly purchased buck into a high health status
herd may be a possibility.
Abortions tend to occur during the second half of
pregnancy, although earlier abortions have been
reported. The doe is not usually ill, although in
abortion storms individual goats may become
febrile due to weight of infection. The fetus and
placenta are often voided as a single unit, often
with a normal appearing well-formed kid. The Fig. 2.25 Chlamydia abortion confirmed, although
main pathology is associated with the placenta, the stage of pregnancy and gross appearance of the
which shows a severe intercotyledonary pla- placenta is atypical. This demonstrates the importance
centitis, with thickening and congestion of the of laboratory investigation.
38 Chapter 2
infectious cause of abortion. Shedding may continue of practising veterinarians and 83% of farmers were
for as long as a vaginal discharge is evident, and this seropositive to C. burnetii, compared with 2.4% in
may continue for up to 2 weeks after abortion. It is the general population.
not known whether goats can continue to shed infec- Infection with Q fever is undoubtedly more wide-
tion at subsequent pregnancies, even if they kid suc- spread than its clinical appearance suggests, as many
cessfully. On a commercial unit, culling of aborting infected ruminants can carry a fetus to full term, pro-
does is generally recommended, although after any ducing a live viable offspring, yet still shed the organ-
discharge has dried up, they may be allowed to com- ism in fetal fluids and placenta, thus posing an ever
plete the lactation. present occupational risk on many livestock units.
A number of vaccines are licensed worldwide for Because of the zoonotic risks, the organism must
use in sheep, and have been used in the face of infec- be handled in containment level III facilities in the
tion in goats in the UK with unvalidated results. laboratory. It is classed as a Category A biological
The use of tetracyclines in outbreaks in sheep has substance (International Air Transport Association).
been shown to be of economic benefit, and may be
considered in goats at a recommended dose rate of Aetiology
20 mg/kg i/m q3–10d. Q fever is caused by C. burnetii, a pleomorphic, weakly
The aim should be to maintain an EAE-free herd. acid-fast, variably gram-negative bacterium (Fig. 2.26).
Biosecurity is important, and incoming breeding
females should be tested for antibody. A number of Pathophysiology
country-specific health schemes are available, giving In animals infection is mainly subclinical, but abor-
local advice on achieving and maintaining freedom tion may occur in ruminants. C. burnetii has a tro-
from infection. pism for the reproductive tissues and mammary
gland. It is shed in milk, faeces and semen, and is
Q fever present in fetal fluids and placenta of both abort-
Definition/overview ing females and infected females at normal parturi-
Q fever has a worldwide distribution and a wide host tion. The organism has two forms, one of which is a
range including mammals (humans, farmed and wild highly stable spore-like form that can persist in the
species), birds and arthropods. It is extremely infec- environment and is resistant to cleansing and disin-
tious, with only a single colony-forming unit needed fection. In this form the organism is tolerant of acid
to produce infection. The organism Coxiella burnetti pH and is unaffected by UV light. It is also resistant
was first discovered in Queensland, Australia, in 1937
where it caused unexplained fever in abattoir workers.
This so called ‘query’ fever led to the common name
used today.
Q fever is an important zoonotic infection, with
a particularly serious human outbreak (in excess of
3,000 cases) in Holland between 2007 and 2009,
linked epidemiologically to a number of infected
goat units nearby. Seroprevalence studies suggest
that Q fever had been endemic in Holland several
decades before clinical disease was confirmed in
dairy goats and dairy sheep, and Q fever abortions
were registered on 30 dairy goat and dairy sheep
farms between 2005 and 2009. Fifty-nine percent of
human cases in 2009 lived within 5 km of a farm that
had tested positive by bulk milk PCR. Serological Fig. 2.26 Positive MZN smear prepared from
studies of at-risk groups also showed that over 80% placental exudate. Coxiella was confirmed.
to many disinfectants, including 0.5% hypochlorite and Brucella spp. Confirmatory specific C. burnetii
and 5% formalin. Temperatures reached during pas- PCR tests are now available. Serological testing of
teurisation are effective at killing C. burnetii. dam’s blood using an ELISA test is useful, particu-
Environmental contamination with the spores larly as a screening tool alongside PCR testing of bulk
can be high on infected units, particularly in bed- milk, although serological results should be inter-
ding as it is removed from buildings (occupational preted carefully if vaccine has been administered.
risk to those working in the vicinity), but also as this It is important to bear in mind that C. burnetii
material dries out, with spore carrying dust particles can be shed heavily at the time of a normal kidding,
being distributed by the wind into local communi- therefore demonstration of the organism may not
ties. Abortions are most likely to occur after infection necessarily confirm disease.
is introduced into a naive herd (or subgroup within
a herd) or in times of stress such as overcrowding, Differential diagnosis
environmental extremes or nutritional shortfalls. Other potential causes of abortion.
Clinical presentation Treatment/management/control

Abortion is associated with a progressive placen- There is good evidence to suggest that prophy-
titis: the placenta shows a generalised thickening lactic antibiotic administration in the face of
often covered with an abundant thick discharge an abortion storm is beneficial (e.g. using tet-
(Fig. 2.27). There are no obvious lesions in the racyclines). This likely reduces the number of
fetus, other than some post-mortem autolysis. abortions, but does not prevent shedding or the
The doe is not affected clinically unless there is underlying zoonotic risk.
intercurrent disease. The products of abortion should be removed and
Q fever abortions tend to present at a significantly aborting goats segregated to reduce lateral spread.
high level in year one, but in a stable herd reduce There is likely to be heavy environmental con-
dramatically by year two. tamination when a herd becomes infected, so test
and cull strategies are unlikely to be very effective
Diagnosis overall.
Examination of MZN-stained placental smears will The overall management and nutrition of the
demonstrate acid-fast pleomorphic organisms, but affected group should be reviewed, and improved if
these can be difficult to differentiate from Chlamydia found to be deficient, to reduce overall stress factors.
There are a number of vaccines available, some of
which are licensed locally for use in goats. There are
differences in the notifiable or reportable status of
Q fever between different countries. For example, in
the UK Q fever is not notifiable. In the Netherlands
the disease was made notifiable in small ruminants
in 2008, and in Australia it is notifiable.
Brucellosis
Definition/overview
Brucellosis is endemic in many areas of the world
such as the Middle East, India, China and some
southern Mediterranean countries, but many other
countries, such as the UK (in which it is a notifiable
disease), are completely free of infection.
Fig. 2.27 Q fever abortion. Note the thickened Brucellosis is a recognised zoonotic infec-
necrotic appearance overall. tion, being associated with Malta fever in humans,
40 Chapter 2
contracted most commonly from milk or dairy Treatment/management/control

products originating from infected goats and sheep. As stated, many countries are free of infection, and
There is also an occupational risk to those handling great efforts are taken to maintain this status by rig-
infected products of abortion. orous pre- and post-import testing of blood samples,
coupled with post-import quarantine.
Aetiology In endemic areas, a test and cull policy may be
The majority of cases of brucellosis in goats will beneficial in low prevalence herds, and such an
be associated with infection by Brucella melitensis, approach has underpinned control strategies for
a small, faintly acid-fast coccobacillus. The cattle geographical area clearance of infection.
pathogen Brucella abortus has been described in goats, In herds where this is not practical because
but is extremely rare. of widespread infection coupled with a lack of
infection-free replacement stock, the use of available
Pathophysiology vaccines allows such units to continue in production.
Once a goat becomes infected (mainly by the oro- The administration of a parenteral antibiotic, such
nasal route), the organism becomes widely distrib- as long-acting tetracycline, may also be considered,
uted through the body, with trophism for placental although there is limited evidence of its impact.
tissue, if pregnant, and the udder. Abortion tends to Abortions are more likely to occur in goats under
be more likely if infected in late pregnancy, but can stress due to concurrent problems such as inadequate
occur at any stage, particularly as a ‘storm’ follow- or unsuitable nutrition and overcrowding, and, in
ing introduction into a naive herd. Abortion often the face of an abortion storm, a review of husbandry
results in a persistent vaginal discharge rich in the and management could be beneficial.
infective organism. Shedding can also occur in The continuous environmental occupational risk
urine, faeces and milk. Kids born alive to infected to human health should be emphasised, particularly
does may themselves be infected and continue to on heavily infected units.
shed the organism.
Listeriosis
Clinical presentation Definition/overview
Abortion is the most common presenting sign in goats, Listeriosis is a disease of goats causing a variety of
and there are usually no characteristic signs evident. clinical signs, including abortions, encephalitis, sep-
Asymptomatic disease can be identified by serological ticaemia and sudden death – these other presenta-
surveying either for brucellosis disease surveillance or tions will be dealt with in the relevant chapters.
following epidemiological tracing from a human case It is a potential zoonosis, linked either directly or
of Malta fever. indirectly to contamination of dairy products such
as cheese, with the added problem of multiplication
Diagnosis within the infected product at fridge temperature.
The organism can be demonstrated in MZN-stained
smears from placenta, but is difficult to differenti- Aetiology
ate from other similar staining organisms such as The causative organism is Listeria monocytogenes, a
Coxiella and Chlamydia spp. B. melitensis can be cul- ubiquitous organism in soil and the general environ-
tured using specialist media such as Farrell’s. A num- ment including harvested forage such as silage. It is a
ber of serological tests have been developed for both gram-positive, predominantly rod-shaped organism,
diagnostic and surveillance testing of blood samples. which is able to survive and multiply at low tempera-
Bulk milk testing by either PCR or ELISA is a fur- tures and has a number of distinct serotypes.
ther diagnostic tool. Silage becomes contaminated mainly due to
excessive soil contamination during harvesting and
Differential diagnosis ensiling. This is often associated with mole activity
Other potential causes of abortion. in fields or setting the cutting blades too low. A poor
the potential for transfer into milk during the milk-

ing routine.
Diagnosis
Abortions will often occur during a herd episode
of listeriosis in which other clinical manifestations
have been identified. Unlike other causes of abortion
described, the doe is often sick shortly before or at
the time of abortion. Laboratory diagnosis is based
mainly on the isolation of Listeria organisms from
fetal stomach content or placenta.
Differential diagnosis
Fig. 2.28 Poorly made silage – this clamp was the Other potential causes of abortion.
source of a severe outbreak of listeriosis in goats.
ensiling process encourages multiplication of the In commercial units, control is based on avoiding
organism, particularly when secondary fermenta- soil contamination when making silage or other
tion occurs and the pH rises above 5.0 (Fig. 2.28). conserved forage, and ensuring a good ensiling and
Silage ash levels can give a good indication of likely feeding process.
soil contamination. Silage should be kept under Clinical cases in which encephalitis or septicae-
anaerobic conditions until use. Once spread out as mia are presenting signs may respond to an intrave-
a feed, low levels of Listeria organisms can rapidly nous antibiotic such as potentiated sulphonamides or
multiply to dangerous levels. Therefore, the advice is benzylpenicillin sodium and supportive therapy with
to remove any uneaten silage after 24–36 hours and non-steroidal anti-inflammatory drugs (NSAIDs),
replace with fresh silage. which may have a beneficial effect on reducing the
Miscellaneous sources of infection have included overall abortion rate. Vaccination in the face of an
wet pea straw bales that were heavily contaminated outbreak may be effective if commercial vaccines are
with soil, and thistle and bramble trauma to the available. Autogenous vaccines have been utilised
mouths of goats browsing around manure heaps or with variable results.
old spoiled forage.
Less common infectious causes of abortion
Pathophysiology
Abortions usually develop as one of a series of dif- Salmonellosis
fering clinical manifestations in an outbreak, and Salmonellosis is an unusual cause of abortion in goats,
most often follow a septicaemic episode as a result and most fetal losses result from systemic infection in
of either maternal illness and pyrexia, or because of the doe. Serotypes involved have included S. dublin,
colonisation of both fetus and placenta causing fetal S. typhimurium and S. montevideo. Infection is often
death and expulsion. the result of environmental contamination by other
clinically infected livestock such as cattle, or by wild
Clinical presentation bird or rodent carriers contaminating feed, water
Aborting does are often, but not always, systemi- and bedding. Sewage spills or overflows contami-
cally ill with pyrexia and inappetence prior to abor- nating pastureland or watercourses are other poten-
tion occurring. Recovery after abortion can be tial sources. Confirmation of infection is normally
rapid (aided by antibiotic therapy), although a per- achieved by isolating the organism from aborted mate-
sistent vaginal discharge (rich in L. monocytogenes) rial supported by other associated clinical signs such as
can be a sequela, causing udder contamination and severe fibrinonecrotic diarrhoea and systemic illness.
42 Chapter 2
Neosporosis •• Schmallenberg virus (Europe).

Neospora caninum is a microscopic protozoan parasite •• Cache Valley virus (USA, Canada and Mexico).
with worldwide distribution, and is recognised as a
major cause of abortion in cattle. Sporadic abortions Each of these infectious agents is transmitted
associated with infection in goats have been confirmed, between susceptible species, including goats, by a
but its presence has also been confirmed by serological wide variety of biting flies and midges. If infected
surveys in goat herds with no associated clinical signs. while naive and pregnant in the first trimester, the
Dogs, including some wild canids, are the definitive virus crosses the placenta after a period of viraemia,
hosts of N. caninum and are capable of shedding oocysts and causes a variety of fetal abnormalities that may
in faeces after eating placental tissues of infected ani- result in immediate abortion or the later birth of a
mals. Neospora oocysts have an impervious covering that deformed kid. The dam is usually unaffected clini-
enables survival in soil and water for prolonged periods cally. Fetal abnormalities described include:
after canine faeces have decomposed. Goats may become
infected by ingesting these oocysts, but just how sus- •• Severe damage to or absence of the cerebral
ceptible they are is unclear. Confirmation of infection cortex, leading to microencephaly and
is by histological examination of the brain and myocar- hydrocephalus.
dium of aborted fetuses and immunohistochemistry. •• Neurogenic atrophy of fetal muscles, such that
limbs develop arthrogryposis and are fused at
Tick-borne fever abnormal angles, often leading to fetal dystocia.
Anaplasma phagocytophilum, previously referred to as •• Mummification.
a rickettsial organism, causes an acute febrile con-
dition that can result in abortions in immunologi- Laboratory confirmation is based on demonstra-
cally naive goats and other ruminants in a number tion of the virus or maternal antibody. Vaccines are
of countries including the UK and parts of Europe, available in affected countries for Schmallenberg
Africa and India. It is transmitted from animal to virus and for Akabane virus.
animal by the feeding activities of the hard tick
Ixodes ricinus and possibly other tick species. Campylobacter infection
Diagnosis is based on demonstrating the patho- Although Campylobacter infection is a common cause
gen in polymorphonuclear leucocytes in Giemsa- of abortion in sheep worldwide, its involvement in
stained smears or by demonstrating a rising antibody goat abortion appears to be more sporadic, and vari-
level in paired blood samples. able between countries. Infection most often involves
Pregnant, previously unexposed does should not Campylobacter fetus fetus and Campylobacter jejuni, both
be grazed in known tick infested areas during the of which can be carried in the gut of healthy carrier
tick activity seasons where possible. In endemically sheep and goats who can introduce infection into a
infected areas, however, it is likely that most goats clean herd.
will have been exposed in early life and hence will Infection in naive pregnant does, particularly
be immune. If clinical infection is suspected, the during late pregnancy, can lead to abortions. The
organism is susceptible to tetracyclines, which can placenta may be thickened and oedematous, and
be used either therapeutically or prophylactically. occasionally characteristic focal liver necrosis can be
seen in expelled fetuses. Confirmation is based on
Arbovirus infections the demonstration of the causative organism in fetal
Arthropod-borne bunyavirus infections reported stomach content.
to have been associated with abortions (and birth In the face of an outbreak, prophylactic use
defects in kids) include: of long-acting tetracyclines may be of benefit.
Control should be aimed at preventing introduc-
•• Akabane virus (Australia, Israel, Japan, Korea, and tion and spread of Campylobacter infection, particu-
parts of Southeast Asia, the Middle East, and Africa). larly by keeping each group of late pregnancy goats
as a stable unit, thus minimising the impact of any Rift Valley fever
clinically healthy carrier animals. Any re-grouping Rift Valley fever is a mosquito-borne viral infection
of animals should be done at another time. causing sporadic outbreaks of disease among domes-
tic and wild ruminants, including goats, in Africa.
Leptospirosis During an outbreak, the characteristic pattern is for
There are occasional (and often anecdotal) reports of numerous abortions to occur with increasing mor-
abortion associated with infection by Leptospira inter- tality among young animals, together with disease
rogans serovars including hardjo, icterohaemorrhagiae, in humans (it is an important zoonotic infection).
sejroe and pomona. Confirmation is often based on Pregnant animals affected by this disease will almost
the demonstration alone of antibody in the aborting always abort (80–100%).
doe’s blood.
Maceration – non-specific
Border disease virus/bovine viral Maceration is the result of fetal death accompa-
diarrhoea virus (BDV/BVDV) nied by loss of the CL, opening of the cervix and
These antigenically similar viruses are associated entry of autolytic and other bacteria into the uterus.
predominantly with disease in sheep and cattle, The fetus decays in utero: soft tissues break down and
respectively, although there is cross susceptibility are passed as malodorous vaginal discharge; bones
between both viruses and goats. However, reports of may be too large to pass through the cervix and
reproductive failure in goats are scant. remain in situ.
Infection with BDV has been linked to early Indication is a malodorous vaginal discharge in
embryonic loss, reports of increased barren rates an animal thought to be pregnant. Ultrasonography
at scanning, or returns to oestrus after apparent or radiography is used to confirm the diagnosis.
pregnancy. Fetuses that survive this early insult can Prognosis is guarded, with treatment – consisting
show a variety of congenital abnormalities depend- of physical removal and lavage – often unsatisfac-
ing on the stage of pregnancy when first infected. If tory because of the difficulty in removing all bone
the insult is severe, then the fetus may be aborted; fragments from the uterus. If the cervix is largely
mummification is often described, and gross abnor- closed, a combination of oestrogen injections and
malities may be visible. Some fetuses will survive prostaglandin E pessaries placed into the cervix may
to term and be born alive (with abnormalities cause relaxation. Hysterotomy can be employed if
described in other chapters), or may show no visible economically justified.
abnormalities yet be persistently infected with the
virus. Non-infectious causes of abortion
Caprine herpesvirus Pharmacological products

CpHV1 can cause sporadic outbreaks of late-term Prostaglandins (administered throughout pregnancy)
abortions, often with no other clinical signs in and corticosteroid products (administered in later
the dam. The virus is also potentially associated pregnancy) can each result in a termination of the
with vulvovaginitis, balanoposthitis and respira- pregnancy and resultant abortion.
tory disease in adult goats, and enteric and sys- There are a number of reports of many other
temic disease in neonates. Aborted fetuses may products potentially causing abortions, but these
be fresh or autolysed, and show no gross lesions. are often anecdotal. The pharmacological safety
Presumptive diagnosis is by microscopic identifi- data necessary for modern products to receive a
cation of necrosis with the presence of intranuclear marketing licence are robust, and as such will result
inclusion bodies in the fetal liver, lungs and other in a reasonable safety margin. The greatest risk will
organs, or by demonstrating the virus in fetal tis- be from the gross overdosing of a licensed product,
sue and/or maternal antibody. (See earlier in chap- the use of unlicensed products or stress induced by
ter for more details.) handling and administration.
44 Chapter 2
Toxicity accumulation of excessive intrauterine fluids and

Plants and shrubs are often recognised locally as fetal oedema, a retarded fetal heart rate and eventu-
potential causes of abortion. These are impossible to ally congestive heart failure and fetal expulsion. It is
confirm by laboratory examination of aborted mate- now recognised that this same physiological pro-
rial, and diagnosis often relies on circumstantial evi- cess may also occur in other stressful situations in
dence that consumption has occurred. pregnant Angoras, such as cold inclement weather
Chemical toxicity has also been incriminated, shortly after shearing.
with abortions most often associated with wide-
spread organ failure and other clinical signs rather Mummification – non-specific
than a specific effect on the pregnancy itself. Mummification is a result of fetal death in utero, with
the cervix remaining closed. Resorption of fetal and
Vitamin/mineral deficiencies body fluids leads to mummification (Fig. 2.29). The
A number of deficiencies have been linked to abor- CL normally remains active and thus the dam does
tions in the literature, but are often difficult to not return to oestrus. Only part of the litter may be
reproduce experimentally, and as such may be com- affected.
ponents of a multifactorial cause. These include: Clinical suspicion may arise because the doe
is overdue or does not show as much abdomi-
•• Retinol (vitamin A). nal distension as expected for the stage of preg-
•• Selenium. nancy. On abdominal palpation, mummification
•• Copper. may be confused with an intra-abdominal mass.
•• Manganese. Ultrasonography aids diagnosis. Luteolysis is
•• Iodine. induced with PGF 2α . (Note: Because no active
placenta is present, corticosteroids are ineffective
There are often other clinical manifestations, in inducing abortion.) The fetus typically enters
such as stillborns or weak kids (retinol [vitamin A] the vagina 2–3 days later and must be removed with
and iodine) or congenital abnormalities (copper and great care and plenty of lubrication. Caesarean
manganese). section is a possible approach, but difficult to per-
form satisfactorily.
Malnutrition/pregnancy toxaemia
If goats are severely malnourished in late pregnancy
or, conversely, are overweight and develop preg-
nancy toxaemia, late abortions or the birth of weak
kids may occur.
Angora goats appear to be particularly susceptible
to late abortions if placed under nutritional stress in
late pregnancy (see below).
Habitual abortion in Angora goats

In South Africa, where marked genetic selection
for fine-quality mohair has been undertaken, there
has been an apparent parallel selection for genetic
habitual abortion. It is thought that the nutritional
stress associated with producing this high-quality
mohair results in chronic hyperadrenocorticism.
This in turn interferes with the normal regulation of Fig. 2.29 Mummification results from fetal death
the water and electrolyte balance of the body, caus- while the cervix remains closed and the corpus luteum
ing placental dysfunction and thus the progressive is maintained.
THE BUCK The buck produces about 30 million sperm per

gram of testicular tissue per day. Spermatogenesis
NORMAL STRUCTURE AND FUNCTION takes about 48 days, resulting from 4.5 cycles of
seminiferous epithelium each of 10.6 days duration.
Male kids are precocious, and puberty commonly Maturation and progression along the epididymis
starts around 4 months of age. It is important, how- takes another 10 days or so.
ever, not to confuse onset of puberty with sexual
maturity. The latter will follow some months later and OUT-OF-SEASON BREEDING
result in sperm production of satisfactory quantity and
quality. Indications
Bucks are not fully seasonal, although in breeds Out-of-season breeding may be desirable to put young
from temperate regions sexual behaviour, testes size bucks to use early (including for progeny testing),
and sperm production is markedly reduced during allow breeding soundness examination before the
the females’ anoestrus period. natural breeding season, in AI centres or to have sex-
Testicles are oval-shaped, paired and arranged ually active bucks available for doe synchronisation.
in a vertical orientation in a pendulous scrotum
(Fig. 2.30). The epididymis is arranged such that Technique
its head lies dorsal to the testicle and its tail ventral. Artificial lighting regimes or melatonin may be used,
Some breeds (e.g. Somali) have a split scrotum. The as discussed under oestrus manipulation in the female.
accessory sex glands consist of seminal vesicles, pros-
tate gland and bulbourethral glands. The ductus (vas) EXAMINATION FOR BREEDING
deference widens into an ampulla prior to merging SOUNDNESS
with the urethra.
The penis is fibroelastic and has a sigmoid flexure, Indications
and there is a urethral process (syn. filiform appendage; Ideally, all bucks should undergo a physical health
Fig. 2.31) extending beyond the glans penis. check 8–10 weeks prior to being used (to allow for
Fig. 2.30 The buck has a pendulous scrotum. Fig. 2.31 Extruded penis showing the glans penis
The testicles are arranged vertically. and urethral process (syn. filiform appendage;
indicated by arrows).
46 Chapter 2
resolution of any general health issues and a full return to oestrus in the does, and examination for
cycle of spermatogenesis), plus a breeding sound- insurance purposes or prior to entering a buck into
ness examination about 1 month prior to being used. an AI facility.
The timing of this examination in relation to the
buck’s natural breeding season must be taken into Aetiology
account when interpreting findings. Other indi- The causes of failed breeding soundness components
cations include unsatisfactory pregnancy rates or are shown in Table 2.1.
Table 2.1 Aetiology of failed breeding soundness components.
COMPONENT CAUSES COMMENTS

Deficient libido Hormone deficiency Negative energy balance may affect LH pulsatility
Age related factors Natural decrease from 5–7 years of age. Sexual maturity may not
be reached yet if under 1 year of age
Breed Differences recognised in other species, but little known in goats.
Estimated heritability is 0.59 in cattle, suggesting that selection is
possible
Over- or underuse Difficult to control in multiple sire groups. (See earlier in chapter
for buck:doe ratios)
Systemic disease Especially those affecting body condition, causing a systemic
inflammatory response or pyrexia, or affecting the locomotor
system
Psychological factors Fear or pain experienced during previous mating attempts.
Selective libido in group-mating systems may occur
Inability to mount Problems of the musculoskeletal system Potential problems include: degenerative joint disease, arthritis,
or spine, or neurological deficits spondylitis, foot disorders, ataxia
Inability to achieve Size disparity May be solved by use of ‘service crates’
intromission
Conformation Poor conformation (e.g. straight-legged or sickle hock) may
result in poor positioning of buck relative to the doe’s perineum
Anatomical defects Persistent frenulum or other penile deviation. Erection failure
caused by hereditary or acquired vascular shunt
Injury, adhesions, neoplasia For example, penile haematoma, phimosis, papillomatosis
Inability to fertilise Aspermia Infectious disease of genital system, congenital or acquired
obstruction of vas deference, testicular degeneration. Rarely,
anti-sperm antibodies
Low sperm count Excessive use, testicular hypoplasia or atrophy, cryptorchism
Poor motility No recent mating activity (‘stale sample’), sperm tail
abnormalities, handling error during semen evaluation (such as
cold shock, exposure to water or other spermicidal agents)
Morphological abnormalities (Fig. 2.32) Heat or cold stress, testicular abnormalities including epididymis,
seminal vesiculitis
Venereal disease CpHV-1 and certain Mycoplasma spp.
Urethral process abnormality Failure to detach from penis or absence may affect sperm
deposition
Genetic defect Lethal gene preventing fertilisation or causing early embryonic
death
The buck should display a strong scent. While

this does not reflect on the buck’s fertility, it influ-
ences standing oestrus in the doe.
Karyotyping may be used to identify specific
genetic abnormalities.
Genital tract examination

In the normal buck, the scrotal skin is soft and
undamaged. Attention is paid regarding vasectomy
scars. The testicles are freely mobile within the
scrotal sac, roughly of equal size, and have the con-
sistency of a ripe tomato. The head, body and tail
of the epididymis are palpated for presence, normal
Fig. 2.32 Morphological abnormalities of size and closeness to the testes. No pain should be
spermatozoa, such as proximal droplets (arrow) elicited when palpating scrotal contents.
or detached heads (arrowhead), may render a buck A minimum scrotal circumference of 25 cm is
subfertile. expected in dairy breed bucks weighing more than
40 kg (Fig. 2.33).
History Examination of the penis and prepuce may be
Knowing the buck’s history will influence the list of performed with the buck sitting on its haunches
differential diagnoses and interpretation of results. (but is less tolerated in goats than in sheep) or in the
Of particular interest is whether the buck has bred standing position (elevated on a table or bale of straw
successfully before or is a maiden, is currently with for ease of examination). The penis, including its
a group of cycling females, is presented within the sigmoid flexure, is palpated through the prepuce; it
breeding season, has had any recent illnesses or should be mobile, without any swelling or enlarge-
treatments and whether libido and mounting ability ment and pain free. After extrusion, the glans penis
have been observed. and urethral process are examined. In the prepu-
bescent male, normal preputial adhesions prohibit
Physical examination extrusion. The integrity and health of the prepuce
Bucks are often poorly cared for outside the breeding and parapreputial abdominal skin is established
period, potentially resulting in poor foot health and (Fig. 2.34). Preputial hair should be moist, with no
body condition, and heavy ecto- and endoparasite bur- evidence of urolithiasis or discharge.
dens. In addition to the feet, joints are examined for Assessment of the accessory sex glands is lim-
arthritis, in particular the elbows. The target body con- ited in the buck. While the prostate gland is within
dition score is 3–3.5 (scale 1 to 5). Overconditioning may digital reach, its diffuse nature prevents meaningful
negatively affect libido, as well as sperm quality, with examination. However, pain may be elicited on digi-
fat deposition increasing scrotal temperature. Scrotal tal rectal palpation if severe pathology of any acces-
mange may also lead to increased scrotal temperature. sory gland is present.
Negative energy balance affects LH pulsatility. Further diagnostic aids include ultrasonography
The cardiovascular and respiratory systems are of the testicles (transcutaneous) and accessory sex
examined to determine physical fitness. Vision and glands (transrectal), and culture or other patho-
smell are important, especially where group mating gen isolation of either a preputial wash or a semen
is used. Where bucks are kept together, the poll and sample.
horns are examined for signs of fighting injuries.
The brisket area is checked for trauma, especially if Semen evaluation
a raddle harness is used. Attention is paid to urinary Semen may be collected using either an artificial
tract health. vagina or electroejaculation (EEJ). When using EEJ,
48 Chapter 2
(a) (b)

Fig. 2.33 Scrotal circumference indicates sperm output capacity. (a) Measured correctly: testicles fully
descended and held in place by tightening the scrotal skin in the neck area, with the measurement over the
widest part of the scrotum. (b) Incorrect holding of the testicles: the thumb of the left hand pushes the testicles
apart, resulting in an elevated measurement.
Fig. 2.35 For electroejaculation, a 3 cm diameter

probe with ventrally placed electrodes is suitable.
(Probe shown is by Lane Manufacturing, Denver,
Colorado.)
ring-electrode one, and the unit should allow grad-

Fig. 2.34 Lesions around the prepuce will reduce ual increase of stimulation. EEJ is a veterinary pro-
libido and mounting willingness. cedure and heavy sedation is recommended. (Note:
Anaesthesia is a requirement in some countries.)
the ejaculate is commonly diluted by accessory Semen evaluation parameters include (Fig. 2.36):
gland fluid. This will result in reduced density and
lower apparent gross motility, but not affect other •• Volume: typically 1.0–1.5 ml.
semen evaluation parameters. For EEJ, a ram probe •• Colour and appearance: a rough estimate of
(circa 3 cm diameter; Fig. 2.35) is used. A probe density can be made based on appearance
with ventrally placed electrodes is preferable to a (beware EEJ dilution effect). In a creamy
TESTICULAR AND EPIDIDYMAL

ABNORMALITIES
Testicular hypoplasia
Definition
Testicular hypoplasia is a congenital defect with a
genetic basis.
Unilateral or bilateral underdevelopment of testicle,
recognisable from puberty onwards.
Fig. 2.36 Handling errors, like cold shock, must be Diagnosis

avoided when assessing semen quality. Note the use of Suboptimal scrotal circumference. For unilateral
a hotplate to pre-warm slides and the heated stage on cases, also unevenness between testes size.
the microscope. The procedure should be carried out
in a draught-free, warm environment. Differential diagnosis
Testicular degeneration developing later in the
sample, the presence of pus must be buck’s life.
ruled out (e.g. by examining a stained
smear). No blood contamination should be Treatment/management/control
present. Moderately high hereditability, therefore selection
•• Sperm concentration: varies from 2–10 × 109 against is possible.
spermatozoa/ml (beware EEJ dilution effect).
•• Gross motility: 2.5 or higher (on a scale of 0 = no Testicular degeneration or atrophy
movement, to 5 = strong swirling waves; beware Definition
EEJ dilution effect). This acquired reduction in testicle size is one of the
•• Progressive motility: minimum targets are 30% common testicular problems seen. The buck typi-
for natural service in a multiple sire group, 50% cally has been fertile before, and continues to show
for a single sire group, and 70% for AI. normal service behaviour.
•• Morphology: target is >70% morphologically
normal, with no one abnormality exceeding Aetiology
20% (taking into account whether defects are Testicular degeneration or atrophy is often a result
compensable or not). of elevated scrotal temperature (e.g. secondary
•• Live-to-dead ratio: for routine examinations, to heat stress or pyrexia). Other possible insults
this step may be omitted. Gross and include trauma and genital tract infections leading
progressive motility will indicate proportion to regional inflammation or vascular compromise,
of live sperm. Where performed, strict frostbite and a systemic illness-induced inflamma-
adherence to protocol is important to obtain tory response. Toxic damage, high oestrogen diet,
meaningful results (quality of reagent, correct gonadotrophin deficiency and autoimmune disease
temperature maintained throughout, accurate are rarer causes. Testicular degeneration has been
timing). observed as part of caprine contagious agalactia
•• pH: target is 6.8–7.0. (see Chapter 12).
•• Cellularity and bacterial contamination:
Gram stain or Diff-Quik ® are suitable Clinical presentation
to assess excessive cellular debris or Testicular consistency is soft and fibrosis may be
bacterial count. palpable. Scrotal circumference is often reduced.
50 Chapter 2
Diagnosis
Systematic clinical and reproductive tract examina-
tion, together with history (e.g. exposure to extreme
weather). The exact cause may be difficult to identify.
Ultrasonography is useful to establish the extent and
type of changes within the testes.
Testicular hypoplasia, which is present from a
young age.
Addressing the underlying cause, including NSAID
therapy. Prognosis is generally guarded to poor, but
depends on type and length of insult. Gonadotrophin
treatment may be tried. Monitoring for resolution
should take into account the 58 days required for
spermatogenesis.
Orchitis and epididymitis Fig. 2.37 Noticeable scrotal enlargement in a ram

Definition with epididymitis.
Orchitis and epididymitis are more commonly rec-
ognised in the buck compared with some other spe-
cies, but often not detected until severe pathological Testicular mobility within the scrotum is reduced.
changes are present. May be unilateral or bilateral. If accessory glands are affected, pain on rectal palpa-
tion may be present. Gangrenous changes are occa-
Aetiology sionally present in the scrotal skin.
Post-traumatic invasion with opportunistic patho-
gens may occur, typically as an ascending infec- Diagnosis
tion. Specific pathogens associated with orchitis Clinical signs, combined with ultrasonography
and epididymitis include Corynebacterium pseudo- showing tissue oedema and irregular echogenicity
tuberculosis, Brucella melitensis, Actinobacillus seminis, (Figs. 2.38).
Staphylococcus pyogenes, Chlamydia abortus, Escherichia
coli, Pseudomonas spp. and Besnoitia spp. Differential diagnosis
Inguinal herniation (Fig. 2.39), testicular haema-
Pathophysiology toma, spermatic cord torsion, neoplasia.
Infection causes rapid damage to seminiferous
tubules, reducing sperm output. The inflammatory Treatment/management/control
response may result in heat insult of the unaffected If only one testicle is affected, unilateral castration is
testis, and pressure build-up in the tunica albuginea a viable option. Sperm output in the remaining testi-
leading to internal tissue necrosis. Infection may cle may reach 80% of normal total output. However,
spread to the epididymis and accessory sex glands. the client should be advised that the inflammation
may have caused secondary damage to the unaffected
Clinical presentation testicle. For bilateral cases, aggressive antibiosis
Pyrexia is common in the early stage. The testicle (e.g. macrolides) combined with anti-inflammatory
is enlarged and painful (Fig. 2.37), often result- therapy, and emollient cream if the scrotal skin is
ing in reluctance to move and an abnormal stance. affected. Prognosis for suppurative cases is guarded.
(a) (b)

Fig. 2.38 Irregular echogenicity indicates testicular pathology (such as orchitis, degeneration or neoplasia,
as in [a]), compared with the homogeneous appearance of normal testicular tissue (b).
gonad may increase the risk of neoplastic changes.

Prevalence in the goat appears to be low.
Aetiology
Likely to have a genetic component, with irregu-
lar transmission by parents and their offspring.
Insufficiency in testosterone and Müllerian-inhibiting
hormone may be involved. Cryptorchism is frequently
seen in intersex animals. In the goat, testicular descent
is usually complete at birth.
One or both testicles are absent from the scrotal
Fig. 2.39 A loop of intestine (longitudinal section) is sac. They may be located at any point along their
apparent on the left-hand side in this ultrasonography normal migration path between the external ingui-
scan of the scrotum. This indicates an inguinal hernia nal ring and the kidneys. Occasionally, they are
as the cause of scrotal enlargement. positioned cranial to the scrotum along the ventral
abdominal wall.
The epididymis and deferent duct may become Diagnosis

obstructed secondary to the inflammation. Palpation confirms absence from the scrotal sac and
may reveal the position along the abdominal wall
Cryptorchism (syn. retained gonad) or near the inguinal ring. Ultrasonography is used
Definition to locate intra-abdominal gonads (Fig. 2.40) or to
Cryptorchism is the absent or incomplete descent confirm the testicular nature of any mass detected
of one or both testicles. Subfertility often results, on palpation. The retained gonad is typically smaller
mainly due to a lower sperm count. Exposure to than normal and the parenchyma often appears less
higher than normal temperatures of the retained uniform.
52 Chapter 2
accessory sex gland, and may be unilateral or bilat-

eral. Cysts in the bulbourethral gland have also
been reported.
The animal may display dysuria or stranguria. Pain
is elicited during digital rectal examination. The
ejaculate contains inflammatory cells and bacteria,
and sometimes outright pus. Very rarely, the affected
seminal vesicle may rupture, causing peritonitis, or
fistulate into the rectum.
Urolithiasis or urinary tract infection for dysuria
or stranguria. Pelvic trauma for pain on rectal
Fig. 2.40 Intra-abdominal testicle, with intestinal examination.
loops visible to the left. The normal, homogenic
appearance is often lost in retained gonads, and they Treatment/management/control
are often smaller than normal (about 3.5 cm length in Aggressive antibiosis (e.g. macrolides) in the early
this case). stages, but prognosis is guarded with often remis-
sion rather than cure being achieved. Aspiration of
cysts may be attempted.
Monorchism is much rarer than cryptorchism, PENIS AND PREPUCE ABNORMALITIES
but may be ruled out by a LH stimulation test
2 months after surgical removal of the testicle that Penile deviation
is present. Overview
Persistent frenulum in a young buck and acquired
Treatment/management/control deviation in older males are the main causes of penile
Because the retained gonad may produce fertile deviation.
sperm, and because of the increased risk of neo-
plasia, surgical removal is recommended in males Aetiology
destined to be kept into adulthood or housed with A persistent frenulum results from failure of the
does. A scrotal approach is usually successful for preputial attachment to break down fully, leaving
gonads lying near the inguinal ring. The gubernac- a remnant connecting the ventral penis with the
ulum testis can be used as a guide towards a gonad prepuce (Fig. 2.41). A lack of testosterone exposure
lying in the inguinal canal. A laparotomy is usu- may be responsible.
ally necessary to remove gonads located near the A loose attachment of the dorsal penile ligament
kidney. to the dorsal surface of the tunica albuginea results
in lateral deviation during erection. The penis may
ACCESSORY SEX GLAND DISORDERS adopt a corkscrew shape (spiral deviation) in severe
cases. Degeneration or trauma to the ligament are
Definition possible precursors.
The most widely recognised accessory sex gland An hereditary component has been postulated
disorder is seminal vesiculitis. This is caused for both conditions. Affected bucks should not be
by inflammation or infection, either as part of a used to sire offspring destined for a pedigree breed-
wider genital tract infection or just affecting this ing pool.
Aetiology
Penile haematoma is usually caused by the
male thrusting without having achieved intromis-
sion, thereby deflecting the fully erected penis
ventrally. This results in a tear in the dorsal tunica
albuginea, often around or anterior to the sigmoid
flexure, with subsequent haemorrhage into the sur-
rounding tissues.
Initially a soft, fluctuant, typically bilateral sym-
metrical swelling develops on the ventral abdomen
cranial to the scrotum. Pain may be present on
palpation. Over time, the swelling becomes harder
and may reduce in size. If presentation is delayed, it
may be difficult to exteriorise the penis because of
adhesions.
Fig. 2.41 Persistent frenulum in a yearling bull. Diagnosis

Palpatory findings and history of recent mating
Clinical presentation activity. Ultrasonography confirms the presence of
The buck fails to achieve intromission. Close obser- a haematoma associated with the penis.
vation of mating activity is required to detect this, as
sexual behaviour is normal including possible ejacu- Differential diagnosis
lation and thrusting outside the vagina. Ruptured urethra secondary to urolithiasis, with
subcutaneous accumulation of urine. The swelling is
Differential diagnosis more extensive and the condition more common in
Spiral deviation during semen collection using EEJ a castrated male, rather than in an entire male. Also,
can occur, but this does not mean that deviation also history of dysuria or anuria and elevated blood urea
occurs during natural service. and creatinine levels.
Treatment/management/control Treatment/management/control
A persistent frenulum can be surgically corrected. Routine wound management principles are applied
After digital or EEJ stimulation to cause an erec- to shearing injuries.
tion, the penis is ‘snared’ (e.g. with a loop of gauze For penile haematoma, conservative treatment
bandage). The frenulum is ligated and cut at both consists of cold or hot packing, if discovered early,
ends. For lateral or spiral deviation, suturing the combined with anti-inflammatory therapy.
dorsal ligament onto the tunica albuginea may be Surgical repair of the rent may be attempted,
attempted. However, improvement is often only either under epidural, local infiltration or general
temporary. anaesthesia and with the buck in dorsal recumbency.
After blunt dissection to expose the penis, the blood
Penile trauma clot is removed and the defect in the tunica repaired
Overview with absorbable suture material. Routine antibiosis
In fibre breeds, careless shearing may result in injury and anti-inflammatory therapy is given.
to the penis or prepuce. Penile haematoma (syn. bro- To avoid adhesions, the buck is teased without
ken penis) is reported much less in small ruminants being allowed to mate, starting from 2 weeks after sur-
compared with bulls. gical repair and 4 weeks after conservative treatment.
54 Chapter 2
Prognosis is about 50% with either approach, with for paraphimosis: extruded parts are cleaned, if nec-
recurrence and adhesions the most common problems. essary using surgical debridement. After thorough
lavage with saline or a mild disinfectant, an antibi-
Phimosis and paraphimosis otic ointment, with or without corticosteroids, or
Overview udder cream is applied, and the penis is replaced. If a
Phimosis and paraphimosis are an inability to extend risk of re-prolapse is perceived, a purse-string suture
the penis or withdraw the penis back into the pre- may be placed into the preputial orifice, encasing a
puce, respectively. Both are relatively rare in the tube to facilitate urination. The penis is manually
buck, but result in marked loss of libido and fertility. exteriorised every 1–3 days, with repeated lavage and
ointment application.
Aetiology Phimosis carries a poor prognosis, in part because
Causes include hair rings, trauma and balanoposthitis. of loss of libido. Prognosis for paraphimosis is poor
if presentation is delayed or the swelling continues
Clinical presentation to prevent withdrawal of the penis after a few days.
Phimosis presents as failure to extrude the penis Where hair rings are the cause, regular shearing
when sexually stimulated. With a traumatic aetiol- of the hair just cranial to the prepuce may prevent
ogy, adhesions may prevent manual exteriorisation. the problem.
Paraphimosis presents as a continuous extrusion of
the penis, with secondary inflammation, swelling Balanoposthitis
and trauma (Fig. 2.42). Overview
Two main forms of balanoposthitis are recognised
Differential diagnosis in goats: infectious and enzootic (syn. ‘pizzle rot’).
Urolithiasis or urinary cystitis, if dysuria or stran-
guria is present. Aetiology
Pathogens associated with the infectious form include
Treatment/management/control CpHV-1, contagious ecthyma (orf) and Mycoplasma
The buck is sedated. For phimosis, any hair rings and Ureaplasma spp.
are removed and the penis manually exteriorised to The enzootic form is associated with high dietary
check for trauma. Where penile adhesions prevent protein (e.g. in bucks on lush spring pasture or during
this, treatment becomes unrewarding. Any traumatic feeding-up for shows or sales). This leads to high urea
lesions found are treated along the same principles as levels in the urine, which is hydrolysed to ammonia by
the commensal Corynebacterium renale. Both very short
and very long preputial hair are recognised as risk fac-
tors. The condition is more common in castrated males.
Early castration may increase the risk, with lack of expo-
sure to testosterone leading to failure of the frenulum to
detach and subsequent urination into the prepuce.
The irritation leads to severe inflammation of
the penile shaft, parapreputial skin and preputial
mucosa, often with pustules, ulceration and scab for-
mation. Secondary bacterial infection is common.
Dysuria and stranguria may be observed. Complete
occlusion may result, leading to death.
Fig. 2.42 Paraphimosis in a ram. (Image courtesy Venereal transmission of the infectious form will
Daniel Scovenna.) result in infectious vulvovaginitis in the does.
Urolithiasis if dysuria or stranguria is observed.
Topical and systemic antibiosis, combined with anti-
inflammatories, emollient cream and sexual rest. For
the enzootic form, penicillin against C. renale and
reduction of dietary protein.
Neoplasia of the male

reproductive tract
Overview
Various tumours may affect any part of the repro-
Fig. 2.43 Marked enlargement caused by
ductive tract, but overall neoplasia is rare in bucks.
unilateral testicular neoplasia affecting both
Unlike in bulls and boars, there is no specific virus-
germ and stromal cells. Severe adhesions
associated neoplastic disease in bucks.
necessitated scrotal ablation during surgical
removal.
Aetiology
Both benign and malignant tumours of a variety of
tissues may occur, including squamous cell carci-
noma, Leydig or Sertoli cell tumours, adenoma/ade-
nosarcoma, teratoma, seminoma and haemangioma/
haemangiosarcoma. Metastasis into reproductive
tract tissues from other sites is very uncommon.
Proliferative penile lesions may interfere with intro-
mission, and bleeding is often observed during or
after mating activity. Associated pain often leads to
loss of libido.
Tumours affecting the testes may lead to disrup-
tion of spermatogenesis (Fig. 2.43). Epididymal or
accessory gland neoplasia often leads to secondary
sperm abnormalities.
Behavioural changes may be apparent with either
Leydig (aggression) or Sertoli (feminisation) cell
tumours.
Diagnosis
A definitive diagnosis is achieved with histology of
tissue biopsies.
Unilateral castration may be an option for unilat- Fig. 2.44 A catheter placed into the urethra is
eral testicular neoplasia. Penile tumours sometimes useful during penile surgery to avoid accidental
can be excised, with optional cautery or cryosurgery trauma to the urethra. (Image courtesy Peter G.G.
(Fig. 2.44). Jackson.)
56 Chapter 2
CASTRATION Preparation and equipment

Tetanus cover (vaccination or antitoxin), routine
A rubber ring may be used in kids up to 7 days of antibiosis and NSAIDs. If performed with goat in
age (Fig. 2.45). Under UK regulations, anaesthesia recumbency, preoperative starvation. Simple proce-
must be used in animals over 2 months of age, but is dure kit, absorbable suture.
recommended in animals of any age.
Restraint
Indications Typically performed in the standing animal under
Easier management of pet goats and fibre breeds, local infiltration of the scrotum and/or spermatic
in particular allowing cohabitation of males and cord and/or testicle. Sacrococcygeal epidural is also
females. Avoidance of meat taint if reared to a more suitable (2% lidocaine HCl at 1 ml/45 kg, possibly
mature age for slaughter. combined with 0.07 mg/kg xylazine HCl).
Technique
The scrotum is incised on both lateral aspects with
a J-shaped incision, starting one-third to halfway
up the scrotal sac and ending close to the median
raphe. For open castration, the tunica vaginalis is
incised (Fig. 2.46) and the testicle exteriorised.
The attachment of the tunica near the epididymis
is broken (Fig. 2.47) and the tunica pushed back
into the scrotal neck. For closed castration, the
tunica vaginalis is kept intact (Fig. 2.48). The cord
is either ligated with absorbable suture material
or clamped for 2 minutes above the pampiniform
plexus (Fig. 2.49). The cord may also be broken
by the ‘twist and pull’ method in young animals.
The skin incision is left open.
Fig. 2.45 Castration using a rubber ring (here
shown in a lamb).
Fig. 2.46 Maintaining firm pressure on the scrotal Fig. 2.47 Breaking the tunical attachment near the
sac aids exteriorisation of the testicle. Incision of the epididymis with an instrument (rather than manually)
tunica vaginalis has been started in this image. reduces contamination of tissues to be retained.
Fig. 2.48 The tunica vaginalis is kept intact for Fig. 2.49 Clamping or ligation must be done
closed castration. proximal to the pampiniform plexus.
tunica vaginalis prolapses through the skin incision;

this is cut off at the level of the scrotal skin. Abscess
formation is dealt with by drainage and lavage.
VASECTOMY
Indications
Creating a teaser buck that is sexually active, but
incapable of fertilisation. Mainly used to advance the
breeding season. (Note: Other techniques to create
a teaser male, such as penile diversion or amputation,
are banned in the UK.) Anaesthesia must be used for
vasectomy in the UK.
A sexually mature (>1 year of age), physically fit
male showing good libido should be used.
Preparation and equipment

Tetanus cover (vaccination or antitoxin), routine
antibiosis and NSAIDs. If performed with goat in
Fig. 2.50 Postoperative haemorrhage addressed by recumbency, preoperative starvation. Simple proce-
packing the scrotal sac with gauze swabs. dure kit, absorbable suture.
Aftercare Restraint
Clean bedding, encouragement and space to move Performed with the buck sitting on its haunches
around. Fly repellent if necessary. or in dorsal recumbency. Mild sedation, if neces-
sary. Local infiltration over the cranial neck of the
Complications scrotum.
Postoperative haemorrhage is addressed by locating
the stump of the spermatic cord (in severe cases, via a Technique
laparotomy) and renewed ligation. Packing of the scro- A 3 cm long, longitudinal skin incision is made on
tal sac is less effective, as bleeding may continue intra- the cranial aspect of the scrotal neck over each sper-
abdominally (Fig. 2.50). Occasionally, part of the matic cord (Fig. 2.51). Using blunt dissection, the
58 Chapter 2
cord is freed and lifted into the incision (e.g. by plac- cord slightly facilitates identification. The tunica is
ing a pair of tissue forceps underneath it). The vas incised over the vas (Fig. 2.53) and the latter grasped.
deference, lying slightly medial to the cord’s midline, Haemorrhage from the tunica incision readily
whitish in appearance and feeling firm under digi- obscures the surgical field, therefore identification of
tal palpation, is identified (Fig. 2.52). Rotating the the vas prior to incision greatly aids its location after
the incision. The vas is ligated with absorbable suture
at either end, and a section of at least 3 cm removed
(Fig. 2.54). A few simple interrupted sutures are
placed into the subcutaneous layers, and the skin is
sutured in a routine way (Fig. 2.55).
Aftercare
Clean bedding, fly repellent if necessary, sexual rest
for 1 month.
To confirm removal of the correct structure,
the contents of the removed section of vas can be
squeezed onto a slide and examined for spermato-
zoa. Alternatively, the removed sections are placed
into formal saline, providing the option to perform
histology should a dispute arise.
Complications
Haemorrhage tends to be minimal. A post-
vasectomy spermatocoele is a common compli-
Fig. 2.51 Holding the spermatic cord firmly through cation, occurring in a large proportion of teasers
the skin, a 3 cm long incision is made over the cranial within 2 years of surgery, seen or palpated as dis-
aspect of the scrotal neck. tension of one or both testes within the scrotum.
Fig. 2.52 The spermatic cord is freed and brought into Fig. 2.53 The vas becomes visible (here underneath
the incision. The vas deference lies medially (arrow). the point of the scalpel blade) after incision of the tunica.
Fig. 2.54 The vas is clamped and ligated at either end, Fig. 2.55 The incision is closed in a routine
making sure a minimum of 3 cm length is removed. manner.
TEMPORARY SUPPRESSION
OF FERTILITY
Indications
This may be asked for by smallholders, where either
housing of the buck separate from non-pregnant
does may not be possible or where owners wish to
suspend breeding activity for 1 year.
Technique
A commercial anti-GnRH vaccine was effective in
90% of Australian bucks, resulting in temporary
suppression of spermatogenesis and male odour and
behaviour for up to 1 year. Some regions use canvas Fig. 2.56 Gynaecomastia.
or leather belly-aprons to prevent intromission.
Alternatively, progesterone may be administered
to the female goats, either daily in feed or as an Treatment is generally unsatisfactory, although cab-
implant (not in UK). ergoline therapy has been tried with some success.
The problem usually resolves with time.
OTHER MALE DISORDERS
Venereal disease
Gynaecomastia Vulvovaginitis and balanoposthitis can be associated
Commonly seen in males of heavily milking strains, with the venereal spread of both CpHV-1 (see above)
especially in the British Saanen breed (Fig 2.56). and certain Mycoplasma spp. (see Chapter 10).
CHAPTER 3
PREGNANCY AND PARTURITION

61
PREGNANCY
Fertilisation occurs in the ampulla of the oviduct

several hours after ovulation. The conceptus reaches
the uterus 4–5 days after conception. Fixation occurs
around day 18 to day 22.
Gestation is on average 150 days’ duration
(range 147–155) and is corpus luteum (CL) depen-
dent throughout. The doe has an epitheliochorial
cotyledonary placenta. The maternal caruncles and
fetal cotyledons form multiple concave placentomes
(Fig. 3.1).
In the UK, the kidding period is typically from
January (Anglo-Nubians) or February until March.
Pregnancy diagnosis
Indication
Confirming pregnancy and identifying non-
pregnant animals for re-breeding or culling are of
equal importance. Additional uses include determi- Fig. 3.1 The concave placentomes typical of the
nation of litter size, fetal gender, gestational length doe’s placenta.
and fetal viability.
Technique
Pregnancy diagnosis methods include real-time
(syn. B mode) ultrasonography transrectally from
day 25 to day 30 and transabdominally from day 40
to day 45 (Figs. 3.2–3.5), blood or milk oestrone
sulphate from day 45, and abdominal radiogra-
phy from day 70 to day 80. A caprine pregnancy-
specific protein (interferon tau) has been identified
and could be used from day 25, but field testing
kits are not currently available. The fetus may be
detected on abdominal palpation in the second half
of gestation. Supportive signs include non-return Fig. 3.2 A uterus filled with anechoic fluid is
to oestrus, elevated milk or blood progesterone lev- indicative of pregnancy. A single, fluid-filled structure
els from day 18 to day 21 and, least accurate, live may be the urinary bladder, therefore both uterus and
weight gain. bladder must be visualised to avoid misdiagnosis.
62 Chapter 3
Fig. 3.3 As pregnancy progresses, fetal structures Fig. 3.4 In late-stage pregnancy, there is often
become apparent, such as the stomach (arrow), heart little obvious free fluid. Yellow arrows = outline of
(wide arrow) and ribs (arrowheads; with reverberation placentomes; white arrows = outline of fetal head.
artefacts below).
Fig. 3.6 Mushroom-shaped placentomes become

visible from day 40.
from day 40, and reach 2–3 cm in length by day

Fig. 3.5 Ultrasonography is useful to confirm fetal 60 (Fig. 3.6). In dairy breeds, fetal age can be cal-
health. Here, two amniotic vesicles are present, but culated between 40 and 100 days using the bipari-
only the right-hand one contains a conceptus. etal diameter (BPD; Fig. 3.7) of the head and the
formula:
Gestational age (days) = 1.71 × BPD (mm) + 14.6
Ultrasonographic determination of litter size
is best performed with a 3.5 MHz 170-degree Sexing may be attempted by ultrasonographi-
sector probe between 40 and 75 days of gestation. cally assessing the position of the genital tubercle at
Placentomes become visible on ultrasonography 60–69 days.
P r e g n a nc y a n d Pa r t u r i t ion 63
Fig. 3.7 The biparietal diameter is the distance

between the eye sockets (indicated by the dotted line
between the two white crosses [×]). The nose of the
fetus points towards the 2 o’clock position in this
image.
PREPARTUM PROBLEMS
Hypocalcaemia and
pregnancy toxaemia
(See Chapter 14)
Fig. 3.8 Abdominal distension in a doe with
Mummification, maceration
pseudopregnancy.
and fetal maldevelopment
(See Chapter 2)
appearance of pregnancy (Fig. 3.8). In non-lactating
Pseudopregnancy (syns. does, mammary development sometimes follows in
cloudburst, hydrometra) the later stages. Lactating does may show a drop in
Definition/overview milk yield.
Pseudopregnancy is an abnormal accumulation of Sudden loss of fluid occurs (giving rise to the col-
sterile uterine fluid in the absence of a fetus. A mean loquial term ‘cloudburst’), usually near or beyond
herd incidence of 9% has been reported (range normal term (150 days) in mated does and before
3–30%). normal term in unmated does. Indirect signs that
fluid loss has occurred include the abdomen return-
Aetiology ing to a normal size, damp bedding and a moist vulva
The exact cause of pseudopregnancy is unknown. and perineum.
Incidence appears to increase with age, and it may be
more common after oestrus has been induced and in Diagnosis
certain family lines. It can occur in both mated and Transabdominal ultrasonography shows clear fluid
unmated does. in the uterus in the absence of a fetus, placenta or
amniotic vesicle. A ‘honeycomb’ appearance may be
Clinical presentation present (Fig. 3.9). Other pregnancy diagnostic tests
Following oestrus (with or without mating), abdom- are equally negative (including oestrone sulphate
inal distension slowly increases, giving an external levels, abdominal palpation, radiography).
64 Chapter 3
Fig. 3.9 Honeycomb appearance of the uterus on Fig. 3.10 Marked abdominal distension, excessive
ultrasonography - here in a case of pyometra. The same for the stage of pregnancy, in a doe with hydrops
appearance is commonly found in pseudopregnancy, allantois.
although then the fluid will be anechoic.
Differential diagnosis allantois, respectively. It is unestablished in goats

Normal pregnancy or pregnancy accompanied by whether there is an association between hydrops
hydrops allantois or hydrops amnion are ruled out allantois and an abnormal placenta and hydrops
by real-time ultrasonography. amnion and fetal malformation, as in cattle.
Treatment/management/control Clinical presentation

Prostaglandin-F 2 alpha (PGF2α) given i/m usually Hydrops amnion tends to be insidious in onset from
results in loss of fluid within 36 hours (e.g. 10 mg the second half of gestation. The condition often
dinoprost or 62.5–125 µg cloprostenol; dinoprost goes unnoticed until parturition, when excessive
may have a beneficially more direct action on the fluid is noticed. Hydrops allantois shows a rapid
myometrium). A repeat dose of PGF2α after 12 days development, leading to marked abdominal disten-
is recommended. Oxytocin may aid involution. sion (Fig. 3.10). This may lead to respiratory dis-
Affected does that remain unbred are likely to have tress, discomfort and recumbency.
the problem repeatedly, therefore mating, culling or Should pregnancy continue to term, contractions
spaying should be considered. may be weak and the fetus may display oedema,
anasarca, hydrothorax or ascites with both condi-
Hydrops uteri tions, all potentially leading to dystocia.
Overview
Hydrops uteri is a rare condition in the goat, but Diagnosis
often life-threatening to both dam and fetus, espe- Ultrasonography to detect excessive fluid and
cially hydrops allantois, which is the more common placental, cotyledonary and fetal abnormalities.
form. Centesis may be used to confirm the type of fluid,
with sodium and chloride levels much higher in
Aetiology amniotic fluid (bovine values: sodium 120 versus
Excessive accumulation of either amniotic or allan- 50 mmol/l, and chloride 90 versus 20 mmol/l,
toic fluid leads to hydrops amnion or hydrops respectively).
Large litter and pseudopregnancy for uterine dis-
tension. For hydrops allantois, also other causes of
abdominal distension and respiratory distress, in
particular rumen tympany, peritonitis or ascites.
If the doe is not unduly affected, pregnancy may be
allowed to continue to term, but assisted delivery is
typically required, as well as intensive care for the
neonate. If the doe is close to term, induction of
birth and an elective caesarean section are options.
In both, the rapid loss of abdominal pressure may
trigger splanchnic disturbances, and fluid replace-
ment therapy is advisable. If the doe is affected but
far from term, abortion should be induced and occa-
sionally euthanasia is indicated. Neither diuresis nor
uterine drainage are effective long term.
Prognosis is guarded to poor, and recurrence in
subsequent pregnancies cannot be ruled out. Fig. 3.11 A recent vaginal prolapse in a ewe.
Vaginal and cervical prolapse of the vaginal wall with intestinal prolapse is a rare
Overview complication.
Vaginal and cervical prolapse is an important prob-
lem in the prepartum doe, requiring careful man- Diagnosis
agement. While usually only seen sporadically, herd Clinical examination confirms the condition and
‘outbreaks’ may be encountered. Occasionally, it is allows assessment of tissue viability. Pregnancy sta-
seen in the post-partum doe. tus should be confirmed.
Aetiology Differential diagnosis

Principally, excess relaxation or weakness of pelvic Rectal prolapse may be confused with vaginal tissue,
tissues, possibly combined with increased intra- and sometimes both occur concurrently.
abdominal pressure. Predisposing factors include
genetic predisposition, high body condition score Treatment/management/control
(BCS), ageing, oestrogenic diet and bulky feeds Mild or intermittent cases may be dealt with by
(e.g. turnips). A sloping environment aids develop- cleaning, lubricating and replacing the prolapse,
ment. However, the exact aetiology remains unclear, followed by one of several retention methods. In
and two herds with equal genetics and management more severe cases, substantial trauma is addressed
may have a very different incidence rate. (e.g. by suturing) and a sacrococcygeal epidural
given. It is useful to add 0.07 mg/kg xylazine HCl to
Clinical presentation the epidural to suppress straining for several hours.
Eversion of the vagina (sometimes including cer- Retention methods include:
vix), leading to exposure of the mucosal surface
(Fig. 3.11). The prolapse may be intermittent, and •• Plastic retainer (Fig. 3.12) or body truss
partial or complete. The exposed tissues quickly (Figs. 3.13). (Note: While not advisable,
become dry and traumatised. The doe often displays kidding is possible without removing these
a raised tail and moderately arched back. Rupture devices.)
66 Chapter 3
(a)
Fig. 3.12 A plastic spoon-shaped retainer for vaginal
prolapse.
•• Retention sutures placed in the vulva, such as

Bühner or simple mattress. Careful placement is
required to avoid discomfort and tissue trauma.
Use of suture buttons is advised.
•• Vulvoplasty, such as Caslick’s, may be considered
in chronic cases that are far from term.
Any sutures must be removed and the vulvoplasty

reversed by an episiotomy prior to stage 2 of labour.
NSAIDs should be routinely given and antibiosis
is strongly advised. Parturition must be supervised
in affected does. Whether prepartum prolapse is
recurrent in the doe (like in the ewe or cow) is not
known, making culling advice difficult. Both pre-
and post-partum prolapse leads to reduced fertility.
For post-partum prolapse, the Farquharson tech-
nique (submucosal resection) or Winkler’s cervi-
coplasty (external cervical os secured to prepubic
tendon) may be considered. (b)
Fig. 3.13 A sheep prolapse harness or truss is also
Rupture or herniation of the uterus
suitable for goats with a vaginal prolapse (a). It exerts
Overview
pressure over the perineal area (b).
The gravid uterus may rupture prior to term or her-
niate through an existing or acquired body defect
(including inguinal, umbilical, diaphragmatic, peri- hydrops uteri in a goat. In general, abnormally high
neal, prepubic tendon). While rare, these are life- uterine weight contributes to herniation.
threatening conditions.
Aetiology With herniation, the abdominal contour appears
External trauma appears to be the most common rea- abnormal, and gait and stance may be altered.
son for uterine rupture. Herniation through a rent in Prepubic tendon rupture is often accompanied by
the prepubic tendon has been reported secondary to painful oedema just cranial to the udder.
Rupture of the gravid uterus may go unnoticed, as has equally been used successfully, with p
arturition
the sterile fetal fluids will not induce a septic peritoni- 90–150 hours later.
tis. However, haemorrhage may be substantial, lead-
ing to dyspnoea, weakness, anaemia and collapse. If Aftercare/prognosis
caused by external trauma, other signs such as body Retained fetal membranes (RFM) are not a common
wall haematoma and fractures may be apparent. problem after induction, rarely exceeding 10% of
induced animals. Kids born more than a few days
Diagnosis prematurely are unlikely to survive.
Observation and palpation of abdominal contour.
Ultrasonography to confirm fetal parts in an abnor- Ante-natal preparation
mal location. The doe is dried off 6–8 weeks prior to term at the
latest. A clostridial vaccine booster is given 4–6 weeks
Differential diagnosis prior to the doe’s due date. Exercise opportunities
Other causes of dependent oedema (e.g. c ongestive should be made available in late pregnancy. Dietary
heart failure), haemorrhage and abdominal disten- protein and energy are increased to account for fetal
sion (e.g. rumen tympany). growth, and post-natal dietary feeds introduced to
allow for adaptation of the rumen microflora.
Ventral herniation rarely breaches the abdomi- PARTURITION
nal skin, and if the doe is reasonably comfortable,
she may be allowed to carry to term, potentially Normal parturition
aided by a belly bandage. Blood loss is assessed and The fetus controls the time of parturition. In the
addressed as usual. Alternatively, the pregnancy may goat, PGF2α secretion by the mammary gland is
be terminated. important for initiation of normal parturition, with
Assistance at parturition is invariably required, dystocia resulting in goats that underwent udder
with surgical delivery if the fetus fails to present removal as a young female.
at the pelvic canal. Repair of an acquired hernia is Labour has a normal duration of: first stage 6–12
often not rewarding long term. The udder may be hours, second stage 0.5–1 hour (Fig. 3.14), and third
inaccessible for suckling by the kid, necessitating stage 3–4 hours. Cervical dilation appears to be of
supplementation with colostrum and milk. relatively short duration in the doe, with closure
Great care should be exercised when handling commonly starting 2–3 hours after onset of stage 2.
heavily pregnant does to avoid uterine or body wall
ruptures.
Induction of parturition
Indication
Reasons for induction include prolonged gestation
with risk of feto-maternal disproportion, prepartum
metabolic disease in the doe (e.g. pregnancy t oxaemia),
injury or trauma in the doe. Elective induction may
be indicated if the sire is found to produce large off-
spring, thereby avoiding potential dystocia.
Technique
PGF 2α (5–10 mg dinoprost or 62.5 µg cloprostenol) Fig. 3.14 Second stage labour typically lasts 0.5 to
given i/m after day 140 typically results in partu- 1 hour. Not all does adopt lateral recumbency, as in this
rition 30–72 hours later. Dexamethasone (16 mg) case. Straining and abdominal contractions are seen.
68 Chapter 3
Anterior longitudinal presentation is the norm in •• During stage 2, unproductive straining for over
the goat. Posterior longitudinal presentation occurs 15 minutes or failure of the kid to be delivered
in up to 10% of births, but almost always involves after 1 hour.
multiple births and typically the first-born kid is •• Obvious maldisposition.
presented correctly (i.e. anteriorly). •• Malodorous fetal fluids, haemorrhage or
premature separation of fetal membranes.
Dystocia
Overview History
Average reported dystocia rates are 4–17%, but The two main aims of history taking in obstetrical
may reach 50% in individual herds. Fetal mald- cases are establishing a prognosis and narrowing
isposition and obstruction of the birth canal are down possible causes, both of which will influence
common causes worldwide. Prompt attention is management of the case. Prognosis is generally
warranted, with the life of the fetus and dam at negatively influenced by previous dystocia, recent or
risk. Dystocia is always costly, even if both neo- concurrent illness of the dam, attempts at assisted
nate and dam survive. delivery and time elapsed between onset of labour
and attention. An obstruction is unlikely if one kid
Aetiology has already been delivered, whereas an overdue dam
In common with other species, the incidence of is likely to carry a large fetus.
dystocia is higher in primiparous does and those
carrying a single male fetus. General approach
The reported incidence of maternal causes ranges The general health status of the dam is established
from 30% to 58%. A frequent maternal cause is with a brief clinical examination, paying particular
obstruction of the birth canal. This may be bony (e.g. attention to any respiratory distress, metabolic dis-
skeletal immaturity or secondary to pelvic trauma), ease, position and trauma.
but more often is a soft tissue obstruction and in
particular failure of cervical dilation or cervical clo-
sure in delayed parturition. Primary uterine inertia
appears to be rare. Other maternal causes include
secondary uterine inertia (‘exhaustion’ of uterine and
abdominal musculature), concurrent illness, rupture
or herniation of the uterus, or neoplastic growths in
the birth canal.
Fetal causes most commonly involve maldis-
positon. In single births, lateral deviation of head
and neck or bilateral shoulder flexion is common.
With multiple fetuses, simultaneous presentation
is common. Feto-maternal disproportion accounts
for about 20% of dystocia cases. Other fetal causes
include fetal monsters or fetal death (Fig. 3.15).
Indications of dystocia include:
•• During stage 1, no progression to stage 2 after

several hours (i.e. fetal parts not becoming
visible or labour signs subsiding) or doe showing Fig. 3.15 Fetal monsters, such as the double-head
marked restlessness or discomfort. formation in this kid, often lead to dystocia.
If necessary, the doe is moved into a clean, well- the correction method (vaginal delivery, fetotomy,
lit and well-bedded area. Manual restraint is usually caesarean section, euthanasia of dam). As a general
sufficient in does. If low-level sedation is desired, rule, vaginal delivery is possible if there is room for
detomidine HCl or butorphanol are preferable over one finger to be passed all around the fetus once it
xylazine HCl, which has a direct oxytocin-like myo- is engaged in the dam’s pelvis. Oversize should be
tonic action, making the uterus more friable. suspected if the head fails to stay aligned despite use
The birth canal of the doe is tight and fragile, of a rope or snare, the fetus’s front legs are crossed
and great care must be exercised during vaginal over or bilateral shoulder flexion is present.
manipulations (Fig. 3.16). A sacrococcygeal epidural
(1 ml/45 kg 2% lidocaine; see Chapter 18) is strongly Fetus alive versus dead
recommended. A smooth muscle relaxant (e.g. clen- Signs of fetal life include movements visible in the
buterol) may be useful. Plenty of obstetrical lubri- dam’s flank, spontaneous limb movements and a
cant should be used and can, if necessary, be applied variety of positive reflexes. In anterior presentation,
to the birth canal with the help of a lamb feeder tube these include suck, deep pain (interdigital space or
and catheter-tip syringe (Fig. 3.17). tongue), palpebral and corneal. In posterior presen-
Both the perineal area and the obstetrician’s hands tation, the anal and deep pain reflex can be used. It is
and forearms must be clean throughout, using either important to remember that absence of reflexes is not
a mild disinfectant (povidone–iodine or chlorhexi- a definite sign of death; the fetus may be unable to
dine) or soapy water. After gentle insertion of the move (being wedged in) or too depressed to respond.
well-lubricated hand into the vagina, the degree If in doubt, the fetus should be assumed to be alive.
of relaxation (especially cervical) and fetal disposi- Feeling for a pulse in the umbilical cord can
tion (presentation, position, posture, singleton or sometimes be useful, but in general the presence of a
multiple) are established, and a decision made on pulse is difficult to establish.
Fig. 3.17 Both owners and veterinarians should

have a fully stocked parturition kit readily available.
It usefully contains (from top left in a clockwise
Fig. 3.16 The pelvis and birth canal are narrow in direction): rectal gloves, iodine or chlorhexidine
the doe (for reference, the person’s hand shown in the disinfectant, obstetrical lube, catheter-tip syringe to
image takes surgical glove size 7.5). One to two cm aid lubricant application, disinfectant for navel, torch,
extra space may be gained by rotating the fetus weighing scales, plasma, colostrum, oesophageal
30–45 degrees clockwise or anticlockwise. feeder tube, resuscitator, lambing snare and ropes,
navel clip, tail bandage, swabs, thermometer.
70 Chapter 3
If the equipment is available, other techniques snare (Fig. 3.18) or gentle digital pressure behind
include detection of a heart beat by Doppler or the poll (if necessary via gentle insertion of a finger
B-mode ultrasound, fetal ECG, PO2 levels on fetal into the rectal canal) can be used to achieve this.
blood gas or pulse oximetry. In both anterior and posterior presentation, the
Signs of fetal death include corneal opacity and fetus may be rotated by 30–45 degrees around its
collapse of the eyeball, emphysema or autolysis, sep- longitudinal axis to make best use of the widest
aration of the placenta and a fetid discharge. diameter of the dam’s pelvis (Fig. 3.16).
Signs of fetal distress include excessive move- The natural arc of expulsion is followed and the
ments visible in the dam’s flank, breathing or vocal- fetus’s head or hip aided through the vulva by gen-
ising, or a heart rate consistently below 120 bpm or tly pushing the vulval lips over the fetus. Traction
above 180 bpm. is applied in synchrony with the dam’s contractions
and straining as much as possible.
General principles of vaginal correction
and delivery Control
In multiple births, it is important to allocate limbs Prevention of dystocia relies on suitable matching
and head to the correct fetus. of sire and dam, adequate growth of doelings prior
Correction of a maldisposition is usually a com- to breeding, dams being in target body condition,
bination of repulsion of one fetal part while apply- nutritional and health status, and close supervision
ing traction to another. Where this needs to be done with knowledgeable intervention of parturition.
simultaneously, a rope on the relevant fetal part is Unsuitable dams (e.g. ones with pelvic abnormalities)
used for traction with the obstetrician’s hand carry- should be promptly removed from the breeding pool.
ing out repulsion. Repulsion is often easier if a rock-
ing movement, rather than continuous pressure, is Failure of cervical dilation
used on the fetus. Sharp pointed extremities of the (syn. ringwomb)
fetus are covered with a hand as much as possible Overview
during traction to avoid trauma to the reproductive Insufficient cervical dilation is the commonest
tract. In the goat it is sometimes possible, with great maternal cause of dystocia in the goat, reported to
care, to deliver a small fetus in an uncorrected mald- account for 12–23% of all dystocia cases, or 45% of
isposition (e.g. unilateral shoulder flexion). As a rule maternally caused dystocia.
of thumb, if correction is not possible or no progress
in delivery is made within 20 minutes, a caesarean
B
section should be considered.
Failure of vaginal or vulval dilation can typi-
cally be addressed with gentle manual stretching for
10 minutes or so. A true persistent hymen is easily
C
broken down manually, but one should rule out a
rare case of vaginal stenosis. Where the vulva fails
to relax fully, an episiotomy is useful; an incision is
made with a scalpel blade at either the 10 or 2 o’clock
position, followed by post-partum closure with an A
absorbable suture.
Once correction has been achieved, the natu-
ral birth posture should be observed as much as Fig. 3.18 A lambing snare (A) is easy to apply and
possible. For the goat fetus in anterior presenta-
ensures that the head stays in its normal position during
tion this is elbow flexion, with the nose resting on traction. Leg snares (B) or lambing ropes (C) should be
the feet. Therefore, traction on the limbs must be used with care, as they easily disrupt the normal elbow
accompanied by expulsion of the head. A lambing flexion with which the caprine fetus presents.
Aetiology Aetiology
The normal cascade of hormonal factors and physical The aetiology remains unclear but causes may
dilation by the fetal sacs (or fetus itself, for example in include an unstable suspension of the uterus in mul-
breech presentation) fails. It can also occur secondary tiparous animals, a singleton occupying mainly one
to fibrosis after previous cervical trauma, and has been horn, vigorous fetal movements and possible reduced
linked to hypocalcaemia and hypophosphatemia. exercise in late pregnancy. The torsion may be up
to 360 degrees, with a clockwise (towards the right)
Clinical presentation rotation possibly more common.
Stage 2 of labour has commenced, but no fetal parts
become visible. Vaginal examination reveals a par- Clinical presentation
tially opened cervix. Unproductive straining without fetal membranes
becoming visible. Any signs of parturition may
Differential diagnosis cease altogether after some time. In the major-
Premature births or abortions may present with ity of cases, the point of torsion is the anterior
a lack of cervical dilation. It is important to estab- vagina, and the deviation is detectable on vaginal
lish that parturition has commenced and abdominal examination (manually or visually via a specu-
straining is not caused by urinary tract disease, colic lum). Occasionally, a precervical torsion occurs, in
or another cause. which case there are no detectable signs on vaginal
In delayed parturition, or missed cases of dysto- examination. Rectal examination is a challenge in
cia, the cervix may be in the process of contracting goats, but may be possible in a large framed doe:
down again. A uterine torsion may present as an the broad ligaments are palpable as tight bands
apparent failure of cervical dilation. across the pelvic inlet.
Treatment/management/control Differential diagnosis

For manual dilation, the fingers of a clean, well- As for failure of cervical dilation above.
lubricated cone-shaped hand are inserted into the
cervix and gently opened and closed, repeatedly, for Treatment/management/control
several minutes. Caesarean section is often the best approach. Failure
Response to medication is variable. A smooth of cervical dilation may occur once the torsion is
muscle relaxant (clenbuterol, 30–60 µg slow i/v; or corrected, not least because the dystocia has often
butylscopolamine bromide 4 mg and metamizole gone unnoticed. In addition, the uterine wall may
500 mg combination product, 0.05–0.1 ml/kg) may have become fragile because of compromised blood
help. Using valethamate bromide (15 mg) and clo- supply.
prostenol sodium (250 µg) has been successful in The technique for non-surgical correction is
33% of cases. If no immediate effect is seen, one can as follows: for an anti-clockwise torsion, the doe
wait for 30–60 minutes, providing the fetal mem- is cast into left lateral recumbency. While kneel-
branes are intact and there are no signs of fetal dis- ing at a right angle to the doe’s ventral abdomen,
tress. Otherwise, a caesarean section is indicated. one person folds their hands and pushes their
Oxytocin must not be used, as it carries a high risk parallel-held lower arms onto the fetus through
of resulting in uterine rupture. the abdominal wall (Fig. 3.19). Two assistants
slowly and carefully rotate the doe over her back
Uterine torsion into right lateral recumbency, while pressure on
Overview the fetus is maintained. The process is repeated
This occasional disorder (average 2% incidence) may for torsions of more than 180 degrees. For a clock-
not be recognised even by experienced breeders. wise torsion, the technique is reversed (i.e. the doe
It almost always occurs during stage 1 or stage 2 of is rotated from right lateral recumbency over her
labour in the goat. back into left lateral recumbency).
72 Chapter 3
from the transverse processes to near the midline.

In long-haired breeds, duct tape can be usefully
employed around the edges of the clipped area to
keep the fleece away from the surgical site. The sur-
gical site is aseptically prepared.
The owner or assistant is briefed on neonatal
resuscitation (see Chapter 4), and relevant equip-
ment for this laid out.
A full caesarean section kit includes: razor
blade for shaving or clippers, povidone–iodine or
chlorhexidine disinfectant and methylated spirit,
local anaesthetic (with syringes and needles), nail
Fig. 3.19 Position adopted by veterinarian to fix the brush, sterile gown and gloves, sterile lavaging
fetus in position through the abdominal wall during fluid, large instrument kit, suture material; and,
correction of a uterine torsion (shown here on a dog optionally, sedative, sterile drape, intra-abdomi-
mannequin). The doe is rolled underneath onto her nal antibiotics.
other side.
Restraint
Caesarean section Sedation and local anaesthesia is favoured for
Indications this procedure, as the rapid recovery of the dam
In approximate order of importance, reasons for allows her to nurse her offspring, and there is gener-
emergency caesarean section in the doe are: obstruc- ally less effect on the neonate from the anaesthetic
tion of the birth canal, feto-maternal disproportion, drugs used.
uterine torsion, rupture and tears to the reproduc- Suitable sedative drugs include detomidine HCl,
tive tract, malpresentation and, rarely, abortion or butorphanol and xylazine HCl. For local anaesthe-
fetal monsters. Not surprisingly, does with male kids sia, options include line block, inverted L-block,
and primiparous ones are overrepresented in case paravertebral block and lumbosacral epidural (see
reviews. Chapter 18).
As an elective procedure, it may be indicated where The goat is placed into right lateral (for left flank
disproportion is suspected, gestation is prolonged, approach) or dorsal recumbency (for paramedian or
or the doe is suffering from disease. Induction is ventral midline approach; Figs. 3.20). If the fetus is
carried out whenever possible prior to an elective emphysematous, the ventral midline approach offers
caesarean section. A combination of corticosteroids, good access, allowing exteriorisation of the uterine
followed 12–24 hours later by PGF2α , works well to horn prior to incision, thereby reducing abdominal
support neonatal lung function, release of placental contamination. From the dorsal position, the patient
attachments and luteolysis. The ideal time for sur- is leant 30–45 degrees towards the surgeon to aid
gery is at the start of cervical dilation. Note that kids this. The uppermost hind leg of the doe may be tied-
more than 5 days premature have a slim chance of out, if necessary.
survival. Steps to reduce the risk of aspiration and hypo-
thermia are taken (see Chapter 18).
Preoperative medication includes antibiosis, Technique – left flank approach
NSAIDs, tetanus cover if not vaccinated and a A vertical flank incision of about 20 cm length is
uterine relaxant (e.g. clenbuterol). Intravenous flu- made in the centre to slightly caudal left flank,
ids are indicated in a compromised patient. starting approximately one hand-width below
For a left flank approach, the left flank is clipped the transverse processes (Fig. 3.21). The inci-
from the penultimate rib to the tuber coxae, and sion must be undertaken with care, as the patient
(a) (b)

Fig. 3.20 Possible incision sites for a caesarean section in the left (a) or right (b) flank. Yellow = vertical
sublumbar; green = angled sublumbar; blue = paramedian; red = ventral midline.
direction of the muscle fibres in the various layers

greatly helps to ascertain depth and level of inci-
sion. These are:
•• Head to hind foot for the external oblique

muscle.
•• Hip to front foot for the internal oblique.
•• Vertical for the transverse abdominis muscle.
Haemostasis is achieved with artery forceps, all of

which are removed prior to exploring the abdominal
cavity.
A hand is inserted into the abdomen and the
pregnant uterine horn nearest the flank incision
found and manoeuvred into the incision (Fig. 3.22).
Orientation within the abdomen is often helped by
Fig. 3.21 A 20 cm long incision is made in the initially placing the hand into the pelvic inlet, feel-
centre to caudal flank. The scalpel blade is held as ing the fetus within the uterus in that location and
parallel to the flank as possible, to avoid accidental then following the fetus and uterus down onto the
puncture of deeper structures should the goat move. horn. Usually, it is possible to exteriorise the horn
In this case, the goat was placed onto a tarpaulin to containing the fetal extremities. The uterine inci-
provide a reasonably clean surgical environment. sion is started between the claws of the fetus and
(Image courtesy Adelle Isaacs.) extended to the hock (if hind leg) or carpus (if front
leg). To minimise blood loss, the incision is made
along the greater curvature where blood vessels are
is conscious and therefore liable to move occa- minimal (Fig. 3.23), and care is taken to avoid incis-
sionally, the tissue layers are relatively thin and ing into placentomes. The incision should be made
a distended viscus (rumen, uterus) may be pres- reasonably close to the uterine body to aid delivery
ent adjacent to the body wall. Remembering the of any additional fetus from the other horn through
74 Chapter 3
Fig. 3.22 A leg is grasped through the wall of the Fig. 3.23 To avoid unnecessary blood loss, the uterine
uterine horn and brought into the incision. (Image incision is made along the greater curvature where
courtesy Adelle Isaacs.) vessels (some highlighted with arrows) are smallest.
Fig. 3.24 An assistant takes the fetus and provides Fig. 3.25 Both horns are thoroughly explored for
first care and resuscitation. The surgeon holds the additional fetuses. (Image courtesy Adelle Isaacs.)
uterus to stop it falling into the abdominal cavity.
(Image courtesy Adelle Isaacs.)
the same incision. Occasionally, this is not possible persistence that may lead to scarring compared with
and a second uterine incision has to be made. synthetic suture materials. However, synthetic mate-
The fetus is removed and passed to an assistant for rials, such as polyglactin 910, offer more consistent
further care (Fig. 3.24). Both horns are thoroughly material strength and better knot and handling quali-
explored for further kids (Fig. 3.25). The placenta ties. Great care must be taken to avoid including the
is only removed if it comes away easily. Otherwise, fetal membranes. The knots should be buried.
any protruding parts are resected, with the bulk left After uterine closure, the uterus is lavaged with
in place. warm sterile fluid, paying particular attention to
The uterus is sutured with a continuous inverting removing any blood clots around the ovaries. Prior
pattern (e.g. Lembert or Cushing) through the serosa to routine closure of the abdominal wall (Fig. 3.26),
and muscular layer, using absorbable material, ideally the surgeon may wish to instil intra-abdominal
on a swaged needle to reduce tissue trauma. Catgut antibiotics (soluble and non-irritant, for example
is a good choice, with less tearing of tissue and less benzylpenicillin sodium). If the doe was tied-out
Fig. 3.26 Routine closure of the abdominal wall. A Fig. 3.27 Depending on the time of year, fly
continuous pattern may be used for both musculature repellent ointment is applied to the wound. (Image
and skin. However, in case of seroma formation, it courtesy Emily Reeves.)
is good practice to place 1 or 2 simple interrupted
sutures at the ventral end of the skin suture.
during surgery, abdominal wall closure is aided by

releasing the leg ties.
Aftercare
The flank and udder are cleaned thoroughly.
Postoperative medication includes analgesia, oxyto-
cin to aid involution and fly control where applicable
(Fig. 3.27). Any hypothermia in the doe is addressed,
and any concurrent disease treated. Bonding and
colostrum intake is monitored (Fig. 3.28).
Complications
Reported kid survival rates range from 40% to 65%. Fig. 3.28 Successful delivery of triplets by caesarean
Stage 2 labour of more than 6 hours prior to inter- section. The newborn kids are placed near the doe’s
vention carries a poor prognosis for kid survival. head to encourage bonding. (Image courtesy Adelle
Doe survival rates of >90% are achievable. Isaacs.)
Common complications include RFM, metri-
tis, endometritis, wound breakdown or seroma
formation, subcutaneous emphysema and peri- Fetotomy
tonitis (which typically presents clinically within Indication
72–96 hours postoperatively). Good surgical tech- Fetotomy may be considered in cases of fetal mald-
nique is paramount, including asepsis, generous isposition, feto-maternal disproportion, partial fetal
incisions, suture techniques that achieve a good seal delivery (for example ‘hiplock’) or when dealing with
and reduce dead space without being overly tight and fetal monsters. It may be of particular benefit where
avoid incorporation of fetal membranes, clean surgi- fetal death occurred some time ago and autolysis has
cal environment, clean preoperative vaginal exami- set in, and therefore a caesarean section carries a
nation and routine antibiosis. high risk of peritoneal contamination.
76 Chapter 3
An absolute requirement for a fetotomy is that clenbuterol are administered. Obstetrical lubrication
the fetus is dead and that there is sufficient cervi- and water and mild disinfectant are prepared.
cal dilation both for carrying out the procedure
and retrieving fetal parts. Because of the space Technique – front leg removal
constraints and the relative fragility of the uterus, This is a relatively easy and quick to perform partial
a complete fetotomy is seldom performed in small fetotomy that often enables vaginal delivery after-
ruminants. Partial fetotomy, however, has its place. wards. The aim is to remove one (or both) front legs
Contraindications include: fetus still alive via a subcutaneous method.
(although euthanasia in utero may be considered), Using a scalpel blade, a circular cut is made
insufficient dilation of the birth canal and in par- through the skin just above the fetal carpus, taking
ticular the cervix, fractured pelvis, severe trauma of care not to sever any tendons (Fig. 3.29a). A 2–3 cm
the birth canal or uterine tears, compromised dam long cut along the long-axis of the leg is made in a
(e.g. septicaemic). proximal direction, connecting with the circular cut
at its distal end. Using digital pressure and probing,
Restraint and position the skin is lifted off the leg’s soft tissue (Fig. 3.29b).
The doe may be standing or in lateral recumbency Tension is maintained on the lower limb to aid break-
(with the fetal limb to be removed lying upper- ing down of muscular attachments, especially of the
most), under mild sedation if necessary. A sacrococ- shoulder blade (Fig. 3.29c). The freed ‘skinned’ leg
cygeal epidural (1 ml/45 kg 2% lidocaine HCl) and is removed (Fig. 3.29d).
(a) (b)

(c) (d)

Fig. 3.29 Partial fetotomy to remove a front leg, demonstrated on a dead lamb ex utero. The gloved hands on
the right mimic the vulva of the dam. A circular incision is made just above the carpus (a) followed by an incision
at right-angle to this along the long axis of the limb. Soft tissue attachments are broken down with fingers (b),
while maintaining tension on the lower limb (c). The removed, de-gloved limb (d).
Aftercare
It is important to ensure that all fetal parts have been
removed. In cases of severe autolysis, uterine lavage
with saline may be indicated. Medication consists of
antibiosis, NSAIDs and analgesia. Oxytocin is advis-
able, especially if clenbuterol was used. The doe is
monitored for pyrexia, metritis and inappetence over
the next several days.
POST-PARTURIENT PROBLEMS
Haemorrhage
Overview Fig. 3.30 Bleeding from the umbilical stump (arrows;
Internal or external post-partum haemorrhage is shown here in a cow in left lateral recumbency).
possible.
Aetiology For cervical or vaginal haemorrhage, pressure is
Trauma to the soft tissues of the birth canal, espe- applied by packing the birth canal: a stockinette (or
cially the vagina and cervix and their associated ves- freshly laundered sock as first aid) is placed into the
sels, in particular the vaginal artery. Internal blood vagina and filled with gauze swabs or cotton wool to
loss may arise from uterine trauma, including plac- its maximum capacity. It is left in place for at least
entomes accidentally incised during a caesarean sec- 72 hours. The stockinette may be soaked with 1%
tion, and bleeding into the broad ligament. alum or 1:1,000 adrenaline. If the origin is a ves-
sel and this is accessible, it may be clamped using a
Clinical presentation pair of haemostats, which are secured to the dam’s
External haemorrhage is apparent at the vulva. tail. Ligation can be attempted, but often results in
A uterine bleeding point does not usually result in more tissue trauma. Oxytocin is useful to support
large quantities of blood externally, but the animal involution.
will show systemic signs of blood loss. Bleeding into For internal haemorrhage, treatment consists of
the broad ligament may present as acute or chronic sedation or enforced rest, blood transfusion, antio-
blood loss. biosis, and possibly a laparotomy to find the source
of the haemorrhage.
Diagnosis
Careful examination, if necessary with the aid of a Laceration of the cervix
speculum, is required to locate the source. The vagi- Overview
nal arteries are located roughly at the 3 and 9 o’clock Uncommon, but can affect future fertility. Scar tis-
positions in the vagina and should be inspected sue may compromise the cervical seal or dilation at
for integrity. Blood accumulation in the peritoneal subsequent gestation and parturition.
cavity may be confirmed via abdominocentesis or
ultrasonography. Aetiology
Trauma at parturition, especially if delivery
Differential diagnosis attempted while cervix not fully dilated. The weak-
Temporary bleeding from the umbilical stump can est point is dorsally (12 o’clock position).
appear as severe external haemorrhage, but will not
deplete the dam’s circulatory volume (Fig. 3.30). For Clinical presentation
internal haemorrhage, any other causes of acute or Detected at post-partum or infertility examination,
chronic blood loss (see Chapter 7). with the aid of a speculum.
78 Chapter 3
Treatment/management/control structures from the rectum (Fig. 3.31). Where only

Surgery is possible, but access typically proves dif- the vaginal roof is involved, there may be no outward
ficult. Culling is advised if cervical seal fails. sign. However, the presence of faecal material in the
vagina should prompt investigation.
Laceration of the vagina If the case is presented promptly (<12 hours after
Overview injury), there is a reasonable prognosis for achieving
A relatively common complication, causing consid- healing by first intention. Otherwise, surgical repair
erable discomfort and being potentially fatal if posi- should be delayed for at least 6 weeks to allow for local
tioned very cranially. swelling to subside and remodelling of granulation
tissue to occur. Surgery is carried out in the stand-
Aetiology ing animal under epidural anaesthesia. The rectum
Spontaneous tearing may result from vigorous con- is evacuated, the perineal area thoroughly cleaned,
tractions forcing a fetal foot through the vaginal wall. and stay-sutures placed into the vulval lips, which
More common, however, is excessive force during cor- are held open by an assistant. In brief, the technique
rection of a malposture. Contributing factors in other involves freeing a plane of vaginal mucosa (including
species include an overconditioned dam, lack of lubri- edges), folding such created flaps ventrally into the
cation and premature or too aggressive interference. lumen, and suturing the dorsal vaginal submucosa in
a series of interrupted sutures from cranial to caudal
Clinical presentation to form a new vaginal roof.
Laceration is only detectable on vaginal examina-
tion. Care must be taken during exploration to avoid
turning a shallow tear into a deeper defect. Most are
positioned retroperitoneally, but if full thickness and
cranial enough to connect to the peritoneal cavity,
signs of peritonitis develop 24–96 hours after kidding.
For treatment and prognosis, categorisation as fol-
lows is useful: grade 1 = mucosa only affected; grade
2 = submucosa also involved; grade 3 = full thickness,
with prolapse of pelvic fat or able to feel serosal sur-
face of uterus or intestines, depending on location.
•• Grade 1: the mucosa normally heals rapidly

without treatment.
•• Grades 2 or 3: if discovered when fresh, best
repaired surgically. A sacrococcygeal epidural is
given and stay sutures placed into the vulval lips
to aid visual and manual access (held open by
an assistant). Commencing at the cranial end of
the tear, a continuous absorbable suture is placed
incorporating the submucosal and mucosal layers.
Systemic antibiosis and NSAIDs are given.
Recto-vaginal fistula
Trauma to the roof of the vagina and vestibulum may Fig. 3.31 A recto-vaginal fistula. The tissue plane
lead to loss of the tissue plane that separates these between rectum and vagina has been lost.
Prevention is by early consideration of an episi- A large defect should be repaired as best as possi-
otomy or delivery by caesarean section. ble, either per vaginam or via a laparotomy. Another
approach involves creating a uterine prolapse after
Vaginal prolapse – post-parturient administration of adrenaline (does not work if an epi-
Overview dural was used), repairing any defects then replacing
Vaginal prolapse may be a standalone problem or the uterus. High-dose antibiosis, NSAIDs and oxy-
recurrence of a preparturient prolapse. It is some- tocin are given. If repair proves difficult, euthanasia
times accompanied by rectal prolapse. should be considered.
Treatment/management/control Uterine prolapse

As for prepartum prolapse (see earlier). Prognosis is Overview
better than in prepartum cases. Uterine prolapse appears to be less common in the
doe compared with the ewe or cow. Typically a spo-
Uterine rupture radic condition, but occasionally ‘storms’ may be
Overview observed.
Ruminants appear more prone to uterine rupture
than other species. Aetiology
Suggested contributing factors include: poor uter-
Aetiology ine tone (e.g. caused by hypocalcaemia); increased
Typically caused by trauma during assistance such post-partum straining because of pain or discomfort
as correction of maldisposition, repulsion of fetus or secondary to reproductive tract trauma; increased
prolonged attempt at delivery. Rarely spontaneous intra-abdominal pressure (e.g. caused by rumen tym-
due to contractile forces. Cases with uterine torsion pany or recumbency); or excessive traction. Possible
or fetal autolysis are especially vulnerable because of other factors include high oestrogen content of diet,
uterine wall compromise. overconditioned dam and excessive weight of fetal
The weakest point in the wall is dorsally, but dam- membranes.
age may occur at any location where undue pressure
has been exerted (e.g. near the pelvic brim during Clinical presentation
correction of a breech presentation). Most cases present within 24 hours of parturition.
One or both uterine horns are prolapsed, expos-
Clinical presentation ing the mucosal surface with the caruncles visible
If the defect is caudal enough, it will be obvious on (Fig. 3.32). The fetal membranes are often still
palpation during the routine post-partum check. attached. The dam may be in any state from stand-
Loops of intestine may prolapse through the defect ing and systemically well, to recumbent and in cir-
and must be confirmed as belonging to the doe culatory or toxic shock. The uterus is contaminated,
rather than to another fetus (if not delivered yet). engorged and oedematous, and often traumatised
If the defect is out of reach, signs of peritonitis will with tears. Initially warm, the uterus increasingly
develop within 72–96 hours of parturition. becomes cold to the touch and discoloured.

For a small defect, where parturition was without Owners may be uncertain whether they are pre-
excessive contamination and the fetus is alive, oxy- sented with fetal membranes or a uterine prolapse.
tocin to cause uterine contraction is sufficient.
For a small defect, but involving a dead fetus or Treatment/management/control
contamination, oxytocin, antibiosis and NSAIDs are First aid includes restraining and separating the
given. dam (e.g. with the use of hurdles or bales of straw).
80 Chapter 3
Fig. 3.33 A cow in the ‘New Zealand’ position for

replacing a prolapses uterus. The animal is in sternal
recumbency and both hind legs are pulled backwards,
resulting in the pelvis tilting forward.
Fig. 3.32 A uterine prolapse (in a ewe). The mucosa

is exposed and caruncles visible. Fetal membranes are
still partially attached.
If possible, a moist wrap made from a clean sheet or

towel is placed around the uterus.
The doe’s general condition is assessed, and a
decision made as to whether treatment is feasible.
A sacrococcygeal epidural is given (see Chapter 18).
The doe is placed in either lateral or sternal recum-
bency with her hindquarters moderately raised
(e.g. over a bale of straw), taking care not to cause
respiratory compromise. Alternatively, she may be
placed in the ‘New Zealand’ position – in sternal
recumbency with both hind legs pulled backwards;
Fig. 3.34 Suturing of the vulval lips is typically not
this results in the cranial part of the pelvis tilting
required. However, if performed, the suture is fed
downwards, thereby aiding the uterus to resume its
through buttons or lengths of tubing to reduce the
normal position (Fig. 3.33).
risk of cutting into the soft tissues.
The uterus is thoroughly but gently cleaned using
a mild disinfectant solution (e.g. 0.1% iodine). Fetal
membranes are removed if they come away easily. is fully inverted. Vulval suturing is typically not nec-
Any tears are sutured. Using the flat of one’s fin- essary, but if desired, a Bühner or horizontal mat-
gers or a fist, the uterus is gradually inverted while tress suture may be placed. For the latter, the suture
pushing it back through the doe’s pelvic canal. An is fed through buttons or short lengths of tubing (e.g.
assistant parting the vulval lips is of great help. Once a giving set or flutter valve) to reduce the risk of it
replaced, palpatory examination ensures the uterus cutting into the tissue (Fig. 3.34).
Medication consists of antibiosis, NSAIDs and Aetiology

oxytocin. Subcutaneous calcium borogluconate The separation process starts well before parturi-
(50–100 ml of 20% solution) should be considered. tion. Various pathological processes can disrupt this
Uterine prolapse tends to be a one-off event in complicated event, such as immaturity of placent-
any particular doe. The female can, therefore, be omes, oedema or necrosis of chorionic villi, placen-
retained for future breeding, although there is a risk titis or metritis, and uterine atony. Postulated risk
of infertility due to endometritis. factors include:
Amputation of the uterus may be considered as a
salvage procedure if the prolapsed organ has become •• Physiological: litters >3 kids, induction,
devitalised or too fragile to replace. This may enable shortened or prolonged gestation, dystocia,
survival of a pet goat or completion of the lactation increasing age of dam.
in a commercial goat. The technique involves plac- •• Infectious: e.g. abortive agents and also
ing a ligature using thick material (e.g. a Penrose generalised disease.
drain or Foley catheter) tightly around the uterine •• Nutritional: deficiency in retinol (vitamin A),
body just cranial to the cervix. The uterus is dis- tocopherol (vitamin E)/selenium, beta-carotene,
sected 2–3 cm from the ligature, any bleeding vessels calcium, copper, iodine; high BCS, fatty liver.
are ligated and the stump oversown, before inverting •• Hormonal: lack of PGF2α , low progesterone/
the reproductive tract remnant. high oestradiol.
•• Environmental: heat, season, previous RFM,
Retained fetal membranes breed.
Overview
RFM is defined as stage 3 not completed and the Clinical presentation
membranes not detached and passed by 12 hours The fetal membranes often protrude from the
post partum (Fig. 3.35). Retention is relatively rare vulva. Otherwise, a malodorous haemomucoid dis-
in the doe, but impaired fertility and reduced milk charge may be obvious on the tail and perineal area
yield are likely sequelae in affected females. In small (Fig. 3.36). In dairy goats, the malodour may be
ruminants, there is also the risk of secondary infec- noticed in the milking parlour.
tion with life-threatening clostridial pathogens such A good proportion of does are systemically
as tetanus or malignant oedema (Clostridium septicum, affected, so as a minimum the vital signs should be
Clostridium perfringens type A). established.
Fig. 3.35 Fetal membranes passed in the normal Fig. 3.36 Partial protrusion of retained fetal
time frame of 3–4 hours post partum. The brown membranes and staining of the perineal area and
material (arrow) is meconium. caudal aspect of the udder.
82 Chapter 3
Diagnosis the authors have no experience with its use in goats.

Vaginal examination using a speculum if membranes Oestrogens have a direct uterotonic effect and
are not protruding. increase the effect of prostaglandin and oxytocin,
but beneficial effects in cases of RFM have not been
Differential diagnosis proven so far, and their use may increase the absorp-
Retained fetus, metritis. tion of toxins.
Treatment/management/control Other agents

Antibiosis Two not yet commercialised agents are collagenase
Antibiosis may lead to reduced phagocytosis, anti- (to aid breakdown of collagen binding in placent-
body response and T-cell function, and delay in omes) and relaxin (to loosen connective tissue).
the necrotic process necessary to cause separation.
Therefore, it is best reserved for systemically affected Manual removal
does. Various factors limit the choice: aminoglyco- Manual removal is no longer advocated, with good
sides have reduced activity in the low-oxygen, acidic evidence that the trauma caused by the manipulation
environment of the uterus; trimethoprim/sulphon- leads to reduced fertility. It should never be used in
amide combinations are inhibited by the organic a septicaemic animal, as toxin release is triggered by
debris; the commonly involved Trueperella pyogenes is the manipulation. At the most, gentle traction for
resistant to streptomycin; anaerobes and Streptococcus up to 1 minute, and grasping the membranes outside
spp. are resistant to enrofloxacin; penicillinase pro- the vulva only, may be tried.
ducing bacteria are often present in the first 5 weeks
post partum. This leaves tetracycline (≥10 mg/kg), Metritis
potentiated penicillin and cephalosporin as the main Overview
groups. Metritis is acute to peracute inflammation of the
Systemic administration ensures even tissue endometrium and myometrium soon after kid-
concentrations throughout the reproductive tract. ding. Outbreaks are occasionally encountered in
Inflammation may reduce drug absorption into herds where hygiene has deteriorated throughout
uterine tissue, therefore high dose rates should the kidding period, or where tight batch kidding is
be used. Intrauterine administration is not useful; practiced. Metritis is one of the main differential
organic debris inactivates drugs quickly, distribu- diagnoses for depression in a post-partum doe, but
tion is haphazard, straining may expel the drug and its incidence tends to be low (around 2%).
some drugs are irritating to the endometrium in
direct contact. Aetiology
Post-partum uterine infection occurs in all females,
Hormonal treatment but some do not resolve or bacterial growth becomes
Hormonal treatment has shown equivocal results overwhelming. Commonly involved pathogens
in cattle. PGF2α appears beneficial in some females include Trueperella pyogenes (potentially acting syn-
and should be used immediately post partum (i.e. ergistically with Fusobacterium spp. and Bacteroides
in females considered at risk of RFM). Oxytocin spp.), and Escherichia coli, Staphylococcus spp. and
receptors are lost within a few hours post partum Streptococcus spp., plus occasionally clostridial
in ruminants, and oxytocin may only be beneficial pathogens. Metritis and salpingitis are reported as
in the few females where hypomotility is a prob- part of the disease picture of caprine contagious
lem. It may be used as a slow i/v infusion or 2 IU agalactia (see Chapter 12).
every 20 minutes for the first 3 hours post partum; Risk factors include abnormal parturition, unhy-
resulting uterine contraction may lead to marked gienic kidding environment, excessive manipulation
discomfort. Carbetocin is an oxytocin analogue, but during assisted delivery, concurrent disease or stress
possibly with better distribution and longer effect; in the doe and high BCS.
Metritis commonly results in systemic illness
with pyrexia, toxaemia, septicaemia, dehydration,
reduced rumen activity, diarrhoea and inappetence.
A fetid, haemopurulent uterine discharge (Fig. 3.37)
is either outright apparent or signs are found on the
tail and perineum.
Diagnosis
Vaginal examination using a speculum.
Retained fetus or fetal membranes for this type
of vaginal discharge. Other causes of systemic ill-
ness (e.g. mastitis). Not to be confused with normal
lochia: reddish-brown, non-malodourous discharge
for up to 3 weeks post partum (Fig. 3.38).
Systemically affected does are treated aggressively
with antibiosis (see RFM regarding choice of anti-
microbial), NSAIDs and fluids, supported by good
nursing care. I/v fluids are ideal (used judiciously
to avoid pulmonary oedema), with oral fluids often
effective providing some rumen activity is still
present. Treatment of mild to moderate cases may be
beneficial in terms of future milk yield and fertility. Fig. 3.37 Fetid, haemopurulent discharge typical of
Uterine irrigation is detrimental in most cases, with metritis. (Image courtesy Ann Courtenay.)
a risk of causing rupture of the fragile uterus, delay-
ing involution, irritation of the endometrium by some
solutions (e.g. iodine) and lowering the natural defence
mechanism of the uterus. Lavage with sterile saline
may be considered, as an exception, in cases with large
amounts of fetid fluid to dilute toxins present. As much
of the lavage fluid should be siphoned off as possible.
Prevention and control involve attention to hygienic
kidding environment, sound kidding assistance (degree
of manipulation, timing, implements used, hygiene),
avoiding dystocia (breed, metabolic disease, body con-
dition), preventing concurrent disease (in particular
metabolic disease, which may impair neutrophil func-
tion) and adequate nutrition (body condition, deficien-
cies such as retinol [mucous membrane function] or
ascorbic acid [modulates disease resistance]).
Where clostridial pathogens are implicated, a vacci- Fig. 3.38 Normal lochial secretions: reddish-brown,
nation programme should be instigated. Prophylactic and without purulent material or malodour (may have
use of intrauterine antibiotics has failed to show a a faint smell of fresh fish or chocolate).
84 Chapter 3
positive effect and may be detrimental to fertility. In Treatment/management/control

at-risk does, antibiotics should be used systemically. Emollient cream (e.g. udder cream, Dermisol®),
antibiosis, NSAIDs.
Necrotic vaginitis
Overview Bladder eversion or herniation
Necrotic vaginitis is an occasional complication of Overview
dystocia managed by vaginal delivery, leading to Bladder eversion or herniation is an uncommon, but
severe discomfort. life-threatening, malposition of the urinary bladder.
Aetiology Clinical presentation

Pressure insult of vaginal wall, either by oversized The bladder either everts through the urethra or
fetus or obstetrician’s manipulation. herniates through a vaginal tear. It is found within
the vagina and may protrude from the vulva. The
Clinical presentation bladder mucosa is exposed in a case of eversion,
Foul vaginal discharge, signs of discomfort includ- whereas the serosa is exposed in a case of herniation.
ing straining, moderate depression of appetite and
milk yield. The vaginal mucosa is inflamed, hard Treatment/management/control
and painful to the touch. Green-coloured plaques For eversion, the bladder is manually replaced
may be present on the mucosa. Typically no pyrexia, under epidural anaesthesia by pushing it back down
unless concurrent uterine infection. through the urethra. For herniation, the bladder
is emptied, replaced and the vaginal tear repaired.
Diagnosis A Foley catheter (14–16 Fg) is inserted via the ure-
Manual examination of the vagina should be avoided, thra for 48 hours to prevent filling. Antibiosis and
using a speculum instead. NSAIDs are given.
CHAPTER 4
NEONATOLOGY
85
INTRODUCTION Congenital abnormalities

Although relatively uncommon, all newborn kids
Whether born naturally, delivered manually or by should be examined for congenital abnormalities
caesarean section, once the cord has broken the new- and these will vary in their influence on survivabil-
born kid must rapidly become a viable unit and adapt ity. However, not all are apparent immediately, and
to life ex utero. The fetal membranes are removed some may not manifest for months or even years
from around its mouth and if obviously viable, the after birth.
kid is best placed next to the dam’s head to facilitate Some of these conditions will be covered in more
quick bonding. detail in this and other chapters.
First movements should be evident within 1–2
minutes of being born, with sternal recumbency Genetic abnormalities
being achieved by 5–15 minutes. ‘Time to sternal’ is Genetic abnormalities occasionally encountered
a good indicator of vigour. Most kids will be standing across all breeds include:
within 60 minutes post partum. A kid whose coat is
stained with meconium likely has suffered a stressful •• Cleft palate.
delivery, and should receive extra care and attention. •• Undershot/overshot jaw.
•• Atresia ani or coli.
WEAK NEWBORN KIDS •• Rectovaginal fistula.
•• Penile abnormalities such as hypospadias.
There are a number of possible reasons why vigour •• Cryptorchidism.
and normal adaptation may be suboptimal in a new- •• Teat abnormalities such as ‘fish-tail’ and
born kid: supernumerary teats.
•• Entropion.
•• Injuries and trauma related to the kidding •• Umbilical hernia.
process (e.g. ribcage trauma associated with •• Skeletal malformations.
compression during delivery). •• Spastic paresis.
•• Anoxia associated with a prolonged birth or
premature placental separation. Developmental insult
•• Swollen head and tongue associated with abnormalities
prolonged birth. Abnormalities associated with developmental insult
•• Environmental conditions leading to hypo- or by teratogenic infections during pregnancy include:
hyperthermia or preventing normal adapation.
•• Poor in-utero development (e.g. caused by •• Arthrogryposis and other leg abnormalities
abortive agents or nutrition-related poor (Orthobunyavirus infection such as
placenta formation). Schmallenberg or Akabane virus)
•• Prematurity, potentially linked to infectious •• Neurological abnormalities including cerebellar
causes of abortion (e.g. Toxoplasma spp., and cerebral hypoplasia/aplasia (border disease
Chlamydia spp., Coxiella spp.). and Orthobunyavirus infection).
86 Chapter 4
Mineral shortfall abnormalities Aetiology

Abnormalities associated with specific mineral Dystocia-induced hypoxia and acidosis may dimin-
shortfalls during critical stages of fetal development ish the kid’s ability to initiate ventilation. Partial
include: or complete failure of the lungs to inflate (atelec-
tasis) may be caused by ineffective gasping or an
•• Congenital swayback. obstruction (fetal membranes, aspiration of fluid or
meconium). Trauma to the ribcage (Fig. 4.1) may
Known heritable abnormalities lead to pain-induced failure of the first deep breath
Abnormalities associated with known heritability or, if a lung is punctured or with diaphragmatic
include: rupture, failure of sufficient negative pressure to
build up.
•• Beta-mannosidosis, an inherited lysosomal
disease of Nubian goats. Clinical presentation
•• Intersex associated with polledness. The kid may be in any of the following stages of
acute asphyxia:
RESPIRATION
1 Shallow breaths.
Normal adaptation 2 Primary apnoea of 1–2 minutes duration, but
Lung alveoli form pre-partum and surfactant, which responsive to external stimuli. Perfusion and
enables the lungs to expand and retain air without body tone are still good and heart rate is normal
individual alveoli collapsing, is produced in late to elevated. Mucous membrane colour may be
gestation. cyanotic.
The physiological stimulus for the first breath 3 Period of gasping.
comes from a mix of hypoxia, hypercapnia and respi- 4 Terminal apnoea unresponsive to stimulation.
ratory acidosis. Physical stimuli include reduced Perfusion and body tone are poor, and marked
ambient temperature, tactile stimulus and possibly bradycardia is present. Mucous membranes
gravity. The hypoxic stimulus is often reduced in appear very pale.
kids delivered by caesarean section, therefore extra 5 Cardiac arrest.
attention to respiratory function must be paid in
these neonates. They may also suffer from the seda-
tive effects of the anaesthetic agent used (or if deliv-
ered after barbiturate euthanasia of the dam).
The kid needs to generate substantial negative
pressure to inflate its lungs (each lobe independently),
and in part achieves this by gasping against a closed
glottis. The ribcage is pliable in newborns, therefore
active inspiration and expiration is required.
The amniotic fluid produced in the fetal lungs
is physically removed by external pressure on the
thorax during the passage through the birth canal,
and by absorption via the lymphatics and pulmonary
capillaries after lung inflation. The process is com-
pleted within a few breaths in a normal neonate.
Fig. 4.1 The metal stilet points to bruising on the
Asphyxia inside surface of the ribcage caused by a fractured rib.
Overview Trauma such as this may lead to failure of the neonate
Asphyxia is severe oxygen deprivation. to take an effective first breath to inflate its lungs.
Ne on at ol o g y 87
(a) (b)
Fig. 4.2 Radiographs showing severe atelectasis in a 2-day-old neonate (a) and lack of lung aeration in a
neonate with a ventricular septal defect (b) – the lungs almost appear like solid soft tissue. In both cases, the
affected kids appeared normal for the first 2 days post partum.
Signs of atelectasis, in the form of respiratory

istress and cyanosis, may not become clinically
d
apparent until day 2 or 3 post partum (Figs. 4.2).
Similarly, signs of periparturient anoxia or hypoxia
may take a few days to become apparent. The kid ini-
tially appears normal, then ‘crashes’ at 2–4 days old.
Clearing airways
Remove membranes and amniotic fluid from upper
airways by manual removal or suction. The kid’s
hindquarters may be raised briefly (<10 seconds;
caution: pressure on diaphragm hinders inflation).
Handling must be delicate because of the pliable rib
cage.
Induction of respiration
•• For mild asphyxia. External stimulation by Fig. 4.3 Rubbing (kid on red towel) is one of
rubbing (Fig. 4.3), irritating the nasal mucosa the physical stimuli that can be tried to stimulate
with straw, pinching the tongue or nasal breathing. The lower kid has been placed into sternal
septum or interdigital space, or using hot or recumbency to aid lung inflation.
cold stimuli.
•• Acupuncture. Insertion of a 25 gauge 1.5 cm but does not aid opening of collapsed airways or
(5/8 in) needle into the nasal philtrum at right alveoli. Oxygen requirement is increased.
angle to the skin. •• Artificial respiration and inflation. Application
•• For primary apnoea (respiratory centre of intermittent chest compression or movement
still responsive). Analeptics (e.g. doxapram of the ribcage (hold by humerus and last rib)
hydrochloride) can be tried. Increases ventilation may help lung expansion, but will not aid
88 Chapter 4
Fig. 4.4 Simple resuscitators, such as the one

shown using atmospheric air, are effective in causing
lung inflation. The lamb size is suitable for kids.
Alternatives include the Ambu-Bag or Breath of Life.
With the kid in lateral recumbency, the head and
neck are extended fully, the face mask placed over
the nose and mouth and the cylinder pulled out and
pushed in 4–5 times about every 4 seconds. The kid is
placed onto its opposite site, and the same repeated.
If available, an assistant can clasp their fingers around
the cervical oesophagus to prevent air entering the
forestomachs.
initial inflation, and care must be taken not Absent heartbeat

to cause trauma to the ribcage or internal An apex beat should be visible or palpable (Fig. 4.5).
organs. Resuscitators, utilising atmospheric If not present, external cardiac massage or intra-
oxygen, are easy to use and quite effective cardiac adrenaline combined with intubation and
(Fig. 4.4). Placing an endotracheal tube (size 5) PPV, and i/v atropine (0.01–0.03 mg/kg) and adrena-
and exhaling into it is also effective. Positive line (0.1–0.2 ml/kg of 1:10,000 IU solution) may be
pressure ventilation (PPV) is ideal, with a rate tried, but success rates are poor.
of 15–25 bpm and sufficient tidal volume to
inflate the chest. Once breathing is established Cardiovascular defects
and if available, oxygen delivery via a face Cardiovascular defects typically do not become
mask or nasal tube for 1–2 hours at 5 litres/ apparent until the kid is several days old and its
minute is useful, in particular in kids delivered increased activity accentuates circulatory and oxy-
by caesarean section. (Note: Mouth-to-mouth genation problems, unless a severe defect is present
respiration is ineffective and carries zoonotic such as tetralogy of Fallot. (See Chapter 7.)
risks.)
Placing the kid into sternal recumbency also aids

lung inflation (Fig. 4.3).
CARDIAC FUNCTION AND
CIRCULATION
Normal adaptation
Closure of the foramen ovale is in response to an
increase in lung circulation, leading to increased
pressure in the left atrium. Initially consisting of
only a thin septum, full-thickness closure happens
quite a while post partum. The ductus arteriosus
Botalli closure is a reflex response to oxygenated
blood, and is typically complete by 24 hours post Fig. 4.5 Palpation for apex beat in a newborn, with
partum. The umbilical vein collapses in response to fingers and thumb placed either side of the ribcage
absent blood flow, and the umbilical arteries contract close to the elbow. If present, the beat is easily
when the cord ruptures. detected (and may be visible, as well).
THERMOREGULATION Clinical presentation

The kid becomes increasingly depressed and eventu-
Normal adaptation ally comatose. Oxygen consumption increases if cold
The neonatal kid can employ shivering and non- (i.e. any hypoxia may worsen).
shivering thermogenesis, the latter utilising brown
fat for the first few hours of life. Diagnosis
Easily established by measuring rectal temperature.
Hypothermia
Overview Differential diagnosis
Hypothermia is a common condition and fatal if Hypothermia secondary to septicaemic or toxaemic
untreated, but almost entirely preventable. Usually shock must be ruled out, and concurrent hypoglycae-
in neonates less than 24 hours of age, but can occur mia should be considered. Severe parturition trauma
at any age. or some congenital defects may cause increasing
lethargy.
Aetiology
Risk of excessive heat loss is increased with expo- Treatment/management/control
sure to an inclement environment, especially the The sequence of treatment steps for marked hypo-
combination of wetness and wind. Failure of the kid thermia depends on the age of the kid (if brown fat
to become mobile or dry-off (e.g. in a weak kid) or is depleted, alternative energy must be provided
caused by mismothering (which in turn may be due prior to warming up to avoid increased metabolism-
to dam illness or inexperience, reducing interest in induced hypoglycaemia) and the degree of depres-
later born kids in a large litter, or disturbance during sion of the kid (indicating degree of gastrointestinal
the bonding process). Low birth weights resulting in [GI] atony). Fig. 4.6 gives the options for treatment,
both weakness and increased surface to body mass management and control of hypothermia.
ratio. In general, the relatively little subcutaneous Heat lamps should be avoided for warming up, as
fat deposits and modest insulation characteristics of they cause peripheral vasodilation without increas-
goat fibre increase the risk of hypothermia. ing core temperature. Suitable methods include
Dry kid → stomach tube with colostrum →

37–39°C
return to doe → monitor
Dry → warm up →
Rectal stomach tube colostrum
Under 6 hours old
temperature → return to doe
→ monitor
Dry → stomach tube

Over 6 hours old,
<37°C colostrum → warm up →
able to hold up head
Dry → glucose i/p*→

Over 6 hours old,
warm up → feed →
unable to hold up head
* The dose rate for i/p glucose is 10 ml/kg of 20% bodywarm solution (see Chapter 1 for injection technique).
Fig. 4.6 Flow chart for the management of hypothermia.

90 Chapter 4
Fig. 4.7 A simple but effective ‘hot-box’: a household Fig. 4.8 A straw nest is easily manufactured from
fan heater is used as a heat source and partially a cardboard box, and creates a good transitional
inserted into a hole at the bottom of the box. A grid environment on return of a resuscitated hypothermic
is positioned about one-third up in the box to place kid to the doe. The dam has access to her offspring,
the kid onto. (Note: If a metal grid is used, towels are and the kid can climb out of the box to nurse.
placed underneath the kid.) In this example, the grid
is placed onto removable rods to aid cleaning of the
box. The box has several vent holes in the walls.
a heat box (Fig. 4.7), hot water bottles (or ‘hot colostrum intake for initial immunoglobulin (Ig)
hands’ – see Fig. 18.2, p. 335) placed in the axilla and levels. Little specific data is available for kids, but
inguinal region, heat blankets or a Bair Hugger™. extrapolating from lambs and calves, own-produced
The kid is monitored every 30 minutes for response Ig first appears at a few days old for IgA and IgM,
and overheating. Any hyperthermia (indicated by about 1 week old for IgG1, and about 1 month old
panting and rectal temperature exceeding 41°C) is for IgG2. Intestinal Ig appears from about 1 week old
addressed by dousing with lukewarm water, drying (first IgM, then IgA), but is short-lived unless con-
off and returning to the doe. tinuously stimulated.
A ‘nest box’ (e.g. made from a cardboard box Non-immune effector cells (neutrophils, macro-
and straw; Fig. 4.8), heat lamp and coat are useful phages, basophils) are present at birth, but reach full
on return to the doe. The kid is monitored every capabilities only after birth. Noteworthy for haema-
hour for a period to check for relapse and for milk tology interpretation is the higher neutrophil count
intake. in neonates compared with adults. The complement
Prevention involves adequate nutrition of the system is present from the second trimester of gesta-
dam, especially during the first 6 weeks (placenta tion, but activity at birth may be close to 0%, reach-
formation) and last 4 weeks of pregnancy (milk ing 50% at about 2 months of age and full capacity
yield), providing shelter, preventing mismothering after several months.
and prompt intervention in dystocia. Cell-mediated immunity (T cells) is present at
birth. B lymphocytes are present at about one-third
IMMUNE SYSTEM adult levels at birth, reaching adult concentrations at
around 3 weeks of age. They are reduced by steroids,
Normal adaptation including the endogenously produced ones during
Typical for ungulates, the kid is essentially born parturition, which may persist for up to 2 weeks post
agammaglobulinaemic and relies on adequate partum.
Fig. 4.9 Kids should be standing by 2 hours post Fig. 4.10 Equipment used to store and feed
partum, and bonding must not be disturbed to colostrum must be scrupulously clean to maintain
facilitate good colostrum intake. The black kid in the colostrum quality with limited spoilage and reduce
foreground demonstrates the wide-based stance that the pathogen load in the kid.
neonates commonly adopt in the first few days of life.
The neonatal kid is capable of responding to sol- 24 hours of age). (Note: First contact with
uble protein antigens at birth and viral, protozoal colostrum appears to trigger gut closure, so
and bacterial antigens from about 14–30 days old. once some colostrum has been given, the full
However, response is often not 100%, in particular dose must follow promptly.)
memory capacity. These aspects need to be taken
into account for vaccination regimes. Clinical presentation
Kids are at higher risk of neonatal disease, in partic-
Failure of passive transfer ular septicaemia, umbilical infection (and sequelae
Overview such as joint ill) and clostridial diseases.
Failure of passive transfer is a common and largely
preventable condition. Diagnosis
If suspected, or for routine monitoring in a herd,
Aetiology blood is taken from kids at least 24 hours old (to
The causes can be grouped into three main categories: allow time for absorption) but less than 1 week of
age (when production of own Ig begins).
•• Intake of inadequate volume of colostrum. Weak Total protein (TP) is easy to establish in practice
kid, recumbent dam or mismothering (Fig. 4.9), using a capillary tube and refractometer, but hydra-
large litter. Target intake is 10% of birth weight tion status must be taken into account: 55 g/l indi-
in the first 6 hours post partum, plus another cates adequate transfer. Acute phase proteins may
10% in the following 12 hours. artificially increase TP concentrations, which can be
•• Inadequate colostrum quality. Malnutrition and addressed by using globulin levels instead (>20 g/l
illness in dam including mastitis, delay in harvest shows good transfer).
post partum, poor storage conditions, dirty feeding The zinc sulphate turbidity test may be used with
equipment (if artificial feeding is used; Fig. 4.10). either qualitative (adequate transfer if it is impos-
•• Reduced absorption of colostral Ig. Common sible to read newspaper print through test tube),
where the neonate is acidotic or where intake or quantitative (level >20 OD units is adequate)
is delayed (absorption ceases at around interpretation.
92 Chapter 4
(b)
Fig. 4.11 Plasma transfusion is the best option

to address failure of passive transfer. After
centrifugation, the plasma is separated with the
aid of a homemade ‘vice-board’. A human medicine
collection set containing the anti-coagulant CPD has
been used here (a). A blood transfusion i/v set must be
(a)
used to filter out any impurities (b).
Radioimmune diffusion is very accurate, but kits bacterial contamination, air embolism and citrate
tend to be expensive and processing takes 6–24 hours. poisoning.
Gamma-glutamyl transferase. Normal levels in Other options, used with varying success and
the colostrum-deprived newborn are low. A level lacking supporting studies, include continued
>44 IU indicates good transfer. colostrum administration (to provide local IgA in
the intestinal tract), prophylactic antibiosis (risk
Treatment/management/control of influencing GI tract microflora and poten-
Plasma transfusion is the best option, and despite tially supporting fungal infections) or stimulating
there being several blood groups in the goat, cross- the non-specific immune-response (for example
reactions are rare during transfusions. Harvest administering a killed vaccine or foreign protein,
requires a blood centrifuge (Fig. 4.11a). Plasma or immune-modulators such as levamisole, ascor-
will keep at –20°C for up to 12 months, providing bic acid (vitamin C), tocopherol (vitamin E) or
temperature fluctuations are kept to a minimum selenium).
(e.g. by using a dedicated freezer). 30–40 ml/kg of Each herd should have a colostrum bank
plasma are given i/v through a blood transfusion (Fig. 4.12), ideally harvested within 6 hours of
kit at a rate of 20–40 ml/hour (Fig. 4.11b). The birth. Using own does (e.g. those with singletons)
kid is monitored for signs of hypersensitivity, which avoids any biosecurity risks and ensures antibod-
include facial swelling, erythema, dyspnoea and ies against farm-specific pathogens are present.
bronchoconstriction. Treatment for acute hyper- Sourcing bovine or ovine colostrum from high
sensitivity type I reaction includes: dexamethasone health status herds is an alternative. Fresh colos-
at 0.1–4.0 mg/kg i/v, adrenaline 1:1,000 at 0.01 trum will keep for several days at ambient tempera-
mg/kg i/v, or diphenhydramine at 2–4 mg/kg i/m ture. Alternatively, colostrum may be kept frozen
or s/c. Other potential complications include vol- at –20°C for up to 1 year. Thawing has to be done
ume overload, hypothermia (if plasma not warmed), gently to avoid denaturing of proteins (i.e. in warm
Aetiology
Commonly involved pathogens include Escherichia
coli and other Enterobacteriacaea, Streptococcus
spp. (in particular Lancefield group B and C) and
Clostridium perfringens. In-utero infection, leading to
the birth of an already septicaemic neonate, is occa-
sionally seen with pathogens such as Salmonella spp.
Otherwise, pathogens most commonly enter via the
umbilical or oral route, with subsequent haematog-
enous spread (Fig. 4.13).
Fig. 4.12 Ice-cube bags are useful to portion
colostrum for freezing. They must be thawed gently Clinical presentation
to avoid denaturing of proteins. Initial signs are often vague, with owners reporting
the kid being less lively, nursing less and possibly
spending more time recumbent. This progresses
water of 60°C maximum with regular agitation or to signs of septic shock: congested mucous mem-
in a microwave on the lowest setting with periodic branes, dehydration, cold extremities, increased cap-
removal of any thawed liquid). illary refill time, tachycardia, loss of suck reflex and
Routine procedures such as castration should be increasing unresponsiveness. Rectal temperature
delayed until the kid is at least 24 hours old to ensure may be elevated, normal or subnormal.
good colostrum uptake. Death results rapidly in peracute cases. In less
severe cases, additional signs linked to bacteraemic
Neonatal septicaemia (syn. sepsis) infiltration may be seen, such as meningitis, endo-
Overview carditis, kidney and liver abscessation or septic
Neonatal septicaemia generally means an over- arthritis.
whelming infection in the first week of life. It is
often accompanied by a (entero-)toxaemia and bac- Diagnosis
teraemia. One of the most common causes of mor- The sepsis score used in foals can give an indication
tality in neonates. of septicaemia, but has not been validated in kids.
(a) (b)

Fig. 4.13 (a) The dried navel in this septicaemic kid suggests that infection did not occur via the common
umbilical route. (b) Substandard hygiene levels of feeding equipment contribute to a high pathogen load that
may potentially lead to neonatal septicaemia via the oral route.
94 Chapter 4
Blood culture is immensely useful, both for diag- A fluid rate of up to 40 ml/kg/hour may be nec-
nosis and to establish whether a gram-negative or essary initially, but the kid must be monitored
gram-positive pathogen is involved. However, sen- for fluid overload leading to pulmonary oedema.
sitivity of blood culture is not 100%, and clinical Sufficient urine output can be usefully monitored
impression remains important. with the aid of a baby nappy (diaper) strapped over
A marked neutrophilia or neutropenia is the prepuce or vulva (Fig. 4.15). To address the
indicative. likely hypoglycaemia, either glucose is added to the
For treatment and prognosis, liver and kidney chosen fluid or 2.5–5% dextrose is administered
function biochemistry is useful, as are blood acid– simultaneously.
base balance and lactate levels. Until culture results are available, antibiosis must
Arthrocentesis or limb radiography, ultrasonog- be broad spectrum (including anaerobes). Useful
raphy of the heart, kidney, and liver, and a cerebro- antimicrobials include trimethoprim/sulphonamide
spinal fluid tap are used to detect involvement of (data sheet dose, given i/v q8h) and third-generation
organ systems. cephalosporins (e.g. ceftiofur sodium or hydrochlo-
Passive transfer is established using one of the ride at 2 mg/kg q12h). Where aminoglycosides (e.g.
tests discussed previously. amikacin, kanamycin, neomycin, gentamicin) are
available for food producing animals, these may be
Differential diagnosis combined with high-dose benzylpenicillin sodium
Includes hypothermia, hypoglycaemia, uroperito- (25,000–30,000 IU/kg q6–8h), bearing in mind the
neum, severe congenital defect and immaturity. increased risk of nephrotoxicity in a hypovolaemic
animal.
Treatment/management/control Flunixin meglumine (or other NSAID) is use-
Placing an i/v catheter is invaluable (the jugular, ful against toxaemia, providing kidney perfusion is
cephalic or saphenous vein are suitable). In an on- good. After a loading dose of 2 mg/kg, 0.7 mg/kg
farm situation, a large cardboard box, straw bales or q6–8h may be sufficient. Failure of passive transfer,
hurdles are used to restrain the kid, while allowing if present, is addressed as discussed earlier.
the doe to stay in contact if desired (Fig. 4.14). Once a weak suck reflex has returned, the kid
Hypovolaemia is addressed with a sterile crystal- is fed milk in frequent small doses. A prognosis of
loid solution (e.g. Hartmann’s or lactated Ringer’s). about 50% can be expected with intensive care.
Fig. 4.14 This septicaemic kid requiring i/v fluid Fig. 4.15 A baby nappy (here used in a female alpaca
therapy was temporarily placed into a dog crate that cria) is a useful tool to monitor urine output during
was available on farm. Equally, a pen can be created fluid therapy.
from hurdles, straw bales or a large cardboard box.
Fig. 4.16 For navel disinfection, spray application keeps Fig. 4.17 The main differential diagnoses for a
the reservoir solution cleaner compared with a dip-cup, neonate that is increasingly dull and unresponsive are
but care must be taken to cover the navel all the way round. hypothermia, hypoglycaemia, septicaemia and marked
Strong iodine has the advantage over oxytetracycline congenital defect.
solution that it dries out the navel quicker.
Prevention is based on adequate passive transfer, swayback, abortive agents), problems interfering
high kidding environment hygiene and good navel with the kid’s locomotion (e.g. contracted tendons,
care (spray or dip with 7% tincture of iodine or tet- fractures) and exposure to inclement environment
racycline spray within 30 minutes of birth, repeated increasing energy demands.
once or twice over the next 12 hours; Fig. 4.16).
GASTROINTESTINAL TRACT Initially normal at birth, the kid becomes increasingly
weak, incoordinated and unresponsive over 12–24
Normal adaptation hours (Fig. 4.17). Suckle reflex is absent, and dehy-
Hormones, neuropeptides and enzymes have a tro- dration may be evident. Hypothermia is commonly
phic effect on gut development, causing a major present. Eventually the kid becomes recumbent and
growth spurt. Oral uptake of bacteria during the comatose, with death within 24–36 hours.
birthing process and from the kidding environ-
ment starts the colonisation of the GI tract, with Diagnosis
the intestinal flora comparable to adults after sev- A tentative diagnosis can be made in the field, sup-
eral weeks. ported by blood glucose levels (for example using a
The liver changes from its fetal function as a hand-held glucosemeter).
blood-forming organ to its metabolic function.
Hypoglycaemia Hypothermia, neonatal septicaemia, life-threatening
Overview congenital abnormality.
Kids up to 24 hours old are at highest risk, but older
ones may be affected, particularly if the doe develops Treatment/management/control
mastitis or they are exposed to inclement weather. If the kid is able to hold its head up or has a suck
reflex, 150–200 ml of colostrum or milk are given
Aetiology by stomach tube. Otherwise, glucose is administered
Starvation may be caused by milk supply problems i/v, i/p (see Hypothermia for dose rate; see Chapter 1
(e.g. mastitis, teat disorders, mismothering), weak for technique) or as a rectal suppository. Steps to
kids unwilling to suckle (e.g. congenital defects, prevent or address hypothermia are taken.
96 Chapter 4
Fig. 4.18 Meconium retention (shown here in a

lamb) is easily addressed with an enema.
The cause is addressed and the kid continued to

Fig. 4.19 Atresia ani in a newborn male lamb.
be supplemented if necessary.
Because the condition was detected early, no ‘bulging’
Triplets and quads remaining on the doe should
is apparent yet.
always be monitored for sufficient milk intake and, if
lacking, supplemented or fostered on.
over the first week of life. Mild colic may be pres-
Meconium retention ent. A high proportion of affected kids also have
Overview defects in other body systems, which may cause
The meconium should be passed within 24 hours clinical signs and necessitate a thorough examina-
of birth, aided by the laxative effects of colostrum tion to determine prognosis and viability of treat-
(Fig. 4.18). ment attempts.
Treatment/management/control Diagnosis
An enema is gently applied, using either a commer- Absence of an anal opening is obvious on examina-
cial product (such as Micralax®) or 20 ml of warm tion, often with outward bulging of the skin in that
soapy water (with a catheter-tipped syringe). area from pent up faeces. Ultrasonography or (con-
trast) radiography are required to diagnose atresia at
Atresia ani, recti or coli a more proximal point.
Overview
A congenital defect where a section of the lower Differential diagnosis
intestinal tract is missing (Fig. 4.19). Appears to be For abdominal swelling: uroperitoneum, abomasitis,
rare (around 3 of 1,000 kids born). peritonitis.
Aetiology Treatment/management/control
Remains unclear, but may have a genetic component. Atresia ani can often be addressed by making an
incision over the most prominent point of the bulg-
Clinical presentation ing in the perineal area, either under topical anaes-
The kid is normal immediately after birth, but devel- thetic gel, infiltration anaesthesia or sacrococcygeal
ops increasing lethargy and abdominal distension epidural. Wound ointment is applied and the tip of
a finger gently inserted, 2–3 times daily for several URINARY FUNCTION
days.
Surgical treatment of atresia recti may be Normal adaptation
attempted under sacrococcygeal epidural, but it The kidneys are fully formed and functional in the
is often difficult to find the blind end. If it can be second half of gestation. Post partum, the urachus
located, the rectal serosa is freed from surround- closes. In response to increased arterial pressure, the
ing soft tissue, pulled towards the anus and secured glomerular filtration rate increases which, combined
to the rectal sphincter with a series of interrupted with high levels of renin and aldosterone, results in
sutures. production of a large volume of hypotonic urine in
Prognosis for atresia coli is poor. In pet animals, the neonate.
marsupilisation of the intestine to the abdominal
wall can be attempted. However, aftercare is dif- Urine retention
ficult, in particular maintaining skin health and Overview
hygiene and fly control. First urine should be passed within 18 hours of birth.
Cleft palate (syn. palatoschisis) Aetiology

Possible causes include agenesis or atresia of any
Overview
part of the urinary tract, vulval fusion (Fig. 4.20),
Cleft palate is a rare, but typically life-ending, con-
uroperitoneum secondary to a ruptured bladder, or
genital defect in the oral palate. Both the soft and
severe dehydration. Urination in female kids with a
hard palate may be involved.
Aetiology
A genetic component has been considered. It has also
been reported as part of congenital skeletal malfor-
mations induced by ingestion by the pregnant dam
of plants containing piperidine alkaloid toxin (e.g.
lupine, poison hemlock, tree tobacco).
Milk (and later solid feed) will be visible at the nos-
trils. The kid may cough or snort while nursing.
Suckling is not very efficient, leading to poor growth
rate and a potentially distended udder in the doe.
Aspiration pneumonia is a commons sequela, with
dyspnoea, pyrexia and septicaemia.
Diagnosis
Examination of the roof of the oral cavity will show
the defect.
Surgical repair of a small defect in the soft palate
may be attempted. Treatment of larger defects, or Fig. 4.20 Congenital maldevelopment of the vulva
those involving the hard palate, is unrewarding. If may take the form of complete fusion of the vulval
attempted, access is gained by cutting the mandibu- lips, leading to urinary retention (image shows
lar symphysis. hypoplasia).
98 Chapter 4
patent urachus or male kids with hypospadias may Aetiology

be unobserved. Remains unclear. Postulated are a hereditary com-
ponent, position in utero and manganese deficiency
Clinical presentation of the pregnant dam.
The kid probably appears normal in the first few days
of life. As azotaemia worsens, lethargy increases. Clinical presentation
Bulging becomes obvious in females with vulval The flexor tendons of the fetlock, plus sometimes
fusion. the carpus, are contracted, and a plantigrade stance
cannot be achieved. In addition, the leg cannot be
Diagnosis straightened fully by manipulation.
Intravenous urograms are the most straightforward
method to detect agenesis or atresia of the urinary Diagnosis
tract. Ultrasonography will highlight free fluid in the The defect is readily detected on clinical examina-
abdominal cavity and aid aspiration to confirm the tion. However, concurrent congenital defects are
presence of a uroperitoneum. Haematology and bio- common and a thorough and full examination must
chemistry are used to establish levels of d
ehydration be conducted.
and azotaemia. The kid should also be checked for failure of
passive transfer, which is common because of its
Differential diagnosis impaired mobility.
Other causes of lethargy in the neonate (see Neonatal
septicaemia). Differential diagnosis
Arthrogryposis may present similarly, but more
Treatment/management/control commonly involves joints in the upper limb or hind
Vulval fusion is usually easy to treat: topical anaes- leg, as well. Radiography is required to demonstrate
thetic gel is applied to the vulval lips and a verti- joint malformation. Limb joint fixation can also be a
cal incision made at the fusion point of the two lips. feature of Schmallenberg virus infection.
Wound ointment is applied, and the lips manually
parted, 2–3 times daily for several days. Treatment/management/control
Treatment of a ruptured bladder is covered in Conservative treatment is sufficient where the leg
Chapter 10 (Urolithiasis). can be manually extended to achieve a tiptoe stance
Unilateral nephrectomy may be considered in (Fig. 4.21a). After liberal padding, either a splint is
cases of unilateral agenesis of the ureter. secured onto the palmar aspect or the limb is placed
in a cast (Fig. 4.21b), in both cases from the toe
MUSCULOSKELETAL FUNCTION to the proximal metacarpus. The splint or cast is
removed after 10–14 days to check for skin integrity
Normal adaptation and degree of correction. If further support is nec-
The fetus displays leg movements from mid- essary, the cast can be re-used as a half-cast.
gestation, and the bones are generally well ossified at Tendonectomy is indicated if the contracture is
birth. The newborn may display a moderate degree too severe to achieve a tiptoe stance. It can be per-
of tendon and ligament laxity, a wide-based stance formed under general anaesthesia, sedation and
(Fig. 4.9) and an exaggerated gait for a few days. intravenous regional anaesthesia, or local infiltration
of both skin and tendon sheaths. A 3 cm skin incision
Contracted tendons is made on the palmar aspect of the mid-metacarpus.
Overview The superficial flexor tendon is cut across followed, if
A congenital defect, typically bilateral and almost necessary, by cutting the deep flexor tendon and sus-
exclusively involving the fore legs. pensory ligament (Fig. 4.22a). The skin is sutured
(a) (b)
Fig. 4.21 In this calf with contracted tendons, the leg could be manually extended to achieve a tip-toe stance (a);
therefore, application of a splint was a suitable treatment option (b).
(a) (b)
Fig. 4.22 A tendonectomy to address contracted tendons. Both superficial and deep flexor tendons and the
suspensory ligament may have to be cut in severe cases (a). The small incision on the palmar aspect of the mid-
metacarpus was closed with skin staples in this bovine case (b).
or stapled (Fig. 4.22b), and the leg placed into a cast Arthrogryposis
or splinted for 2–4 weeks. Overview
The kid will require aid in standing up and nurs- Congenital joint contracture, typically involving
ing for the first few days. Administration of high- multiple joints and often leading to dystocia.
dose oxytetracycline as a treatment is controversial:
no effect has been proven in ruminants, and the high Aetiology
dose may induce toxic nephrosis. Orthobunyavirus infections, such as Schmallenberg
and Akabane virus, may cause this, as may toxins
Flexor tendon laxity including plant toxins.
Overview
Flexor tendon laxity is commonly linked to prema- Clinical presentation
turity, and carries a good prognosis. The kid shows abnormal angulation of the legs and
is unable to stand. Also, a normal straight posture
Treatment/management/control cannot be achieved with manipulation.
Exercise on a hard surface several times a day is help-
ful. It is also possible to extend the heel with a glued- Diagnosis
on wooden block, for example. Radiography shows abnormal joint formation.
100 Chapter 4
Differential diagnosis Prevention relies on reducing the risk of dystocia

Contracted tendons, fractures, beta mannosidosis and prompt intervention when it does occur.
(see below).
Floppy-kid syndrome
Treatment/management/control Overview
There are no viable options. Floppy-kid syndrome is a metabolic acidosis, with-
out diarrhoea or dehydration, affecting kids typi-
White muscle disease cally between 7 and 14 days of life (range 3 days to
See Chapter 14. 4 weeks). Herd morbidity of between 30 and 50%
is most commonly reported, although in outbreaks
METABOLIC DISORDERS described in North America morbidity approached
100%. Mortality in unrecognised and untreated out-
Because of their clinical presentation, metabolic breaks can be high.
disorders are important differential diagnoses for
apparent neurological disorders. Aetiology/pathophysiology
Remains unknown. In some outbreaks, the biggest
Neonatal acidosis and healthiest kids are affected, and sometimes only
Overview one out of a litter. Both kids nursing their dams and
Acidosis in the neonate is usually a combination of those being artificially reared (on fresh or pasteur-
respiratory and metabolic acidosis. ised milk) are at risk, with a possible link to recent
increase in milk intake. The condition has been rec-
Aetiology ognised in dairy, meat and fibre kids and also in kids
Prolonged parturition or post-partum apnoea are reared indoors and outdoors.
common causes. The current hypothesis is that bacterial over-
growth may play a role (e.g. Escherichia coli, Clostridium
Clinical presentation botulinum). However, kids born to does vaccinated
Often no specific sign, but the newborn may show against clostridial pathogens (e.g. C. perfringens)
reduced vigour. Meconium staining of the newborn appear at equal risk.
indicates that the kid experienced in-utero stress and Some herds report the problem to be contained to
is at higher risk of acidosis. the middle period of the kidding season, with early
or late season kids unaffected. Herds affected in one
Diagnosis or several consecutive years may then not see the
Definitive diagnosis is based on blood gas analysis. problem for a number of years despite unchanged
management.
Intravenous administration of sodium bicarbonate Clinical presentation
will address the metabolic component. The dose rate is Kids are invariably born healthy, consume sufficient
either based on a deficit calculation (body weight × 0.5 colostrum and suckle well either on natural milk or
× base excess) if blood gas analysis is available, or an milk replacer. Early signs include profound muscle
empiric dose of 20 mmol i/v is given, in each case weakness and incoordination, giving the impression
slowly over 10 minutes. Adequate lung ventilation of ataxia, with affected kids appearing intoxicated.
must be ensured to enable removal of the carbon diox- Muscle control is lost across various body systems;
ide produced by the conversion of bicarbonate. for example, tongue paralysis leading to difficulty
Colostral Ig uptake is reduced in acidotic neo- feeding, dyspnoea and GI tract stasis.
nates, therefore a larger volume is required and the Rectal temperature is normal to slightly elevated.
kid should be tested for failure of passive transfer Diarrhoea is absent, but abdominal distension is
once over 24 hours old. sometimes seen.
Diagnosis Clinical presentation

Diagnosis is often based on elimination of other Signs are evident from birth and include inability to
possible causes. Blood gas analysis will confirm rise, intention tremors, nystagmus-like eye move-
metabolic acidosis, typically with an increased ments, deafness, Horner’s syndrome, a mix of joint
anion gap. Hypokalaemia may be present. contractures and hyperextension, and often a dome-
Hydration status is normal, as is kidney function. shaped skull. Kids are typically unable to suckle.
There are no characteristic post-mortem examina-
tion findings. Differential diagnosis
Swayback, other severe congenital disorders,
Differential diagnosis dystocia-induced trauma and hypoxia.
Main differentials include neonatal septicaemia,
enterotoxaemia, peracute enteritis, abomasitis or Treatment/management/control
abomasal bloat, meningitis, cervical spinal cord No treatment is available. Euthanasia is indicated.
lesion, disbudding injury and swayback. The site of mutation for beta-mannosidosis has been
identified.
First aid consists of repeated oral administration Iodine deficiency (congenital
of half a teaspoon of baking soda in some water, hyperplastic goitre)
or frequent oral doses of commercial oral rehydra- Affected kids are typically stillborn or born weak
tion solution. Bismuth subsalicylate may also be and premature. Blindness has occasionally been
beneficial. Good response is seen to i/v NaCHO3 reported, as has coat thinning (see Chapter 15).
over 1–3 hours, with the dose calculated based on
deficit using base excess (body weight × 0.5 × base NEUROLOGICAL FUNCTION
excess), or an empiric dose of 50 mmol. Potentiated
penicillin may be considered, given the possible Normal adaptation
bacterial involvement. Until full suckling func- In principle, all functions necessary for survival are
tion has returned, force feeding may be necessary. well developed at birth. Spinal reflexes develop early
(Note: For i/v use, chemical grade sodium bicar- in utero; in particular the withdrawal and righting
bonate or a commercial NaCHO3 solution must be (into sternal) reflexes are well developed at birth.
used, not baking soda, which contains anti-caking Skin sensation is well developed, including response
agents.) to warmth or coldness. Responses to auditory and
Once recovered, relapses are rare and kids develop tactile stimuli are possibly exaggerated. All reflexes
normally. Recovery rates are about 80% with prompt connected with suckling are present within minutes
treatment and nursing care. of birth.
Control is problematic as the cause is incom- Of note for the neurological examination in neo-
pletely understood. In outbreaks, ad-libitum access to nates are the following: the pupillary light reflex is
milk or milk replacer should be stopped, and strict present at birth, but the menace reflex is a learned
feeding hygiene maintained at all times to prevent response and develops over the first week of life.
pathogen build-up in or on milk utensils. Mentation and senses adjust within 24 hours post
partum, and behaviour within 2–7 days. For gait and
Beta-mannosidosis posture abnormalities it should be remembered that
Overview jerky movements and mild hypermetria are normal
Beta-mannosidosis is an inherited lysosomal disease in the first few days, as is a mild wide-based stance
of Anglo-Nubian goats, leading to oligosaccharide (Fig. 4.9). The normal dominant extensor strength
accumulation in brain and kidney because of a defi- may lead to hyperreflexia. Tendon hyperexten-
ciency in beta-mannosidase. sion or contraction is a common problem without a
102 Chapter 4
neurological basis. In a ‘neurological’ neonate, basic MISCELLANEOUS

disorders such as hypothermia, hypoglycaemia and
septicaemia must always be ruled out. Neonatal maladjustment
syndrome (syn. ‘dummy kid’)
Congenital central nervous Overview
system abnormalities Maladjustment syndrome is a potentially fatal condi-
Overview tion, but with good response to nursing care.
Hypoplasia or aplasia of the cerebrum or cerebellum
may be observed with certain infectious diseases Aetiology
(e.g. border disease virus and Orthobunyavirus [see Potentially linked to milder forms of intrauterine
Chapter 2]). The age at onset of clinical signs can growth retardation. Kids are full term and parturi-
vary from a few days to several weeks old. tion is usually without complications.
Congenital swayback Clinical presentation

Overview The kid appears strong and achieves standing and
Congenital swayback is one of the more common walking within the normal time frame post partum.
abnormalities associated with specific mineral short- However, it demonstrates altered behaviour and
falls during critical stages of fetal development. appears to lack first instincts such as successfully seek-
ing and finding the udder. The kid may drift towards
Aetiology any dark corner and even when aided to latch on, fails
Copper deficiency in the pregnant dam results in to initiate suckling. Righting reflexes may be compro-
spinal cord demyelination in the fetus from the mised. Some kids may suffer myoclonic seizures.
fourth month of gestation onwards. This results in If not detected and treated, secondary problems
a progressive ascending paralysis. Recognised forms ensue such as hypothermia and hypoglycaemia.
are congenital and (acute) delayed swayback.
Diagnosis
Clinical presentation No specific cause is apparent, and no concurrent
Ataxia when driven, muscle incoordination and conditions are evident on clinical and laboratory
inability to stand. Prognosis is poor in neonatal examination.
animals.
Diagnosis Hypoxia, acidosis, hypoglycaemia, congenital defects,
In the dam, liver copper levels are the only reli- neonatal septicaemia and meningitis. Blood and CSF
able indication of copper status, although serum or analysis to rule out.
plasma levels may be reduced in deficient animals.
Treatment/management/control Nursing care is the mainstay, in particular colos-
Copper supplementation of affected kids is trum administration followed by regular milk feed-
unrewarding. ing. Respiratory function may be compromised
Prevention consists of adequate copper supple- and, if available, can be addressed by nasal oxygen.
mentation of the dam. High soil molybdenum Thermoregulation may also be poor, and use of
(‘teart’ pastures) or high soil or water sulphur levels coats and increased ambient temperature is useful.
will interfere with copper uptake. Definitive diag- The kid should be in a low-stimulant environment.
nosis of copper deficiency needs to be obtained, Anticonvulsive therapy may be necessary in some
however, to avoid copper toxicity. (See also kids. It may take several days for the kid to adopt
Chapter 15.) normal behaviour.
Prematurity Diagnosis
Overview In herds with good breeding dates, diagnosis is often
Prematurity is fairly commonly encountered, with straightforward based on calculation of pregnancy
reasonable prognosis with good nursing care. length. Otherwise, a tentative diagnosis can be made
only based on clinical signs.
Aetiology
Multiple causes may lead to premature live births, Treatment/management/control
including infectious causes of abortion (e.g. Kids more than 4–5 days premature are generally
Toxoplasma spp., Chlamydia spp., Coxiella spp.), plant not viable and euthanasia should be considered.
toxins, mineral deficiency (e.g. iodine), iatrogenic The two main aspects to address are lung func-
(PGF2α , corticosteroids), placental insufficiency and tion and thermoregulation. Surfactant is often not
illness in the dam. fully developed: a resuscitator will aid inflation
and bronchodilators may help (e.g. aminophylline).
Clinical presentation Thermoregulation is supported by a warm, draught-
Several signs may indicate prematurity, but none are free environment, use of a coat and ensuring energy
specific: incisors not erupted (Fig. 4.23), silky thin intake.
coat, floppy ears and tendon laxity. Abortions may be The kid will require help to stand and suckle, and
evident in the herd. force-feeding colostrum is often indicated, because
The kid may struggle to stand and maintain nor- lactogenesis may not have commenced yet in the dam
mal body temperature and demonstrate dyspnoea. It or because of the kid’s inability to stand and suckle.
may appear normal for the first few hours post par- With regard to passive transfer, the premature gut is
tum before markedly deteriorating. fully capable of absorbing immunoglobulins.
Joint laxity will gradually disappear with exercise.
In the meantime, the kid is aided in standing and
walking (e.g. with a belly sling).
Low birth weights

Overview
A major cause of loss within the first 48–72 hours
post partum. In the Angora breed, survival is less
than 20% for birth weights <1.5 kg, reaching 60%
for birth weights of 2 kg. Peak survival is for birth
weights of 4 kg, after which the higher risk of dysto-
cia reduces survival rates again (Fig. 4.24).
Aetiology
There are two main causes: (1) the doe’s nutrition
status during placenta formation (roughly first
6 weeks of pregnancy); it must stay level or be slightly
increasing; a decreasing level leads to a reduction in
both size and number of placentomes formed; and
(2) abortive agents.
Fig. 4.23 Some body features like non-erupted Treatment/management/control

incisors may indicate prematurity in the neonate, but Nursing care, in particular thermoregulation and
they are not pathognomonic. colostrum/milk intake, may increase survival chances.
104 Chapter 4
Fig. 4.25 Just as in lambs, the skin of a dead neonate

may be placed onto another kid to facilitate fostering.
However, this technique is not without disease risk.
but often succumb to secondary disease and, there-

fore, are probably best culled.
Fig. 4.24 Birth weights are easily established using a
spring-loaded or hook scale and suitable container or ARTIFICIAL REARING
sling to hold the neonate. Routine monitoring is very
useful. As a minimum, they should be checked if a Fostering
herd experiences high neonatal mortality. In herds where kids stay on does until weaning, fos-
tering of an orphaned or underfed kid may be tried.
Control of abortive agents is via vaccination and Practices that may increase the chance of acceptance
biosecurity. Nutritional cause is addressed by use of of the foster kid include placing the skin of the doe’s
a suitable ration in early pregnancy. The risk of large own dead kid on the foster one (Fig. 4.25) or smear-
litters versus the benefits of oestrus synchronisation ing the kid with strong smelling or tasty fluids (e.g.
must be weighed up. amniotic fluid, aniseed, molasses). The doe is manu-
ally restrained every 2–3 hours initially to allow the
Sticky kid disease kid to suckle, with monitoring in between for bully-
Overview ing. Foster crates are an option, but can compromise
Sticky kid disease is a hereditary condition of mainly the doe’s welfare.
Golden Guernsey goats. Male kids seem to be more
susceptible than females, and it may affect just one Supplementing
of a litter. Where a doe provides some, but not sufficient, milk
for her kids, finding the right level of supplementa-
Clinical presentation tion can be difficult. If the kid is oversupplemented,
Affected kids do not dry off after birth and become it may stop seeking the doe’s udder and, in turn,
susceptible to other diseases (enteritis, pneumonia). stimulation of milk production ceases.
Excess sebum secretion is evident in skin biopsies. A reasonably successful approach is to estimate
the kid’s 24-hour requirement, based on 15% of its
Treatment/management/control body weight. Then initially feed one-third of this
Treatment with medicated shampoos is not effective. requirement divided over multiple feeds, while mon-
Kids can be successfully reared with lots of nursing, itoring for sufficient weight gain. If weight gain is
suboptimal, increase the supplemented amount to cool milk readily. Where milk is replenished once a
one-half of total requirement for a few days, monitor day and the ambient temperature is above 15°C, the
weight gain and adjust as necessary. milk is chilled prior to being placed into the reser-
voir, and the reservoir ideally insulated to slow down
Routine artificial rearing souring. Ice packs can be placed into the reservoir
Advantages of taking kids off does include more in very warm weather. The reservoir must have a lid
saleable milk in dairy herds, having more control (Fig. 4.29) and, if too heavy to be tipped, a drain-
over growth rates, breaking disease cycles (e.g. age hole for emptying and cleaning. A third option is
Johne’s disease) and dealing with large litters or feeding from an open trough; this is suitable where
orphans. milk is given several times throughout the day, but
requires training of the kids. For teat-based systems,
Feeding considerations the drinking height is 50 cm to start with.
Either whole milk or milk replacer may be used, the Feeding implements must be kept scrupulously
latter with 24–26% protein, 14–22% fat and 12–16% clean (Fig. 4.30), using hot water and disinfectant
dry matter (DM) (e.g. 15% DM equates to 1 part (e.g. sodium hypochlorite [bleach]).
milk powder by weight mixed with 5.7 parts water As a rough guideline, the kid should be fed
by weight; Fig. 4.26). High levels of starch or plant 15–20% of its body weight in each 24-hour period. If
protein in the milk replacer should be avoided. not offered ad libitum, this amount is spread over at
For just a handful of kids, lamb or human baby least 4 feeds during the first week of life, then 3 feeds
bottles placed in a rack work well (Fig. 4.27). Bottles up to 4–6 weeks old and twice daily for the remain-
should not be hand held when feeding male kids, to der. The amount is halved and the frequency reduced
reduce the risk of kids developing ‘berserk male syn- to once a day in the 2 weeks prior to weaning.
drome’. Where larger number of kids require feed- An example protocol is: week 1 feed 4 × 300 ml,
ing, a self-feed milk reservoir with multiple teats is weeks 2–6 feed 3 × 750 ml, weeks 7 and 8 feed
more efficient (Fig. 4.28). Starting with bodywarm 2 × 1–1.5 litres, week 9 feed 1 × 1–1.5 litres, week
milk for the first few days, kids can be accustomed to 10 feed 1 × 500 ml.
Fig. 4.26 A make-shift weigh scale to measure Fig. 4.27 A bottle rack works well for a small
out milk powder. A timber baton is balanced on a number of kids that require milk feeding.
rod. A known quantity of water is placed at one end.
A container is placed equidistant at the other end and
milk powder added until the baton is in balance again.
106 Chapter 4
Fig. 4.28 Self-feed teat feeders are a labour efficient Fig. 4.29 Where milk is replenished to last 12–24
way for long-term feeding of larger groups of kids. In hours, the container must have a lid to preserve milk
the system shown here, where milk is not available ad quality. It should also be insulated and, depending on
libitum, all kids must have access to a teat at the same the climate, cooled.
time. This type of feeder can be heavy, often resulting
in suboptimal infrequent cleaning.
Fig. 4.30 Good practice. An easily accessible Fig. 4.31 Good access to concentrate, provided from
cleaning area for feeding buckets, well equipped with 1–2 weeks of age, as well as to water (white bucket),
brushes, disinfectant and hot water on tap. aids rumen development (in addition to forage).
Where milk is offered ad libitum, during the mix; 18–25% crude protein) are provided from 1 to
2 weeks prior to weaning the amount is reduced to 2 weeks of age (Fig. 4.31). Kids should be eating
half that consumed in the previous week. 250 g of concentrates at weaning.
Clean drinking water must always be available. Weaning may be attempted at 6 weeks old if the kid
has reached 10 kg body weight. This requires excel-
Weaning considerations lent husbandry and a daily live weight gain of 250 g.
To aid rumen development, hay or eating straw Often more achievable is weaning at 8–12 weeks old
and concentrate (kid, lamb or calf pellets or coarse or once they have reached 18 kg body weight.
Post-weaning growth rates on good quality pas-

ture range from 100–120 g/day for dairy breeds to
185–245 g/day for Boer kids. Kids on pasture may
experience weight stasis in late autumn to early win-
ter, regardless of supplementary feeding.
Housing considerations
Group sizes of 15 work well and should not exceed 25.
Minimum space allowance is 0.6 m2/kid (Fig. 4.32).
Housing must be well ventilated but draught-free,
with plenty of clean bedding. Minimum required
Fig. 4.32 These goatlings are housed in an adequate shed temperature is 5°C, and heat lamps should be
group size (up to 15 works well, maximum of 25). considered depending on air space and number of
However, the stocking density is too high and does not kids. If reared outside, natural or artificial shelter
fulfil the minimum space allowance of 0.6 m 2/kid. from wind, rain and sun must be available.
CHAPTER 5
DIGESTIVE TRACT AND ABDOMEN

109
CLINICAL EXAMINATION OF Abdominal examination

THE DIGESTIVE SYSTEM Abdominal contour
The behaviour of fluid (migrating ventrally) and
Oral and dental examination gas (rising dorsally), together with the anatomical
Examination of the rostral oral cavity is straight- location of various structures of the gastrointesti-
forward; however, the tightness of the goat’s mouth nal (GI) tract, allows narrowing down of the likely
means that sedation may be required to allow full problem when observing the abdominal contour.
examination of the caudal parts (Fig 5.1). A pen Common origins of bilateral ventral distension
torch and mouth-gag are invaluable. Integrity of the are rumen distension (pathological or because of
oral mucosa is of interest. Loss may indicate condi- a fibrous, slowly digestible diet), free abdominal
tions such as dental disease, drenching gun injury, fluid (e.g. ruptured viscera or peritonitis) and late
neoplasia, viral disease or uraemia. pregnancy (Fig. 5.3). Bilateral dorsal distension
Teeth are checked for absence, malocclusion, loss is commonly caused by free abdominal gas (e.g.
of anchoring, overgrowth, angulation and discol- peritonitis) or severe rumenal tympany. Common
ouration. Halitosis and quidding are signs of dental causes for distension of an individual abdominal
disease. A rough assessment of cheek teeth align- quadrant are: left upper = rumenal tympany; left
ment can be made by external palpation of the tooth lower = rumen fluid; right upper = intestine; right
arcades (Fig. 5.2). lower = abomasum, intestine, late pregnancy.
Fig. 5.1 Sedation enabled a thorough examination Fig. 5.2 Skyline view (rostral to caudal) of the
of the caudal oral cavity (here in an alpaca), and a right cheek teeth, with the lip commissure incised.
purulent discharge (arrow) was detected. The abnormal angle of the upper molars could be
palpated externally. The animal was quidding and had
recurrent feed impaction in the cheek.
110 Chapter 5
Fig. 5.3 Distension of the right lower abdominal Fig. 5.4 The mildly arched back and backwards
quadrant in a pregnant doe. The abdominal contour stance of the hind legs indicate discomfort in this
should be noted during examination. goat. Origin of pain may be the abdomen, but also the
udder, thorax or limbs.
A ‘papple’ shape (dorsal and ventral distension on Pain indicators

left, ventral distension on right) may be seen in Colic signs are often subtle, including general restless-
vagal indigestion. More discreet swellings can be ness, shifting weight or lifting a hind leg towards the
caused by haematoma, neoplasia or emphysema in abdomen. The goat may display grunting or bruxism.
the abdominal wall. However, colic signs are not pathognomonic to the GI
tract. Similarly, an arched back may be displayed with
Abdominal auscultation and percussion pain originating in the abdomen, but also in the tho-
In addition to the rumen rate (normal: 2–4 contrac- rax, mammary gland or limbs (Fig. 5.4). A ‘panicked’
tions in 2 minutes), the character of the contrac- facial expression may be present. The withers pinch
tions is of interest (i.e. whether strong and of normal test can be applied in goats; a normal response consists
duration). Quiet sounds mean either reduced rumen of the goat dipping its back in response to the withers
function or that the rumen has been displaced away being grasped. If cranial abdominal pain is present, the
from the left body wall. Rumen fill gives an indica- goat may either grunt on dipping or refuse to dip the
tion of recent feed intake. second time round. Manual palpation and lifting of
Regular intermittent borborygmi of moderate the ventral abdominal wall is also useful to detect pain.
strength should be audible when auscultating the The Eric Williams test is used specifically to
right flank. Of concern would be excessive or absent detect reticular pain. It makes use of the fairly regu-
borborygmi. lar cycle of two B-waves (rumen contraction) to one
A dull, drum-like resonance on percussion sug- A-wave (reticulum contraction), and involves simul-
gests tight distension with gas (e.g. rumen tympany). taneous palpation for the rumen waves in the left
A high-pitched resonance (like fluid dripping into a flank while auscultating the trachea to detect a grunt
metal bucket) indicates a gas–fluid interface, like in or catching of breath.
a distended abomasum. It is important to be familiar
with normal areas of resonance (e.g. a narrow strip Liver examination
just ventral to the lumbar transverse processes asso- The liver is not readily accessible to physical examina-
ciated with the colon). tion. Protrusion beyond the last rib may be detected,
D ige s t i v e Tr ac t a n d A b d om e n 111
as may be pain on percussion over the right caudal guide centesis (see later). In the normal goat, only
ribcage. Mucous membranes are checked for jaun- very small pockets of fluid are present, increasing
dice. In general, detecting liver pathology involves somewhat in a pregnant doe near term.
further diagnostics, such as biochemistry, biopsy and The gas present in the rumen and abomasum
ultrasonography. precludes visualisation of changes in the lumen,
but the position of the viscus and the integrity and
Faecal examination thickness of its wall can be established. Intestines
Volume, consistency and abnormal contents (e.g. can be visualised through the right flank and
blood, mucus, membrane casts) are evaluated. t ypically have a mid-tone echogenicity (Fig. 5.6),
Perineal staining indicates diarrhoea. Presence of with regular and obvious peristaltic movements
tenesmus is noted. (not to be confused with movement caused by
respiration). The loops of the small intestine are
Ancillary diagnostics irregularly arranged, while the loops of the spi-
Ultrasonography ral colon appear more ordered. Of concern are
The presence of free abdominal fluid is easy to estab- absence of peristalsis or incomplete collapse of a
lish by ultrasonography (Fig. 5.5), which may also loop during peristalsis, low echogenicity of gut
contents, wall oedema or a very different appear-
ance of adjacent loops (Fig. 5.7). Intussusception
may display the classic ‘goggle’ appearance (see
Fig. 5.37).
The liver usually has a homogeneous appear-
ance and the main vessels (e.g. vena cava) and bile
ducts can be identified (Fig. 5.8). Calcifications
within the parenchyma or bile ducts are of inter-
est, as are any masses (e.g. an abscess). The gall-
bladder may appear enlarged in an inappetent
animal.
Fig. 5.5 Marked free abdominal fluid (appearing

black on ultrasonography) to the left of a liver lobe.
Fig. 5.6 Mid-tone echogenicity of normal intestine. Fig. 5.7 Cross-sections of adjacent intestinal loops
Some bright gas shadows appear in the lower half of showing different ultrasonographic appearance and
the image. echogenicity in a case of ileal obstruction.
112 Chapter 5
Fig. 5.8 Normal ultrasonographic appearance Fig. 5.9 Landmarks for abdominocentesis: either left
of the liver. The parenchyma is homogeneous paramedian about four finger-widths behind the elbow
and various cross-sections of vessels and bile ducts (arrow), or left or right paramedian just in front of the
can be seen. teats in the male or udder in the female (arrowhead).
Computed tomography and magnetic On farm, the presence of fibrin, ingesta and
resonance imaging blood can be established. A subsample is shaken
Computed tomography (CT) and magnetic reso- vigorously to check for precipitation of excessive
nance imaging (MRI) are becoming more accessible protein. Laboratory analysis includes protein (nor-
and most goats are small enough to fit into a machine mal range 20–25 g/l), nucleated cells (normal range
used for companion animals. These imaging modal- 0.2–0.3 × 109/l) and culture.
ities bypass the limitations of radiography and ultra-
sonography in ruminants, and reference articles for Liver biopsy
normal anatomical appearance are becoming more Liver biopsy is a useful technique to establish pathol-
widely available. ogy in the individual sick goat, but also for routine
monitoring of trace element status (in particular cop-
Abdominocentesis per). The animal is placed into left lateral recumbency,
Ultrasound guidance, if available, is helpful to per- possibly under light sedation. Ideally, it should not be
form abdominocentesis. Alternatively, samples may starved, so that a full rumen pushes the liver against
be taken blindly from the following sites: (1) left the right abdominal wall. An area in the 10th or 11th
paramedian, four finger-widths behind the elbow; or (penultimate) intercostal space, on a line between the
(2) left or right paramedian just in front of the udder tuber coxae and shoulder joint (Fig. 5.10), is clipped
(or teats in the male; Fig. 5.9). The site is clipped and disinfected. After infiltration of skin and inter-
and disinfected. An 18–20 gauge hypodermic nee- costal muscles with local anaesthetic, a 1 cm long
dle, 3.75 cm (1.5 in) long (5 cm/2 in in overcondi- skin incision is made. A Tru-Cut™ or similar biopsy
tioned animals), is inserted at a right angle to the needle is advanced through the incision, either at
skin and gradually advanced. Fluid may be collected right angle to the skin and straight across the body, or
by free-catch or with the aid of a syringe, into both aiming towards the left elbow (Fig. 5.11). The needle
an EDTA and a plain sampling tube. is pushed through the pleura (resistance appreciable,
The omentum is very effective in containing peri- and pain response may be seen) into the thorax. Some
tonitis, and sampling at various sites and to varying centimetres deeper, overcoming resistance indicates
depths may be necessary (also because there may be that the diaphragm has been penetrated (the needle
a substantial amount of intra-abdominal fat). will move in line with respiration). About 1 cm deeper
Fig. 5.10 Landmarks for liver biopsy. Needle Fig. 5.11 Liver biopsy in a goat (the goat’s head is on
entry point is in the 10th or 11th intercostal space the left, with its legs towards the operator). Note that
(arrow) on a line between the tuber coxae and the the needle is angled this acutely only to gain entry
shoulder joint. through the stab incision. After that it will be advanced
at a right angle to the body wall or pointing towards the
opposite elbow. Ultrasound guidance is useful to target
a particular lesion, but the procedure can be done blind.
than the diaphragm, and at a total depth of 7–10 cm in with suspected carbohydrate overload or to assess
the adult goat, renewed resistance indicates the liver rumen health.
capsule. The needle is pushed into the liver tissue for Paracostal collection is carried out in the con-
a couple of centimetres (slightly gritty feel to it, like scious standing animal, with an optional skin bleb
pushing a needle through sand) and the mechanism of of local anaesthetic. The skin is prepared with surgi-
the needle is activated to take the sample. A staple or cal spirit. A 3.7–5 cm (1.5–2 in), 14 gauge needle is
suture is placed into the skin incision inserted perpendicular to the skin in the lower half
If the sample is taken for copper analysis, as of the left flank close to the last rib and advanced
much blood as possible should be washed off with into the rumen. A syringe is attached and the sam-
de-ionised sterile water or saline, before placing it ple collected. Rumen fluid may also be collected by
into a plain sampling pot. For histology, the sample stomach tube, but saliva contamination can artifi-
is placed into 10% formalin. cially increase the pH by 1 to 2 units.
Ultrasound guidance is useful, in particular to Normal rumen fluid in an animal on a forage-
target non-diffuse lesions. Main risk factors include rich diet is green to olive–green in colour and has
penetration of the gallbladder and haemorrhage an aromatic odour. An indifferent smell suggests
from penetrating a large hepatic vessel. Peritonitis inactivity, an acid smell and greyish colour suggests
is very rare. Animals occasionally exhibit dyspnoea low pH, an ammonia smell severe protein overload
after the procedure due to a pneumothorax. This (e.g. urea toxicity) and a foul smell putrefaction
resolves quickly (within 20 minutes) and, because of (overgrowth of coliforms and Proteus spp.). When
the complete mediastinum, does not cause a problem. the sample is left to stand, sedimentation should
Ideally, clotting ability is assessed prior to the proce- take 4–8 minutes. Faster sedimentation, often with
dure (e.g. blood drawn into a plain glass vacutainer absence of floating particles, occurs with inactiv-
will clot within 5 minutes in the normal animal). ity or acute rumen acidosis. Normal rumen pH is
6.5–7.5 on a forage-rich diet, but may be as low as
Rumenocentesis 5.5 about 2–3 hours after a concentrate meal. The
Rumen fluid analysis is useful to assess subacute normal rumen flora is predominantly gram nega-
rumen acidosis on a herd level or in individual cases tive with a wide variety of bacteria (rods, cocci,
114 Chapter 5
Fig. 5.12 Typical appearance of gram-stained Fig. 5.13 Presence of small, medium and large
rumen fluid when the ration is forage-rich. Gram- protozoa suggests a healthy rumen flora. Large
negative bacteria prevail and there is a variety of protozoa are the first to disappear during flora
shapes and sizes. disturbance and the last to reappear after correction.
singly or in clusters; Fig. 5.12) and various sized during cudding. Cheek teeth continue to grow
protozoa (Fig. 5.13). into adulthood.
Dentin is present throughout the length of the
NON-INFECTIOUS DISEASES OF THE tooth, and is covered by enamel in the crown and
DIGESTIVE TRACT AND ABDOMEN cement in the root. Enamel cannot repair itself.
Secondary dentin can be laid down on the biting
Dental problems surface in response to wear, but needs the right
stimulation and good vascular supply and is always
Normal structure and function of lower quality than the original dentin.
Dentition
As is typical for ruminants, the goat has a dental pad Table 5.1 Tooth eruption times in the goat.
in the upper jaw instead of incisors. The dental for-
mula for permanent teeth is: DECIDUOUS ERUPTED PERMANENT CHANGING
TOOTH BY AGE TOOTH AT AGE
0I 0C 3P 3M Incisor 1 Birth Incisor 1 15 months
3I 1C 3P 3M Incisor 2 Birth Incisor 2 19–22 months
The mandibular canine tooth has adopted the Incisor 3 Birth Incisor 3 21–26 months
position and function of a 4th incisor. Eruption Canine 1–3 weeks Canine 29–36 months
times for deciduous and permanent teeth are shown
Premolars 2–4 3 weeks Premolars 2–4 17–20 months
in Table 5.1.
Incisors are used for apprehension of feed. Molar 1 3–4 months
The chewing surfaces of the cheek teeth (pre- Molar 2 8–10 months
molars and molars) are rough with several ridges. Molar 3 18–24 months
The mandibular arcade is narrower than the
maxillary arcade, and each mandibular tooth is Adapted from: Thomé, H (2004) Mundhöhle und Schlundkopf.
In: Nickel, Schummer, Seiferle – Lehrbuch der Anatomie der Haustiere,
offset in a rostrocaudal direction against its cor-
Band II, 3rd edn. (eds. J Frewein, H Gasse, R Leiser et al.) [Oral cavity
responding maxillary partner, with the exception and pharynx. In: Textbook of Anatomy of Domestic Animals, Vol. II,
of M3. They have a combined serrating function 3rd edn]. Parey Verlag, Stuttgart.
Mandibular brachygnathia and The cheek teeth should always be checked, as

prognathia (syns. underbite/overbite) they are often also misaligned.
Overview
Brachygnathia is a shortened mandible, progna- Treatment/management/control
thia a mandible that protrudes beyond the maxilla There is no treatment for an underbite. An overbite
(Fig. 5.14). resulting in clinical problems may be at least par-
tially corrected by trimming the incisors. The goat
Aetiology is lightly sedated. A rolled-up towel or dog tug-of-
Typically congenital, although the extent of the mis- war rope makes a useful gag to hold the mouth open
alignment may alter as the animal grows and matures. and the tongue out the way. The teeth may be cut
A hereditary component is likely and affected animals with embryotomy wire or a Dremel rotary tool.
should be removed from the breeding pool. Water cooling must be applied to the teeth during
the procedure. Great care must be taken not to open
Clinical presentation the pulp cavities.
Teeth alignment and health should always be
checked in an animal failing to maintain a satisfac- Dental disease
tory body condition score. The defect may be obvi- Overview
ous visually, but more subtle cases require lifting of Incisor and cheek tooth pathology are well described
the upper and lower lip to check alignment of the in other ruminants and, despite a paucity of litera-
mandible in relation to the dental pad. Occasionally, ture on the subject, it is likely that the goat is simi-
a lateral head radiograph is required to determine larly affected with conditions such as malocclusion,
whether protruding incisors are due to prognathia tooth loss, periodontal disease and tooth fractures.
or just tooth overgrowth.
Clinical relevance consists of reduced feed intake Aetiology
with an overbite and occasionally broken teeth. Age will cause some inevitable changes, such as uneven
An underbite may damage the oral mucosa with sec- wear and formation of diasthemata. Secondary prob-
ondary infection. lems to these are trauma to the oral mucosa and food
impaction, with periodontal disease.
Occasionally, the eruption of permanent teeth
is abnormal with, for example, deciduous teeth
not shedding on time or eruption at an abnormal
angle.
A high concentrate diet may lead to caries. No
information exists on the possible role of retinol,
ascorbic acid or calciferol (vitamins A, C and D) and
calcium, as implicated in other species.
Tooth root infections may be linked to eruption
of permanent teeth or haematogenous infections.
Tooth fractures may be the result of trauma to the
head or stones or metal in the diet, possibly facili-
tated by any weakening of the tooth structure.
Fig. 5.14 Protruding incisors in an Anglo-Nubian Many affected animals will show no overt signs
buck. Careful examination, possibly combined with until dental pathology is well advanced (Fig. 5.15).
a radiograph, may be required to distinguish true Weight loss or failure to maintain body condition
prognathia from tooth overgrowth. should always trigger a dental examination.
116 Chapter 5
Fig. 5.15 Specimen of severe mandibular bone Fig. 5.16 Radiograph of the mandible showing
pathology. The animal (an alpaca) had not shown extensive bone lysis and sclerosis. To determine
any obvious signs until 1 week prior to referral, and tooth root involvement, the integrity of the lamina
the owners had performed routine body condition dura is established. Normal appearance can be seen
scoring and palpation of the jawline 4 weeks prior. surrounding both roots of M3 and the caudal root of M2:
This lateral view shows the rostrocaudal extent of a radiolucent line adjacent to the root, then a radiodense
the pathology. Also note the normal offset between line (arrows). The lamina dura is lost around the cranial
mandibular and maxillary teeth. root of M2 and the caudal root of M1. The skin staples
were placed over the discharging tracts to establish the
relative location of the bone lesions. Left dorsal to right
ventral oblique view.
(a) (b)

Fig. 5.17 Two radiographs of an alpaca jaw showing the benefit of oblique radiographs. (a) The pathology in
the lateral view looks relatively restricted; (b) the oblique view shows the true extent of the pathology.
Incisor tooth pathology may reduce overall intake the jaw and excessive tear flow (if maxillary tooth
of forage, leading to weight loss. However, if goats affected).
are grazed on varied vegetation, they often compen- Uneven wear may also lead to changes in the
sate by selective feeding. mandibular joint, with associated discomfort.
Cheek tooth pathology will lead to weight loss,
but also signs of poor digestion, such as poor rumen Diagnosis
fill and undigested fibre in the faeces. Other possi- Oral examination, with the aid of a pen torch and
ble signs include quidding (dropping feed or a cud), light sedation, may give an indication of the prob-
feed impaction in the cheek, salivation, bruxism, lem. Diagnosis is aided by radiographs, highlight-
halitosis, tooth discolouration and taking longer to ing involvement of bone structures and tooth roots
feed. Where the tooth root is involved, additional (Fig. 5.16). Lateral, dorsoventral and 30–45-degree
signs include jaw swelling, discharging tracts along oblique views are taken (Fig. 5.17), either in the
standing goat or in lateral recumbency under seda- very important to leave some ridges on the biting
tion. A mouth gag is useful to separate the arcades surface: floating this surface smooth will result in
(e.g. a 20 ml syringe or syringe case, covered in a indigestion.
layer of elastic bandage for grip). Ultrasound is use- The options for tooth root infections are surgi-
ful to investigate soft tissue changes. MRI or CT is cal extraction, surgical curettage (Fig. 5.19), medi-
occasionally necessary to identify the specific tooth cal treatment or a combination of these. Because
involved. of the tightness of the goat’s mouth, the surgi-
cal approach is via the ventral mandible or lateral
Differential diagnosis maxilla. Alternatively, a buccal approach can be
A jaw swelling (Fig. 5.18) may also be caused by used up to molar 2, taking care not to traumatise
infection of the bone (including actinomycosis, the parotid duct. General anaesthesia (GA) is advis-
syn. ‘lumpy jaw’), a fracture, neoplasia, an abscess able, combined with a mandibular and mental block
(including caseous lymphadenitis [CLA]), a saliva for analgesia (see Chapter 18). Any defect created
cyst, foreign body reaction (e.g. a blackthorn), cud is plugged postoperatively to reduce saliva loss and
retention and insect or snake bites. contamination (e.g. with gauze swabs or a tampon;
Fig. 5.19). The plug is replaced, and the wound
Treatment/management/control lavaged daily until granulation tissue is well estab-
A loose or malaligned tooth may be removed orally. lished. Antibiosis, either as stand-alone treatment or
A ‘spike’ that has formed in response to malocclu- postoperatively, needs to be prolonged (4–6 weeks).
sion or a missing tooth can be rasped off. The goat’s A wide variety of pathogens may be involved,
mouth is rather restricted in its ability to open, including anaerobes. Suitable antimicrobials are
but with sedation and using dental floats for min- florfenicol, penicillin, potentiated penicillin (e.g.
iature ponies the task can usually be achieved. It is with clavulanic acid), tetracycline and ceftiofur.
Fig. 5.18 Marked swelling involving the left Fig. 5.19 View onto healthy bone after aggressive
mandible. The main differential diagnoses are: curettage to remove any softened and infected bone
bone infection, soft tissue abscess, cud retention, tissue (animal in dorsal recumbency, with muzzle
salivary cyst. to bottom of image). A gauze swab is placed into a
resulting defect connecting with the oral cavity to act
as a postoperative plug.
118 Chapter 5
(a) (b)
Fig. 5.20 (a) Giant cell tumour in the oral cavity of a mature goat, and (b) associated radiograph showing
extensive bone destruction. (Image courtesy Andrew Dobson.)
Cases with extensive bone involvement may benefit

from oral potassium iodide (0.5–1.0 g per day for
7–10 days) or i/v sodium iodide (1 g/12 kg as 10%
solution, 2–4 times at 7–10 day intervals; an i/v
catheter must be used as the solution is highly irri-
tant to perivascular tissue).
Dietary fibre is important for dental health,
in particular tooth wear and buffering saliva
production.
Fig. 5.21 Oral lymphosarcoma in a 7-year-old
Oral problems (excluding dental) Anglo-Nubian doe, causing separation of incisors and
some food impaction.
Normal structure and function
The tongue has a moderately well developed pro- Aetiology
tuberance in its caudal part, the torus linguae. Neoplastic changes may involve various tissues of
The oral mucous membranes tend to be relatively just the oral cavity (e.g. spindle cell or giant cell
pale and, depending on breed, may show heavy tumours; Fig. 5.20) or be part of a wider spread
pigmentation. neoplasia such as lymphosarcoma.
Neoplasia Clinical presentation

Overview Until the mass becomes externally visible, early
Oral tumours occur regularly. Lymphosarcomas signs include salivation, bleeding, dysphagia and
may be found in young adults, with other tumours tooth misalignment (Fig. 5.21). Regional lymph
typically affecting middle-aged to older animals. nodes may be enlarged, which may contribute to any
There appears to be no breed predilection. dysphagia.
Diagnosis
Histology provides a definitive diagnosis. A punch
biopsy typically gives a suitable sample. Depending
on the site, it is taken under topical anaesthetic gel
application, infiltration anaesthesia or regional
block. Moderate to profuse haemorrhage should be
expected from most oral sampling sites, which can
be addressed with direct pressure application.
Bone proliferation may be caused by dental disease
or bone infection (e.g. actinomycosis). The main dif-
ferentials for a soft tissue swelling are abscess, trau-
matised mucosa with subsequent infection, alveolar
food impaction and foreign body reaction. Clinical,
ultrasonographic and radiographic examination usu-
ally allows a definitive diagnosis.
Fig. 5.22 View onto the roof of the oral cavity of
a lamb, showing extensive infection and necrosis
Prognosis is guarded to poor. It may be possible
resulting from trauma caused by a drenching gun.
to surgically remove very discreet masses, possi-
The entry point was small, with the full extent of
bly followed by radiotherapy. Partial jaw resection
the lesion only apparent after resection. (© Crown
is in theory possible; however, the impact on food
Copyright 2013. Source and kind permission:
intake and mastication must be considered. Spread
Animal and Plant Health Agency and Ian
to regional lymph nodes carries a poor prognosis.
Mawhinney.)
Drenching/bolus gun injury

Overview a few days of the gun being used. Salivation, dys-
This is an entirely preventable problem. A large phagia, halitosis, nasal discharge and enlargement
proportion of goats in a herd may be affected,
of regional lymph nodes may also be seen. Pain
and case mortality rates of around 15% have been is often displayed in the form of bruxism and
reported. i nappetence. Abscesses may erode into local

vessels,
p ossibly leading to bleeding from the
Aetiology nose and mouth, coughing, collapse and sudden
Trauma to the thin mucosa underneath the tongue death. Asphyxia can result from misplacement of
or near the pharynx is caused by forceful place- a bolus. Cases may be peracute, with death within
ment or misplacement of a drenching or bolus gun 24 hours.
nozzle. Occasionally, the soft palate is traumatised. Occasionally, infection tracks into the cervical
The mucosal defect is invaded by commensals and spine, with resulting neurological deficits.
opportunistic bacteria, such as Trueperella pyo-
genes. Clostridium spp., yeasts and fungi may also be Diagnosis
involved. Localised septic cellulitis, tissue necrosis Sudden death is commonly reported, with confir-
and abscessation result (Fig. 5.22). mation on post-mortem examination (PME). In
the live animal, sedation may be required to allow
Clinical presentation thorough inspection of the pharyngeal region.
Submandibular or retropharyngeal swelling, often Ultrasonography may aid in identifying the cause of
extending along the ventral neck, develops within retropharyngeal swellings.
120 Chapter 5
Differential diagnosis oesophagitis caused by choke. May be congenital.

Neoplasia typically affects individual goats The majority of cases appear to affect young adults.
only. Caseous lymphadenitis may present as an out-
break, but swellings are typically confined to lymph Clinical presentation
nodes. Vena cava thrombosis with pulmonary embo- Intermittent regurgitation, weight loss, reduced
lism is a differential for haemoptysis, but usually appetite, salivation, coughing related to food or
only affects single goats. Dental disease is ruled out water intake and possibly recurrent bloat. Pyrexia
during examination. may be present. Where the cervical section is
affected, a swelling in the distal neck may be
Treatment/management/control observed, either permanently or during swallowing
A misplaced bolus may be surgically removed, but or cudding (Fig. 5.23).
prognosis is guarded to poor. Aggressive antibiosis
(broad spectrum, including anaerobes) combined Diagnosis
with NSAIDs may be tried. Euthanasia is indicated Fluoroscopy, endoscopy and contrast radiography
in severe cases. (Fig. 5.24).
Control relies on good drenching technique and
training of all staff undertaking drenching. Of par- Differential diagnosis
ticular importance are the following points: taking Similar clinical signs may be seen with external
enough time over the procedure, restraining the ani- pressure onto the oesophagus. Other causes of bloat
mal effectively, taking into account the angulation of must be ruled out including, in young animals, a
the nozzle (especially when an unfamiliar type of gun persistent aortic arch. Rhododendron poisoning
is used; Fig. 5.71) and placing the nozzle on top of may present with similar signs, but is of acute onset.
the tongue. The minimum body weight of animals Oesophageal sarcocystosis is a cause of dysphagia in
to be treated, which most anthelmintic and mineral some countries (not in the UK).
and vitamin boluses stipulate, must be observed.
Guns must be well maintained (no sharp edges) and Treatment/management/control
replaced regularly. Symptomatic only, including feeding on an incline
(e.g. front feet elevated), small meals and highly
Tongue lesions
Sarcocystosis is common in some countries,
although often without significant clinical impact.
Also reported are foreign body granuloma, erosions,
ulcerative glossitis and fibrosis. Wooden tongue
(actinobacillosis) does not appear to be documented
in the goat.
Oesophageal problems
Megaoesophagus
Overview
Megaoesophagus is a sporadic and relatively rare
disorder involving dilatation and atony of the
oesophagus with poor long-term prognosis.
Aetiology Fig. 5.23 Cervical megaoesophagus (arrow)

Often idiopathic, but also described secondary to in a 3-year-old Golden Guernsey presented for
vagal nerve trauma, hiatal hernia, thymoma and weight loss.
alpha-2 agonist, clenbuterol) and retrograde removal

of the obstruction (massage, probang), or oesoph-
agotomy if this is not successful (risk of stricture
formation).
Forestomach problems

The forestomach system consists of reticulum,
rumen and omasum. The entry point of the oesoph-
agus into the reticulum is connected to the exit point
into the omasum via the oesophageal groove. Its clo-
sure is important in unweaned kids to channel milk
directly into the abomasum. The caudoventral sac of
the rumen is larger than the caudodorsal one in the
Fig. 5.24 Contrast radiograph outlining the dilated
goat, and extends further caudal in the abdominal
oesophagus (arrows) in the thorax of a 7-month-old
cavity. Maximum rumen capacity is around 17 litres.
Southdown sheep.
The omasum is about fist-size in the goat, lying at
the level of the 8th to 10th ribs.
digestible feeds. Because of the necessity for cudding
in ruminants, long-term control is difficult. Rumen tympany (syn. bloat)
Overview
Obstruction (syn. choke) Rumen tympany is a regular problem, with multiple
Overview aetiologies that can broadly be categorised as exces-
Obstruction is occasionally seen, despite the selec- sive free gas production, formation of stable froth or
tive feeding behaviour of goats, especially if grazing secondary due to failure to eructate.
in orchards.
Aetiology
Aetiology Excessive gas production is seen with acute carbo-
May result from feeding dry, hygroscopic feeds (such hydrate overload or milk fermentation in kids (e.g.
as sugar beet pulp), but more commonly in rumi- following incorrect force feeding of milk or ‘rumen
nants when eating large pieces of feed (potatoes, drinkers’). Legumes may lead to frothy bloat.
roots, fruit), especially from overhead height (such Failure to eructate has several categories of
as picking apples out of a tree). More rarely neuro- causes: neurological (vagus nerve dysfunction, teta-
logical in origin or caused by external pressure onto nus), positional (lateral recumbency), physical (exter-
the oesophagus. nal pressure on oesophagus such as neoplasia, lymph
node enlargement, persistent aortic arch; or internal
Clinical presentation obstruction such as choke, proliferative growths),
Excessive salivation is seen. Cervical obstructions and physiological disturbances (hypocalcaemia, tox-
can often be seen or palpated. icities, inflammation).
Chronic bloat is often a sign of disturbed rumen
Diagnosis flora and digestive function, for example in poorly
Inability to pass a stomach tube confirms the diagnosis. weaned animals or with rumen alkalosis.

Treatment consists of administering a smooth mus- The left dorsal abdominal quadrant is visibly
cle relaxant (e.g. hyoscine butylbromide [Buscopan®], enlarged, with a dull resonance on percussion.
122 Chapter 5
Dyspnoea, including mouth breathing, may be Rumen acidosis (syn.

present in severe cases. carbohydrate overload)
Overview
Diagnosis Rumen acidosis is recognised in two forms: subacute
Passing a stomach tube will detect any oesopha- (syn. SARA) and acute.
geal obstruction and confirm the diagnosis of
free-gas bloat. Neck palpation, ultrasonography, Aetiology
endoscopy, thoracic radiography, rumenocentesis SARA is seen in goats on a concentrate-rich ration
and other aids may be necessary to determine the and results from repeated and extended reduction of
underlying cause. rumen pH below 5.5. Dairy goats receiving concen-
Suspicion of frothy bloat is based on history and trate feeds just twice daily, rather than as part of a
confirmed with trial treatment. total mixed ration (TMR), are at risk, as are meat
goats on a concentrate or cereal ration that is not
Differential diagnosis truly offered ad libitum.
Diffuse peritonitis with gas production may lead to The acute form results from carbohydrate over-
dorsal abdominal distension, but the distension is load: animals breaking into a feed store, sudden
usually bilateral and the goat will show additional introduction of a carbohydrate-rich ration or gorg-
signs of severe discomfort and illness. The causes of ing after temporary absence of feed (Fig. 5.25).
secondary tympany, as listed under aetiology, must
be considered. Clinical presentation
Signs of SARA are often vague, including soft fae-
Treatment/management/control ces, reduced milk yield and cudding, and erratic
A stomach tube is passed to release free gas. If the feed intake. Secondary effects become apparent
animal is in severe respiratory distress, emergency some weeks later and include laminitis, liver absces-
treatment consists of inserting a 12–14 gauge needle sation, poor body condition score and reduced
or making a stab incision into the rumen. The land- fertility.
marks for this are on a line from the tuber coxae to Signs of acute acidosis include rumen atony, inap-
the shoulder and close to the last rib. If possible, the petence, trembling and diarrhoea. The acidic con-
area is disinfected first. A stab incision needs to be tents draws water into the rumen, leading to ventral
followed up with surgical wound care. For frothy rumen distension and dehydration.
bloat, the goat is drenched with a surfactant (com-
mercial product such as poloxalene [Bloat-Guard®]
or vegetable oil).
In recurrent or chronic cases, either a trocar is
used or a rumen fistula created (see Surgery of the
rumen).
Supportive treatment consists of transfaunation
or drenching with a rumen stimulant, and offering
a forage-rich diet for several days. Recently weaned
goatlings may benefit from returning to milk feed-
ing for 1–2 weeks.
Control of primary bloat consists of gradual
introduction of carbohydrate-rich rations or
legumes (and pre-emptive surfactant administra-
tion for the latter) and good preweaning man-
agement of goatlings to ensure adequate rumen Fig. 5.25 Grain overload in rumen content. Low pH
development. was confirmed.
Diagnosis tetracycline), and transfaunation or rumen stimulants.

A reduction in milk fat (on individual goat samples) A rumenotomy (see below) or rumen lavage via a large-
reflects suboptimal dietary fibre and gives an indica- bore stomach tube to ‘wash-out’ the feed may be useful
tion. Definitive diagnosis relies on rumen fluid pH if performed within 2 hours of ingestion. Prognosis is
measurement, with samples taken 2–4 hours after guarded overall, and poor in recumbent animals.
concentrate feeding or, in goats on TMR, 5–8 hours In all types of goats, dietary changes must be
after fresh TMR provision (see earlier for rumeno- gradual, with new feeds introduced over 2–3 weeks
centesis technique). Ideally, 12 goats are sampled: a to allow rumen flora adaptation.
rumen fluid pH below 5.5 in more than a quarter Control of SARA in dairy goats relies on opti-
sampled indicates SARA. mal ration formulation, true ad-libitum feeding,
In acute acidosis, a Gram stain of the rumen fluid sufficient trough space and good transition and post-
will show overgrowth of gram-positive, rod-shaped kidding diet management. In particular, neutral
lactobacilli (Fig. 5.26). Blood–gas analysis confirms detergent fibre levels should be 30% of ration dry
a metabolic acidosis. matter (DM), with 70–80% from forage (Fig. 5.27).
Slower fermentable carbohydrates ideally replace
Differential diagnosis some more rapidly fermentable ones. Feeding TMR,
Enteric or toxic causes of diarrhoea and dehydra- rather than twice daily concentrate, is preferable,
tion. Hypomagnesaemia for tremors, but also neu- but care must be taken to mix the TMR well to
rological disorders. Peritonitis for ventral abdominal prevent sorting (while not overmixing, resulting in
distension, and forestomach or abomasal outflow reduction of effective fibre). However, sorting may
problem for rumen distension. not be entirely preventable in goats. Dietary buffers
(e.g. sodium bicarbonate) may be added at a rate of
Treatment/management/control 0.75% of ration DM.
Treatment of acute acidosis consists of increasing Control of SARA in meat goats relies on grad-
rumen pH (1 g/kg sodium bicarbonate orally), correct- ual introduction of the carbohydrate or cereal-rich
ing dehydration and metabolic acidosis, administering ration over several weeks, true ad-libitum feeding
B vitamins (in particular thiamine) and an antimicro- and a clean source of dietary fibre (e.g. straw) being
bial against Lactobacillus spp. (e.g. procaine penicillin or provided separate to bedding.
Fig. 5.26 Overgrowth of lactobacilli Fig. 5.27 Insufficient SARA control. Straw
(gram-positive rods) in rumen fluid during acute to increase the fibre level of the ration must be
acidosis. incorporated into the TMR. If offered separately, as
in this herd, goats are likely to largely ignore it. Also
note that sorting has taken place, and the sparsity of
the TMR (i.e. not true ad-libitum feeding).
124 Chapter 5
Traumatic reticuloperitonitis Rumen fistula

Overview Preparation and equipment
Traumatic reticuloperitonitis is relatively rare in The left craniodorsal sublumbar fossa is clipped,
goats because of their selective feeding behaviour, including over the last rib, and disinfected. A small
but odd cases are reported. The aetiology, clinical procedure instrument kit and non-absorbable suture
presentation, treatment and prognosis are similar to material are required.
cattle.
Restraint
Surgery of the rumen Standing under manual restraint or mild sedation.
Local infiltration anaesthesia (inverted L, line or
Trocarisation rectangular block).
An area in the left craniodorsal sublumbar fossa is Technical description
clipped and disinfected. A stainless steel cannula An elliptical piece of skin (3–4 cm long, 2 cm wide) is
with stylet or ‘Red Devil’ trocar, a scalpel blade and removed just behind the last rib and over the dorsal
suture material are required. gas cap. The abdominal muscles are dissected and
the peritoneum incised. The rumen wall is grasped
Restraint (Fig. 5.28a), pulled into the incision and secured to
Standing under manual restraint. Local infiltration the skin with multiple horizontal mattress sutures.
anaesthesia. The rumen is incised (Fig. 5.28b).
Technical description Aftercare

A skin incision is made close to the last rib and Patency of the fistula is maintained by removing food
just below the most prominent point of disten- and inflammatory exudate, and the surrounding skin
sion. The trocar is inserted through this incision protected (e.g. with petroleum jelly). Antibiosis may
and advanced into the rumen with a quick stab- be considered. Fly repellent is used as necessary.
like action (or rotating action for ‘Red Devil’). The The fistula usually heals over in 3–5 weeks,
stylet is removed. A stainless steel trocar requires but a larger incision can be made for a permanent
suturing to the skin. rumenotomy.
Aftercare Potential complications

The trocar is left in place for 7–10 days. Prior Peritonitis is in part avoided by placing the fis-
to removal, the stylet is intermittently inserted tula dorsal enough (i.e. above the rumen fluid
for several hours to check whether tympany level).
Fly-strike and skin necrosis are potential
recurs. Antibiosis may be considered, and petro- complications.
leum jelly (Vaseline®) applied to protect the skin
below the trocar. Fly repellent should be used as Rumenotomy
necessary. Indication
The skin incision is left to heal by secondary Removal of a reticular or ruminal foreign body
intention after trocar removal. or toxic plant material, rumen ‘washout’ in carbo-
hydrate overload, exploratory in chronic rumen
Potential complications tympany.
Peritonitis from leakage around the trocar. A dwell
time of 7–10 days ensures some sealing adhesions Preparation and equipment
around the trocar without these becoming too The left flank is clipped generously and disin-
firmly attached. fected. Standard surgical kit, stay sutures or pins
(a) (b)
Fig. 5.28 Rumen fistula. An elliptical incision is made through the abdominal wall close to the last rib.
(a) The rumen is grasped and pulled into the incision. (b) After suturing the rumen wall to the skin, it is incised.
(for example Steinman pins) and absorbable and non- Aftercare

absorbable suture material are required. In large Routine antibiosis and NSAIDs. Depending on
goats, a Weingart frame can be used. the findings, rumen stimulant or transfaunation.
Fly repellent if necessary. Oral or i/v correction of
Restraint hydration status and, where indicated, metabolic
Standing under sedation and regional anaesthesia, or acidosis.
in right-lateral recumbency under GA.
Potential complications
Technical description Peritonitis from rumen contents spillage.
A routine laparotomy approach in the dorsocranial
flank, with the incision large enough to accom- Abomasal problems
modate the surgeon’s hand and forearm. A fold of
rumen wall is grasped and pulled into the incision. Normal structure and function
Prior to incising the rumen, it must be secured The abomasum is glandular and has a bagpipe-like
tightly to the skin to reduce abdominal contamina- shape, with a capacity of 1–2 litres. The very acidic
tion. This can be achieved with stay sutures or pins content of the abomasum has a pH of 1.5–3. Its cra-
or, in large goats, by use of a Weingart frame. After nial end lies midline in the ventral abdomen, then
incising, the rumen and reticulum are explored. If courses towards the right paramedian. Its caudal end
necessary, part of the rumen contents is removed to rises up along the right caudal ribcage.
facilitate exploration.
The rumen incision is closed with a continuous Abomasal emptying defect
inverting pattern (e.g. Cushing or Lembert) with (syns. pyloric stenosis, abomasal
absorbable sutures. As much contamination as pos- impaction, distal vagal indigestion)
sible is removed, taking care not to wash it into the Overview
abdomen. The flank incision is closed in a routine Probably the most common abomasal problem in
manner. goats.
126 Chapter 5
Aetiology abdominal pressure. Secondary abomasal ulceration

Tricho- or phytobezoars and enteroliths may cause can lead to anaemia.
physical obstruction of the pylorus (Fig 5.29). Impaction of the abomasum is found on PME,
Functional stenosis can be caused by vagal nerve with content often more similar to rumen content.
disturbance, abomasitis and possibly peritonitis. Muscular hypertrophy of the abomasal wall may be
Granulomatous Actinobacillus lignieresii lesions can evident. The reticulum is commonly enlarged.
affect the proximal digestive tract, including the
pylorus. Differential diagnosis
Duodenal obstruction (enteroliths, bezoars, neo-
Clinical presentation plasia protruding into lumen) or sand impaction of
Affected goats present with abdominal distension, the abomasum. Generalised peritonitis has similar
intermittent diarrhoea or reduced faecal output, clinical signs, but vital signs are altered and toxae-
reduced appetite and gradual weight loss. Heart mia or septicaemia is present. Late stage pregnancy
rate and rectal temperature tend to be within nor- involving a large litter, or hydrops uteri, can present
mal limits. Severe abdominal distension causes dys- similarly.
pnoea. The rumen contraction rate can be increased
or decreased. Milk yield is reduced. Treatment/management/control
Surgery to remove obstructive foreign bodies can be
Diagnosis attempted. Access should be gained via the aboma-
Ultrasonography or exploratory laparotomy are sum or duodenum rather than the pylorus, if pos-
useful to confirm the diagnosis. Sometimes the
sible, to reduce the risk of postoperative pyloric
enlarged, doughy abomasum can be palpated in dysfunction.
the right lower abdomen. A cranial displacement of Treatment with anti-inflammatories or gastric
the diaphragm may be evident on thoraco-abdominal prokinetic drugs typically does not show any long-
radiographs. term effect.
Moderate elevation of liver enzymes may result
from hepatic congestion secondary to increased Abomasal displacement
Overview
Left or right abomasal displacement is only rarely
reported in goats.
Aetiology
Too few reports exist to establish whether similar
factors as in cattle are involved (such as negative
energy balance pre- and post-partum, lack of dietary
fibre, post-partum reproductive tract disease).
Left displacement is reported secondary to pyloric
obstruction caused by a phytobezoar (Fig. 5.29).
With left displacement, milk yield is unsatisfactory
and appetite may be selective (refusing concentrates
but eating forage) or absent. Vital signs are gener-
ally normal, including normal rumen contractions,
Fig. 5.29 Phytobezoars removed from an impacted although it may be difficult to auscultate these
abomasum. because of rumen displacement.
Simple right displacement presents with similar Abomasal ulceration

signs. However, torsion or volvulus on the right Overview
leads to rapid deterioration of the animal with Abomasal ulceration may cause death or clinical
abnormal vital signs, dehydration and abdominal disease, but many cases are undetected in the live
discomfort. goat, with incidental finding on PME or at s laughter
Faecal output may be reduced, but malodorous (Fig. 5.30). Particular risk groups may be dairy
diarrhoea is also possible. goats in the first few weeks post partum, and kids of
Concurrent disease is often present (e.g. ketosis, a few weeks of age on milk.
mastitis, uterine infection), therefore a full clinical
examination is important. Aetiology
Remains unclear: theories include rapidly ferment-
Diagnosis able dietary carbohydrates, finely ground feeds, stress,
Simultaneous auscultation and percussion of the left anti-inflammatory drug therapy and secondary to
(over or close to last rib) or right flank reveals a high- rumen acidosis and abomasal stasis or displacement.
pitched resonance (like water trickling into a metal
bucket). Centesis over this area of resonance reveals Clinical presentation
acidic fluid (pH 2–3), but carries the risk of perito- Non-specific signs of reduced appetite, rumen activ-
nitis. Ultrasonographic diagnosis requires some ity and milk yield, and abdominal discomfort. Vital
experience. signs remain normal unless perforation and peritoni-
tis occur. Mild to moderate anaemia may be present.
Differential diagnosis Perforation can lead to generalised peritonitis
Peritonitis results in bilateral resonance and a with severe systemic disturbance or localised perito-
severely compromised animal. Pneumoperitoneum nitis contained in the omental bursa.
would also be audible bilaterally, with a history of
recent surgery.
Abnormal resonance on the left needs to be dis-
tinguished from rumen tympany (has a duller sound)
and rumen collapse syndrome (resonance more cau-
dal in flank and over larger area). On the right, the
main differentials are caecal dilation and volvulus,
and the normal gas resonance of the colon.
Surgical correction (via right flank or ventral lapa-
rotomy, with abomasopexy or o mentopexy) carries
a good prognosis for left displacement. Right dis-
placement must be addressed promptly and, because
of the more pronounced systemic effect, prognosis
for this is guarded. Dehydration is corrected and
any ketosis addressed. Concentrates are introduced
gradually over 7–10 days. Any concurrent disease is
treated as appropriate.
Despite the aetiology not being confirmed in the
goat, control measures similar to cattle should be
considered. In particular, good transition manage-
ment, avoiding negative energy balance and provid- Fig. 5.30 Circumscribed, non-perforating abomasal
ing sufficient dietary fibre. ulcer.
128 Chapter 5
Diagnosis the oesophageal groove reflex. Extrapolating from

Deep abdominal palpation may locate the source of any studies in cattle and camelids, the following may be
pain to the abomasum. Faecal occult blood is present effective: omeprazole at 0.4–1.0 mg/kg i/v q6–8h;
in some cases. Sampling over several days is advised pantoprazole at 1 mg/kg i/v or 2 mg/kg s/c, both
to increase the detection rate. Ultrasonography of the q24h. The effect of systemic ranitidine or cimetidine
abomasal wall may show disrupted integrity or thick- appears very short lived.
ening, as well as signs of peritonitis in ruptured ulcers Blood transfusion may be indicated if bleeding
(Fig. 5.31). For the latter, abdominocentesis is also has resulted in severe anaemia.
useful but peritonitis may be contained within the Surgical repair of a perforated ulcer is often unre-
omental bursa. warding because of adhesions and established perito-
A moderate inflammatory response and possibly nitis. Localised peritonitis responds reasonably well
anaemia is evident on haematology. to conservative treatment, although surgical drain-
age of the omental bursa may also be considered.
Differential diagnosis Prognosis for generalised peritonitis is poor.
Other causes of colic and peritonitis. Lymphosarcoma
infiltrating the abomasal wall. Abomasitis (syn. abomasal bloat)
Overview
Treatment/management/control Abomasitis is a fatal condition, described in young
Stimulating appetite and feed intake is vital and ruminants including kids of around 10 days to
this may be achieved by offering a choice of palat- 6 weeks of age. Often only a few out of a group are
able feeds and, possibly, administering diazepam (if affected.
licensed). A course of antibiotics should be consid-
ered, but NSAIDs should be avoided as their role in Aetiology
the aetiology is unclear. Two main pathogen groups are implicated: (1) Sarcina
Little information exists on the use of anti-ulcer spp., a common environmental pathogen present in
agents in goats. In general, oral preparations are soil and cereal grain and able to tolerate very low pH
not useful in ruminants, with the exception of pre- levels (Fig. 5.32); (2) Clostridium spp., in particular
ruminant kids if administered in a way to stimulate C. sordellii and C. perfringens.
Fig. 5.31 The excessive, hyperechoic free fluid Fig. 5.32 Histology showing multiple clumps of
(outlined) in this ultrasonography image is suggestive Sarcina spp. (arrows) in a case of abomasitis.
of peritonitis.
The age cut-off is believed to result from increas- Diagnosis

ing carbohydrate digestion in the rumen in older Ultrasonography or radiography shows the dilated
animals, whereby carbohydrates are no longer avail- abomasum (Fig. 5.34). PME shows abomasal
able to the pathogens in the abomasum. haemorrhage, oedema, congestion and emphysema
(Fig. 5.35). Culture of abomasal fluid is usually
Clinical presentation negative. Histology shows anaerobic pathogens and,
Marked abomasal distension developing over several in cases involving Sarcina spp., typical packs of eight
days and leading to bilateral abdominal distension or more gram-positive bacteria (Fig. 5.32).
(Fig. 5.33). The kid remains bright, with largely
unchanged vital signs, but loses body condition. In Differential diagnosis
herds with infrequent animal observation, many are In rumen tympany caused by milk deposition and
simply found dead. fermentation in the rumen (e.g. in ‘rumen drinker’
or secondary to force feeding), gas can be released
by passing a stomach tube. Atresia coli leading to
abdominal distension would be evident at a younger
age. Intestinal obstruction would present with colic
signs and reduced faecal output, and peritonitis
with altered vital signs. Congenital malformations
or birth trauma may lead to an uroperitoneum,
detectable by ultrasonography, biochemistry and
abdominocentesis.
Antibiosis with anaerobic spectrum (e.g. penicillin at
25,000–30,000 IU/kg or ceftiofur) can be attempted,
Fig. 5.33 Marked bilateral abdominal distension in a but is usually unrewarding.
5-week-old lamb with abomasitis.
Fig. 5.34 Standing, left abdominal radiograph of a Fig. 5.35 Severe distension and emphysema
case of abomasitis, showing the extensive abomasal (‘bubble-wrap’ appearance) in abomasitis.
distension and a clear fluid line. Note that fluid
does not reach the ventral abdomen or diaphragm,
indicating that it is contained within a viscus.
130 Chapter 5
Proposed risk factors include unhygienic milk Intussusception

feeding and general poor environmental hygiene. Overview
Intussusception is the invagination of one intestinal
Intestinal problems segment into an adjacent one.
Normal structure and function Aetiology

Intestine A history of diarrhoea a few days earlier is common.
The pylorus leads into the duodenum (which has Young kids may be more affected than adults.
a characteristic S-bend), followed by the very long
jejunum and then ileum. The jejunum is arranged Clinical presentation
in curls and folds on a short mesentery and lies in May cause acute-onset, severe colic, but a gradual
close proximity to, and half encircles, the spiral progression with initially only moderate abdomi-
colon. The ileocolonic junction lies near the most nal discomfort is more common. Not all intussus-
caudal point of the ribcage on the right. The cae- ceptions lead to complete obstruction, therefore
cum is short, has some fermentation function and faecal output may only be moderately reduced
points towards the pelvic inlet. The rest of the rather than completely absent. The degree of dehy-
large intestine consists of the long ascending colon, dration may vary for the same reason. Appetite
whose main part is arranged into the spiral colon (in is typically reduced, with a moderately elevated
parts on two levels), and the shorter transverse and heart rate.
descending colon, followed by the rectum. Because
the stomachs of goats occupy about three-quarters Diagnosis
of the abdominal cavity, the intestines are mainly In a thin animal, the intussusception may be pal-
positioned in the right dorsal quadrant. The average pable as an abdominal mass. Ultrasonography is
length of the intestinal tract is 33 metres. most useful, showing the classic ‘goggle’ appearance
Water absorption in the hind gut is well devel- (Fig. 5.36).
oped, leading to formed faecal pellets.
Omentum Functional ileus, low-grade peritonitis, partial
The main, simplified clinical and surgical aspects pyloric obstruction and other moderately severe
of the omentum are as follows: the greater omen- GI problems. For a palpable mass, also abdominal
tum originates on the left in the horizontal rumen neoplasia.
groove, therefore the dorsal rumen is directly acces-
sible during a left-sided laparotomy. It runs ventrally Treatment/management/control
and connects to the greater curvature of the aboma- Surgical resection carries a reasonable prognosis if
sum. On the right, the greater omentum originates the problem is detected prior to severe systemic com-
high up in the abdomen near the abdominal aorta, promise or peritonitis. Under GA, a ventral midline
and covers most of the abdominal contents. The two or right flank incision is made and the affected part
layers of the greater omentum form the supraomen- resected, followed by an end-to-end or side-to-side
tal process, which is open caudally near the pelvic anastomosis (depending on lumen size of the two
inlet, thereby allowing surgical access to the intes- portions).
tines via a right flank laparotomy. Embedded in Supportive therapy consists of fluid therapy, anti-
the omentum on the right is the outer wall of the biosis (started preoperatively), analgesia, NSAIDs
abomasum and the duodenum. The lesser omentum and gradual reintroduction of the full milk or feed
runs from the portal vein to the lesser curvature of ration over 7–10 days. Complications include nar-
the abomasum. A substantial quantity of fat may rowing of the lumen, leading to functional obstruc-
be present in the omentum of goats in good body tion, and peritonitis.
condition.
(a) (b)
Fig. 5.36 (a) Classic ‘goggle’ appearance of a jejunal intussusception on abdominal ultrasonography. (b) On
laparotomy, the corresponding pathology (on right) with distended loops of jejunum proximal to it (on left).
Torsion of the mesentery

or mesenteric root
Overview
Torsion of the mesentery or mesenteric root is pos-
sibly more common in kids than adults, and carries
a poor prognosis.
Aetiology
Remains unknown. Occasionally, there is a history
of diarrhoea or ileus.
One of the few causes of violent colic, with acute
onset. Vital signs are markedly disturbed, includ-
ing dehydration. Faecal output is reduced or absent.
Rapid deterioration. Fig. 5.37 Distended loops of intestine on
ultrasonography. The loop in the centre of the image
Diagnosis shows wall oedema.
Ultrasonography shows distended intestinal loops
(Fig. 5.37) and absent peristalsis. Abdominocentesis
may show an inflammatory response. Definitive incision. However, the short mesentery often makes
diagnosis is by exploratory laparotomy. it difficult to establish the direction of rotation or,
indeed, correct it. Devitalisation occurs rapidly.
Differential diagnosis If surgery is attempted, fluid therapy support, pre-
Other causes of colic and ‘abdominal catastrophes’. operative antibiosis and postoperative analgesia and
NSAIDs are important. Distended loops may be
Treatment/management/control deflated with the aid of a needle. The short mesentery
Surgical correction under GA may be attempted, makes ‘milking out’ of gut contents (either into adja-
either through a ventral midline or right flank cent unaffected parts or via an enterotomy) difficult.
132 Chapter 5
Intestinal obstruction tends to be more marked if the proximal intestine

Overview is involved.
Functional (ileus) or mechanical obstructions occur
occasionally. Diagnosis
Ultrasonography is the most useful tool; peristalsis
Aetiology is absent and the intestinal wall may appear oede-
Ileus can be a sequela to intestinal or abdominal matous. The intestine proximal to the obstruction
surgery, but also to peritonitis, intestinal inflam- is markedly distended, with the sections distal to it
mation and endotoxaemia. Hypocalcaemia may emptier than normal.
also play a role.
Enteroliths or phyto- or trichobezoars are com- Differential diagnosis
mon causes of mechanical obstruction. Intestine may Intussusception, pyloric outflow problem, rumen
become entrapped in a hernia (umbilical or inguinal; stasis.
Fig. 5.38). Spiral colon impaction has been linked
to dehydration or reduced milk intake secondary to Treatment/management/control
other events (e.g. disease, transport) in other species. A mechanical obstruction can be corrected by an
enterotomy, or by gut resection and anastomosis
Clinical presentation if devitalisation has occurred. Systemic rehydra-
Borborygmi may be increased in the early stage, but tion may be sufficient in mild to moderate colon
are commonly reduced. Faecal output is absent and impaction.
the animal is inappetent. Mechanical obstruction Prokinetics may be tried for ileus, but little informa-
typically causes discomfort, with associated changes tion on these drugs is available in the goat and prognosis
in vital signs. The obstruction may lead to devitali- is guarded. In horses, lidocaine is used prophylacti-
sation of the affected section of intestine, leading to cally either intra- or postoperatively, but can also be
toxic shock and peritonitis. Colic signs are sometimes used as treatment (loading dose of 1.3 mg/kg i/v fol-
also present with ileus. Dehydration is common in lowed by CRI of 0.03–0.05 mg/kg/minute). Similarly,
both functional and mechanical obstruction, and metoclopramide may be used prophylactically or as a
treatment (0.05 mg/kg i/m q6h). Erythromycin was
found to have a positive effect on abomasal tone and
emptying in cows, and is used in ileus in horses (2 mg/
kg i/v in 100 ml of physiologic solution q12h). Another
drug to consider is cisapride.
The risk of postoperative ileus is reduced by gen-
tle tissue handling, keeping exposed intestinal sec-
tions moist during surgery, and prompt correction
of dehydration.
Rectal prolapse
Overview
Fig. 5.38 Incomplete prolapse involves the mucosal layer only.
Typical Eversion of the entire caudal rectum is present in com-
clover leaf plete prolapse. Depending on the length of prolapsed
appearance tissue, mild to severe degrees are distinguished.
of intestinal
incarceration Aetiology
in an inguinal Tenesmus caused by rectal inflammation and irrita-
hernia. tion. Neurological dysfunction is a rare cause.
(a) (b)
Fig. 5.39 Rectal prolapse in a ram. (a) Substantial

tissue eversion exposing the rectal mucosa. Two metal
pins (e.g. Steinman) have been placed through
the prolapse at the level of the skin for temporary
retention during surgery. (b) The prolapsed tissue
is resected about 2 cm away from the skin junction.
(c) Suturing of mucosa to skin completed and first
(c) metal pin removed.

Rectal tissue protrudes beyond the anus, with the Correction is under lumbosacral epidural anaes-
mucosa exposed (Fig. 5.39a). It may be intermittent thesia (see Chapter 18). Addition of xylazine HCl
or permanent. (0.07 mg/kg) to the epidural is useful to prolong
its effect. The goat is kept standing or placed into
Diagnosis ventral recumbency.
Self-evident on clinical examination. For prognosis, A mild prolapse is replaced after cleaning the
the degree and extent of any tissue trauma should be exposed tissue, followed by a purse-string suture
established. placed subcutaneously around the anus using nylon
tape or monofilament nylon. The suture is tightened
Differential diagnosis to leave a one finger-width opening.
Inexperienced keepers may confuse vaginal and rec- Tissue amputation is required in more severe
tal prolapse. Anal or rectal neoplasia may initially cases. For a simple, but somewhat crude approach, a
appear similar. 10 ml syringe (or syringe case) open at both ends and
134 Chapter 5
with the plunger removed, is placed into the rectum. (2) optimal surgical analgesia is provided. The lat-
An elastrator ring is applied over the prolapsed tissue, ter is important, as handling of inflamed viscera will
compressing it onto the syringe. Ischaemic necrosis induce a marked pain response. If performed under
causes sloughing in a few days. Surgical correction local anaesthesia, additional analgesia could be pro-
involves placing two Steinman pins through the vided with a morphine epidural, pethidine or possi-
prolapsed tissue for temporary fixation (Fig. 5.39a). bly opioids (butorphanol, buprenorphine), but these
The prolapsed tissue is resected (Fig. 5.39b), and the drugs are not licensed for food producing animals in
remaining mucosa sutured to the skin in a series of most countries.
simple interrupted sutures, using absorbable mate-
rial. Digital guidance is used, because vision is typi- Technical description
cally obscured by mucosal haemorrhage. The pins A left flank approach is indicated for suspected
are removed (Fig. 5.39c) and the remaining tissue rumen problems, and allows rumenotomy and explo-
replaced into the pelvis. NSAIDs and routine anti- ration of the reticulum. To reduce spillage of rumen
biosis are given. contents, the goat is placed into sternal or 45-degree
The main complication is stricture formation. right lateral recumbency.
A ventral midline approach (Fig. 5.40) is indicated
Exploratory laparotomy for a suspected intestinal problem, but also allows
Indication access to the urogenital tract, abomasum and liver
Exploratory laparotomy is a useful diagnostic tool (by palpation). A right flank approach gives access to
to establish the nature of an abdominal problem. the abomasum, liver (by palpation), urogenital tract
In most goats, all parts of the abdominal viscera and most parts of the intestine.
can be at least palpated, and a large proportion Regardless of the approach, it is important to
exteriorised. Intraoperative ultrasonography is explore both lateral and medial to the omentum,
useful for those parts that cannot be exteriorised. reflecting it where necessary. Viscera and tissues
For this, contact gel and the probe are placed into must be handled gently, and any exteriorised parts
the finger of a sterile glove or sleeve to maintain kept moist.
asepsis. During exploration, the following are noted:
amount, character and abnormal constituents of
Preparation and equipment peritoneal fluid (Fig. 5.41), adhesions, abnormal
A compromised patient is stabilised with i/v fluids location or distension of viscera (Fig. 5.42), viability
and any acid–base imbalance corrected (if detected of organs, foreign bodies and masses.
or suspected). Any free rumen gas is released with Prior to closure, consideration should be given
the aid of a stomach tube to reduce abdominal pres- to thorough lavage with warm sterile fluids,
sure. The stomach tube may be left in place during intra-abdominal antibiosis (e.g. benzylpenicillin
surgery. sodium) and 1% carboxymethylcellulose (to reduce
Standard surgery kit, bowel clamps, sterile solu- adhesions).
tion for lavage, needles and tubing to release gas, Depending on the findings and their prognosis,
suction if available, lap sponges and sterile fluid to intraoperative euthanasia may be indicated.
keep exposed viscera moist, absorbable and non-
absorbable suture material are required. Also eutha- Aftercare
nasia solution. Antibiosis, NSAIDs and analgesia, continued fluid
therapy as necessary. Box rest until wound healed,
Restraint plus possibly a belly bandage.
Unless the goat is too compromised, surgery is
best performed under GA for two reasons: (1) find- Potential complications
ings can be dealt with without time pressure; and Peritonitis, adhesions, wound breakdown or herniation.
(a) (b)
Fig. 5.40 Ventral midline laparotomy. The skin is incised with a scalpel blade; (a) the peritoneum is lifted up
with a pair of rat-tooth forceps and cut with scissors; (b) once the incision is large enough, a surgeon’s finger
is introduced and the incision extended over the finger. This reduces the risk of accidental incision of any
underlying structures, especially if they are distended.
Fig. 5.41 Fibrin or protein clots in the peritoneal Fig. 5.42 Distended jejunum proximal to an
fluid indicates an inflammatory reaction. obstruction. The loops show a change in colour and
fluid accumulation in the lumen, and peristalsis was
largely absent. Note the healthy pink and collapsed
intestinal loops in the background of the image.
136 Chapter 5
Liver and pancreas problems the liver, with non-specific signs of reduced appetite
and milk yield.
Normal structure and function An associated manifestation is caudal vena cava
The liver lies encased in the ribcage in the cranial thrombosis (see Chapter 7).
abdomen alongside the diaphragm, extending along
the right-hand side. The right and left lobes are not Diagnosis
further divided in the goat. The goat has a gallbladder. Ultrasonography to confirm abscessation. Blood
The pancreas weighs about 50–70 g, and lies biochemistry typically shows decreased albumin and
roughly between liver, right kidney and omasum. elevated bilirubin and liver enzymes (gGT, GLDH,
SDH), with a marked inflammatory response on
Liver abscessation haematology.
Overview Liver abscessation can be detected at slaughter or
Although not always causing overt clinical disease, PME.
liver abscessation can lead to substantial financial
losses in meat goats because of carcase rejection at Differential diagnosis
slaughter (Fig. 5.43), and poor performance in both Other causes of abdominal pain or peritonitis. For
dairy and meat animals. jaundice, causes of acute haemolysis. Hepatic insult,
including liver fluke, for elevated liver enzymes.
Aetiology The ultrasonographic appearance may resemble
Usually dietary, with excessive rapidly ferment- neoplasia or tuberculosis lesions.
able carbohydrates leading to a ruminitis, followed
by either direct migration of pathogens through the Treatment/management/control
compromised rumen wall or dissemination via the
There is no treatment option. Control centres on good
portal vein into the liver. Because of the dietary aetiol- management of carbohydrate-rich rations, includ-
ogy, a large proportion of goats in a group are affected. ing gradual introduction of carbohydrates, avoiding
engorgement by making feed available truly ad libitum,
Clinical presentation and avoiding infrequent feeding of large amounts of
Half to two-thirds of liver parenchyma needs to be carbohydrate (e.g. twice daily in-parlour feeding).
affected before overt clinical signs become apparent.
These include jaundice, abdominal pain originating Hepatic lipidosis (syn.
from the liver region and possibly enlargement of fatty liver necrosis)
See Chapter 14.
Ovine white liver disease

See Cobalt deficiency in Chapter 15.
Metastatic tumours
Malignant tumours may result in metastases in the
liver. They may give a similar appearance to liver
abscessation on ultrasonography or cursory PME
(Fig. 5.44).
Pancreatic disorders
Fig. 5.43 Liver abscessation (in a cross-section). The few cases of pancreatic disorders reported
This is often a result of incorrect carbohydrate include diabetes mellitus type I, insulinoma and
feeding management. congenital cystic disease.
(a) (b)
Figs. 5.44a, b Metastatic tumours affecting the liver.
Umbilical disorders

In the fetus, the umbilicus consists of the urachus
connected to the urinary bladder, the umbilical
vein leading to the liver, and two umbilical arteries
connecting to the iliac arteries. When the cord is
torn at birth, the arteries retract and the urachus X
and vein close. Normally, the external umbilical Y
remnants dry out and are shed within about 7 days
after birth.
Umbilical hernia
Overview
Umbilical hernia is one of the more common con-
genital defects, and is occasionally life-threatening. Fig. 5.45 Cross-sectional ultrasonography of
an umbilical hernial sac (arrows). The umbilical
Aetiology remnant (X) is surrounded by some omentum (Y).
This defect in the abdominal wall may be congeni-
tal, with a likely hereditary component, or occur sec- Other congenital defects may be present, affect-
ondary to umbilical infections. Hereditary hernias ing prognosis and treatment economics.
may jump one generation.
Diagnosis
Clinical presentation The defect in the abdominal wall can be easily pal-
A well-circumscribed swelling along the ventral pated after reducing the hernia. Ultrasonography
abdominal midline is present. In uncomplicated is useful to establish whether any viscera have pro-
hernias, vital signs are normal, pain is absent and lapsed into the hernial sac (Fig. 5.45).
the hernia is easy to reduce manually. Rarely, either
small intestine or abomasal fundus prolapses into Differential diagnosis
the hernial sac, leading to colic signs and making Similar swellings may be caused by an umbilical
full reduction difficult and inducing pain. abscess, infected umbilical remnant or a haematoma.
138 Chapter 5
A hernia may occur concurrently with other umbili- Infection of internal structures similarly pres-
cal disorders (see below), and a thorough examina- ents as a swelling, more commonly accompanied by
tion is required. a discharging tract with pus visible at the point of
the umbilicus (Fig. 5.46). Omphalophlebitis car-
Treatment/management/control ries the risk of a bacteraemia. Vital signs may be
If congenital, affected males should not be used for abnormal and signs indicating infection of other
breeding. Unless the defect is very large or a visceral structures may be present, in particular septic
prolapse is present, repair is usually not necessary in arthritis and endocarditis.
goats reared for meat.
Females may be reared for milk or fibre produc- Diagnosis
tion, providing that their offspring are not retained With the goat in lateral recumbency, deep abdomi-
in the herd. Surgical repair (see Umbilical surgery) nal palpation will reveal thickened internal struc-
is advisable as the increased abdominal pressure tures and whether these track cranially (= vein) or
during pregnancy may lead to problems. Delaying caudally (= arteries or urachus). Palpation will also
surgery until 2–3 months of age is a good com- establish the absence or presence of a hernia.
promise between avoiding surgery in the neonate Needle aspiration establishes the presence of pus,
while still dealing with a relatively small, manage- taking care not to penetrate a hernial sac or adjacent
able patient. structures.
Occasionally, applying a belly bandage for a Ultrasonography is very useful to establish
few weeks is sufficient to seal the hernia. Applying the extent of infection and structures involved.
a rubber elastrator ring over the hernial sac is not The probe is initially placed at the junction of the
advisable because necrosis and breakdown of the abdominal wall with the external remnant (caudally
abdominal wall often follow. and cranially, in turn) and then gradually rotated to
Control centres on removing affected animals visualise the abdominal cavity. This will highlight
from the breeding pool. whether the external umbilical structures continue
intra-abdominally and whether any internal struc-
Umbilical infections tures are enlarged (Fig. 5.47) and/or filled with pus.
Overview
Umbilical infections are usually chronic in nature.
Infection may involve either the external remnant
(omphalitis) or tissues (abscess) or the internal umbil-
ical structures (urachitis, omphalophlebitis, ompha-
loarteritis). A hernia may be present concurrently.
Aetiology
Poor navel and environmental hygiene is the main
cause. In group-housed kids, navel sucking may also
play a role. A range of opportunistic and environ-
mental pathogens are involved.
Infection of external structures presents as obvious
swelling in the umbilical region, which is fluctu-
ant in the case of an abscess. The swelling is non- Fig. 5.46 Patent, infected urachus and umbilical
reducible, or partially reducible if a hernia is also hernia in a male calf (lying in lateral recumbency).
present. Occasionally, a draining tract is present. Note the purulent discharge towards the right of the
Pain on palpation is typically mild to moderate. hernial sac (near the prepuce).
Aetiology
The urachus fails to close post partum, leaving a
permanent connection with the urinary bladder.
Concurrent infection is often present.
X Clinical presentation
Urine escapes through the umbilical stump. While
quite easy to detect in the female, close observation
is required in the male because of the close proximity
of the prepuce and umbilicus. Cystitis is a common
sequela, causing dysuria, mild abdominal discomfort
and abnormal urinalysis.
Diagnosis
Fig. 5.47 The enlarged umbilical remnant (here in Clinical observation is often sufficient, but may be
cross-section, labelled X) could be followed all the way confirmed with ultrasonography. Any concurrent
from the hernial sac deep into the abdominal cavity on infection of the urachus needs to be established in
ultrasonography. order to inform the treatment approach.
Differential diagnosis Surgical removal of the urachus (see Umbilical sur-
A complicated hernia (i.e. one with a visceral pro- gery), with resection and oversewing of the bladder
lapse) must be ruled out prior to needle aspiration apex. Even in meat animals treatment is advisable, as
or lancing. urine staining of the ventral abdomen may lead to fly
strike or rejection at the abattoir.
With the goat in lateral recumbency, an abscess Umbilical surgery
(or identifiable pus-filled pocket in omphalitis Indication
cases) is lanced with a scalpel blade, followed by Repair of an umbilical hernia or treatment of infected
drainage and lavage with saline or a 0.1% iodine or patent umbilical structures.
solution. Sedation and local anaesthesia are usu-
ally not necessary. Lavage is repeated once or twice Preparation and equipment
daily for several days until the infection is resolved. If infection is present, lavage and antibiosis are used
Antibiosis is not required unless a hernia is also to at least partially bring the infection under control
present for which surgical repair is planned. Such prior to surgery. Cover against clostridial pathogens
repair is delayed until the infection is brought needs be considered (either vaccination, maternally
under control. derived antibodies or suitable perioperative antibiosis).
Infected internal structures require surgical A generous area of the ventral abdomen is clipped
removal. If a drainage tract is present, careful lavage and prepared. In the male, the preputial opening is
and antibiosis for a few days are used to partially covered with a sterile absorbent swab, held in place
control the infection prior to surgery. with a towel clamp.
A laparotomy surgical kit, including bowel clamps
Patent urachus if the urachus involved, is required.
Overview
Patent urachus is a condition that requires surgical Restraint
treatment to avoid discomfort and chronic inflam- The goat is placed in dorsal recumbency. GA is the
mation from the resulting cystitis. method of choice in anything but a simple hernia
140 Chapter 5
to eliminate any time constraints. A simple hernia freed from surrounding tissues (Fig. 5.48b), the
may be repaired under moderate to deep sedation, hernial sac is inverted into the abdomen. Suturing is
and V-shaped local infiltration (with the point of the as described below.
V towards the sternum, and extending either side of
the hernia). Infected internal structures or patent urachus
The skin incision around the hernia (as above)
Technical description is extended cranially up to the xiphisternum for
Simple hernia removal of the umbilical vein or, for removal of the
In the female, an elliptical incision is made around umbilical arteries or urachus, caudally up to the pel-
the hernia, extending about 1 cm cranially and cau- vic inlet (midline in the female and just lateral to the
dally. In the male, a pear-shaped incision is made prepuce in the male). This cranial/caudal incision is
with the blunt end just cranial to the prepuce. Care is continued through the linea alba (after deflection of
taken in the male not to dissect too far laterally to the prepuce in the male) into the abdominal cavity.
avoid trauma to the nerves in the paramedian region The hernial sac is incised close to the ring, using dig-
that supply the retractor penis muscle. Excessive ital guidance to avoid incision into viscera or omen-
skin from the hernial sac is removed with the inci- tum (Fig. 5.49), and the surplus tissue removed.
sion (Fig. 5.48a). The proximal end of the infection is located, gen-
Closed reduction is preferable, especially for on- tly breaking down any adhesions while taking care
farm surgery, as the peritoneal cavity is not entered. not to rupture any abscess. Two pairs of artery for-
For this, the skin over the hernial sac, including ceps are placed across the uninfected, healthy part
as much of the subcutaneous tissue as possible, is of the structure, followed by a double ligature using
removed with a combination of blunt and sharp 3.5 metric absorbable suture material between the
dissection. Tissues are separated thoroughly down two pairs of forceps. The structure is transected
onto the hernial ring. This is facilitated by placing between the distal pair of forceps and the ligature and
Allis tissue forceps either side of the incision and the removed together with the hernial sac. In cases of a
centre of the sac, and applying tension. The skin will patent urachus, artery forceps are placed across the
be tightly attached to the sac near the umbilical scar, proximal urachus. A bowel clamp is placed across
and accidental incision of the sac may occur (if it does, the bladder apex and, after resection of the urachus,
the resulting defect is oversewn). Once completely the bladder is closed with an inverting suture pattern.
(a) (b)
Fig. 5.48 Closed reduction of an umbilical hernia. (a) The elliptical skin incision around the hernia is made
in such a way that excessive skin is largely removed. Here, the skin is already partially dissected from the
underlying sac. (b) The hernial sac has been freed completely and is ready to be inverted into abdomen.
Fig. 5.49 Open reduction (here to remove an Fig. 5.50 When closing the defect, accurate
umbilical remnant). After making a small opening placement is made easier by first placing all the
through the sac, the incision is extended under digital sutures (securing the ends with artery forceps), then
guidance. tying them off.
Closure of the defect

A modified Mayo-Mattress suture (‘Vest-over-Pants’
suture) or simple interrupted sutures are suitable to
close the hernial defect, using 4 metric polydioxa-
none (PDS). Non-absorbable material may be used,
but carries a higher risk of fistula formation. Sutures
are placed through the outer edge of the hernial
ring, using the index finger or the back of a scalpel
holder inside the abdomen to push away any abdomi-
nal contents and to keep the hernial sac close to the
abdominal wall during closed reduction. It is often
easier to place all the required sutures first, securing
their ends with artery forceps before tying them off
(Fig. 5.50). The edges of the hernial defect should
be overlapped (or pulled together for simple inter-
rupted sutures) as closely as possible. The use of a
polypropylene mesh implant is rarely required in a
goat and is inadvisable if infection is present.
A simple continuous subcutaneous suture is
placed, using 3 metric absorbable suture material and
ensuring that the tissue covers the hernia sutures. Fig. 5.51 A stent made from a gauze swab held in
The skin is closed with simple interrupted or cru- place with two stay sutures exerts some pressure over
ciate sutures with 3.5 metric non-absorbable mate- the wound and keeps it clean.
rial. A rolled-up gauze swab can be placed over the
wound as a stent, held in place with two stay-sutures are administered for 3–10 days (longer duration
(Fig. 5.51). Alternatively, a belly bandage is used. where contamination occurred during surgery or if
the entire infected structure could not be removed).
Aftercare Clavulanic-acid potentiated penicillin is suitable.
NSAIDs are given. Repair of a simple hernia under The goat should be kept confined in a small pen
sterile conditions does not require antimicrobials. for 6–8 weeks, with a companion animal to prevent
Where infection is present, however, antimicrobials escape attempts.
142 Chapter 5
The stent or bandage is removed after 3 days in on the weight of infection, the degree of any hypo-
a female and 1–2 days in a male (when it becomes gammaglobulinaemia present and the involvement
soaked with urine). Skin sutures are removed after of other concurrent enteric pathogens.
12–14 days.
Diagnosis
Potential complications Laboratory detection of group A and B rotaviruses
Breakdown of the repair, caused by residual infec- by polyacrylamide gel electrophoresis (PAGE) or
tion or weakness in suture or excessive exercise post- ELISA tests. Many commercially available ELISA
operatively. Peritonitis because of rupture or leakage kits marketed for detection in calves will detect only
of an infected structure during removal. group A rotaviruses.
INFECTIOUS DISEASES OF THE Differential diagnosis

DIGESTIVE SYSTEM AND ABDOMEN Other causes of neonatal diarrhoea, such as cryp-
tosporidia and E. coli, although rotavirus is often
Rotavirus involved in mixed infections with these same patho-
Definition/overview gens. Also non-infectious causes, including dietary.
Rotavirus is associated almost exclusively with
diarrhoea in young, milk-fed kids, often as part Treatment/management/control
of a mixed aetiology with cryptosporidia and Treatment is aimed predominantly at reducing the
Escherichia coli infection. It can also be demon- effects of diarrhoea (i.e. dehydration and resulting
strated in the faeces of older goats in the absence electrolyte imbalance).
of clinical disease. Emphasis must be placed on attention to detail
when rearing kids, particularly when they are reared
Aetiology artificially. Good colostrum management is a key
Rotaviruses are classified within a number of sero- factor, and many confirmed rotavirus incidents are
groups, with reported disease in goats linked pre- linked to failure of passive transfer. Other risk fac-
dominantly to groups A and B. Group C rotavirus tors include unhygienic kidding environment,
has been identified in faeces from otherwise healthy overcrowding, unhygienic or haphazard feeding
goats. Group A and B rotaviruses are also commonly regimes, a cold and damp environment and concur-
identified as causes of diarrhoea in calves (group A) rent disease.
and lambs (group B), respectively, and these may act Bovine rotavirus vaccines, given to does in late
as sources of infection to young kids and/or their pregnancy, have been used with varying success.
environment. If used, it is important that kids receive colostrum
from vaccinated does for 2–4 weeks after birth.
Pathophysiology
Rotaviruses replicate in the non-dividing mature Cryptosporidiosis
enterocytes near the tips of the villi in the small Definition/overview
intestine, leading to progressive shortening of villi Cryptosporidium spp. infect a wide range of mam-
with villus fusion and thickening of the crypts. The mals and are highly prevalent in ruminants,
villus surface area reduction leads to malabsorp- particularly young calves, lambs and kids. The
tion, with the severity of the diarrhoea linked to the parasite is a major cause of severe diarrhoea in kids
degree of villus damage. <4 weeks of age (Fig. 5.52), particularly in inten-
sive systems of rearing. They are a significant zoo-
Clinical presentation notic pathogen, being a particular risk to young
Diarrhoea in kids <2 weeks old, most commonly in children coming into contact with infected animal
the first 7 days of life, the severity of which depends faeces (Fig. 5.53).
Fig. 5.52 Diarrhoea in a goat kid with confirmed

cryptosporidiosis.
Fig. 5.53 Goat kids are popular at open farms.

Suitable signs should be clearly visible emphasising
the potential risks of zoonotic infections such as
cryptosporidia and E. coli O157.
Aetiology Pathophysiology
Cryptosporidia are small protozoal parasites in the Infection is by the ingestion of infected faecal mate-
phylum Apicomplexa. Over 150 species of mam- rial from the immediate environment. The severity
mals, reptiles, birds, amphibians and fish have been of infection is linked to the dose of oocysts ingested
reported as hosts. Molecular techniques for taxo- (and hence degree of environmental contamination),
nomic classification have identified many different the immune status of the goat (more severe in kids
species, a number of which have reportedly affected with poor passive transfer) and the presence of con-
goats following both natural and experimental infec- current infection such as rotavirus and enteropatho-
tion. While many such infections will be subclini- genic E. coli.
cal, disease in goats is almost always associated with Once the oocyst is ingested, it excysts and releases
Cryptosporidium parvum. sporozoites that then colonise the intestinal entero-
The oocyst stage responsible for transmission is cytes, followed by an asexual phase of schizogony,
ubiquitous in the environment and cryptosporidiosis resulting in a new wave of infected cells by the
can be acquired through a number of routes includ- release of merozoites. This is then followed by the
ing goat to goat (directly or indirectly), from other sexual phase or gametogeny, resulting in further
ruminants (directly or indirectly) or by ingestion of waves of enterocyte invasion and the production of
contaminated food or drinking water. oocysts in faeces and perpetuation of the life cycle.
Oocysts are very resistant in the environment This process leads to progressive destruction of
and are able to survive the effects of many disinfec- enterocytes and of the intestinal villus architecture,
tants. Products are available with declared efficacy of causing malabsorption and maldigestion and result-
reducing environmental contamination. ing in the clinical signs of diarrhoea.
144 Chapter 5
Clinical presentation reducing the effects of diarrhoea (i.e. dehydration

Watery diarrhoea in kids usually aged between 5 and and resulting electrolyte imbalance).
14 days, rapidly leading to dehydration and electro-
lyte imbalance, dullness and inappetence. Cases will Coccidiosis
often become more severe and widespread as the Definition/overview
kidding season progresses, and the weight of envi- Coccidiosis is one of the most important and com-
ronmental infection increases. Explosive outbreaks mon causes of diarrhoea and ill thrift in young goats
of disease can be encountered in intensively reared worldwide. It is caused by a protozoal parasite of the
kids, with up to 100% morbidity and up to 20% mor- genus Eimeria. Although coccidiosis is a problem in
tality (higher in mixed infections). many animals and birds, the causative Eimeria spp.
are predominantly host specific (e.g. cattle Eimera
Diagnosis spp. will not affect goats and vice versa). Goats of all
Laboratory tests include the detection of oocysts in ages may shed Eimeria spp. in their faeces, but it is
faecal smears stained with Ziehl–Neelsen (ZN) or only in younger goats that clinical signs will develop
Giemsa, faecal flotation, ELISA tests, fluorescent- (typically between 4 weeks and 5 months old).
labelled antibody tests and PCR. Disease is more prevalent in goats that are housed
or where stocking density on pasture is high, where
Differential diagnosis environmental contamination can rapidly develop.
Other causes of neonatal diarrhoea, such as rotavi- Conversely, it is rarely encountered in extensive
rus and E. coli, although rotavirus is often involved in management systems.
mixed infections with these same pathogens.
Aetiology
Treatment/management/control Up to 20 different Eimeria spp. have been recorded
Management and control are based on reducing envi- in goats, some of which can cause severe disease;
ronmental contamination with viable oocysts by: others can coexist in the gut with no adverse

effect on the host. The most pathogenic species
•• Ensuring a clean dry environment for rearing, are E. ninakohlyakimovae, E. caprina, E. christenseni,
with clean bedding that is regularly replenished. E. arloingi and E. hirci. Consequently, relying on
•• Ensuring kids have received adequate colostrum. a coccidial oocyst count alone for diagnosis could
•• Ensuring all feeding utensils are scrupulously give misleading results, since a high count of non-
clean. pathogenic oocysts is of no clinical significance
•• Ensuring that a consistent feeding regime is whereas a lower count of a pathogenic species is
followed to avoid dietary upsets. highly significant. Confirming a mixed popula-
•• Practicing an ‘all-in-all-out’ system, in tion of several species of Eimeria is not unusual.
particular avoiding the temptation to hold back Identification is based on the size, shape and struc-
poor performing kids. ture of each oocyst.
•• Practicing a thorough pen cleaning routine The life cycle is direct. Ingested oocysts sporu-
between batches of kids, removing all visual late and release their sporozoites, which enter the
signs of faecal material, followed by steam gut cells to produce schizonts. Following a cycle
cleaning and the use of disinfectants with a of asexual reproduction, a first generation popula-
declared efficacy against oocysts. tion of merozoites is produced. These in turn break
out from the cells and continue the cycle by further
There are no licensed therapeutic or prophylactic cell invasion in a process referred to as schizogony,
products for goats in most countries, but anecdotal of which a number of cycles can occur, thus creat-
evidence suggests that halofuginone lactate at lamb/ ing a massive multiplication potential (Fig. 5.54).
calf dose rates and frequency may be beneficial in The cycle then moves to a sexual stage whereby
severe cases. Treatment is aimed predominantly at male and female gametes are produced, resulting
Fig. 5.54 Eimeria multiplication in intestinal wall Fig. 5.55 Thickened ileum of a goat with chronic
(arrows indicate two examples of the developmental coccidiosis.
stage).
in fertilisation and the production of zygotes, fur-

ther gut cell damage and the eventual release of a
final population of oocysts. The ingestion of a single
oocyst can result in the eventual excretion of up to
one million oocysts.
Pathophysiology
The pathology is associated directly with the dam-
age occurring at gut level as the life cycle progresses.
The affected part of the gut may vary slightly
depending on the dominant species involved, but the
lower jejunum, ileum, caecum and colon can all be
affected. There is variable inflammatory damage and
haemorrhage at the mucosal level, with compensa- Fig. 5.56 Pot-bellied appearance and perineal
tory gut wall thickening (Fig. 5.55). staining in a goat with coccidiosis.
Clinical presentation Diagnosis

Clinical signs will usually develop 7–14 days fol- Faecal oocyst counts, accompanied by speciation to
lowing exposure to oocysts. The pathology results assess whether pathogenic species are present. In the
in diarrhoea, with bleeding and blood loss in severe prepatent period, clinical signs can precede oocyst
cases. Affected goats may show tenesmus and excretion. Hypoproteinaemia and hypoalbuminae-
abdominal pain in the acute phase, and rapidly dete- mia can be marked.
riorate and die if untreated. Subclinical infection At PME, there is characteristic thickening of
may lead to poor growth rates, dull coats and pasty the gut, often nodular in appearance (Fig. 5.55).
faeces with perineal staining (Fig. 5.56). Recovered Oocysts may be present in faeces or, in acute
cases may remain stunted due to chronic gut damage cases, schizonts may be identified in gut scrapes.
and thickening of the gut wall. These chronic effects Histological examination will show the devel-
often cause the main economic loss in an affected opmental stages in gut sections with associated
herd. inflammatory change.
146 Chapter 5
Differential diagnosis classified into a number of groups describing their

Other causes of diarrhoea in young goats. mode of action and virulence, including:
Treatment/management/control •• Enterotoxigenic E. coli (ETEC).

Specific anti-coccidial products for use in sheep and •• Enteropathogenic E. coli (EPEC).
cattle include decoquinate (for in-feed medication), •• Enterohaemorrhagic E. coli (EHEC).
diclazuril and toltrazuril, all of which have been used •• Necrotoxigenic E. coli (NTEC).
effectively in goats (off-licence) at sheep dose rates.
Other products include ionophores, such as monen- The verotoxin producing EHEC, E. coli O157:H7,
sin and lasolocid, amprolium and sulphonamides. rarely causes illness in goats or other ruminants,
Severely affected goats should be isolated, kept but intestinal gut levels and faecal excretion rates
warm and given suitable fluid and electrolyte replace- can be high. The organism is an important zoo-
ment therapy. notic risk, particularly to young children, in which
Control is based on reducing the oocyst envi- a potentially fatal haemorrhagic colitis and haemo-
ronmental challenge. Ideally, young goats should be lytic uraemic syndrome can develop.
exposed to low levels of oocysts to allow immunity
to develop, but this is difficult to achieve in practical Pathophysiology
terms. The problem is greatest on units where succes- Disease producing E. coli (particularly ETEC and
sive populations of young goats move through a rear- EPEC) are potent toxin producers, causing local
ing system, with inadequate cleaning between batches. damage to gut enterocytes by effectively adhering to
Oocysts are resistant in the environment, and any fae- the villi whereby toxins can be readily absorbed.
cal material or contaminated bedding from a previous
batch of infected kids will provide a heavy challenge Clinical presentation
for the next batch. Oocysts can survive from one year Diarrhoea is the main clinical presenting sign in neo-
to the next in contaminated litter. Buildings should be natal kids. Heavy infection, particularly in immu-
thoroughly cleaned between batches (using disinfec- nocompromised animals, may result in more serious
tants with known anti-coccidial properties). An all- consequences such as colisepticaemia, with localisa-
in-all-out system should be practiced; holding smaller tion of infection in, for example, joints or brain, or
stunted kids back may rapidly start a heavy oocyst death from overwhelming septicaemia and toxaemia.
challenge if they are chronic coccidiosis cases. Both
in housed and in grazing groups, floor feeding should Diagnosis
be avoided and feed troughs covered to reduce faecal Isolating E. coli from intestinal content, faeces or a
contamination. Moving feed troughs every few days rectal swab is insufficient evidence due to the ubiq-
may also aid control. uitous nature of the organism and its presence in the
gut of healthy goats.
Escherichia coli More specific evidence includes the demonstra-
Definition/overview tion of specific fimbrial antigens such as F5 or F41,
Unlike coli-enteritis in calves and lambs, there is very although their exact significance or global preva-
little evidence that Escherichia coli is a major problem lence remains unknown. Histological examination
in goats, but its potential role as a causative agent in of very fresh fixed intestine at PME has been used
neonatal diarrhoea outbreaks has been occasionally successfully to demonstrate the adherence capabili-
reported. ties of the bacteria.
There is a zoonotic risk from the serotype O157.
Aetiology Other causes of neonatal diarrhoea such as rota-
E. coli is a ubiquitous organism, with many com- virus and cryptosporidia, although rotavirus is
mensal organisms present as part of the back- often involved in mixed infections with these same
ground intestinal flora. Disease producing E. coli are pathogens.
Treatment/management/control of blood, mucus and ‘shredded’ mucous membranes.

Oral antibiotics effective against E. coli, together Affected goats are often dull and pyrexic, and rapidly
with parenteral antibiotic and NSAIDs in septicae- become dehydrated. If a bacteraemia/septicaemia
mic cases, should accompany fluid therapy. develops, then a variety of other clinical signs may
Attention to detail during kid rearing is key to develop, including abortion in does and meningitis
controlling colibacillosis/colisepticaemia, mirroring and septic arthritis in kids.
the management points highlighted in the section
on cryptosporidiosis. Diagnosis
E. coli vaccines are available for use in pregnant Isolation of the infective organism from faeces or
cows to boost colostral immunity, but there is lim- from gut content at PME. Salmonella organisms will
ited evidence for their potential use in goats. grow readily on blood agar and MacConkey agar,
but can also be enriched through selenite broth.
Salmonellosis Confirmation of serotype and phage type requires
Definition/overview input from specialist laboratories.
Salmonellosis is a worldwide problem in a wide
range of livestock systems including ruminants, Differential diagnosis
pigs and poultry. Goats can be affected at any age. Differentiate from other causes of diarrhoea in goats by
Salmonella organisms can also be carried asymptom- laboratory examination, particularly enterotoxaemia.
atically by wild birds and vermin, which can readily
introduce and spread new infections. The zoonotic Treatment/management/control
risk includes close contact and food-borne infec- Any suspect clinical case should be isolated and barrier
tion via contaminated milk and undercooked meat. nursing employed. A faecal sample is taken for labora-
Salmonellosis is reportable in the UK. tory confirmation. Treatment is most effective in the
early stages and is based mainly on supportive fluid
Aetiology therapy and NSAIDs. Oral or parenteral antibiotics
A gram-negative, rod-shaped organism in the fam- are widely used in clinical cases, but many serotypes
ily Enterobacteriaceae. Salmonellae are classified have developed multiple antibiotic resistance profiles,
according to their serotype or serovar, of which there so antibiotic selection should be guided by in-vitro
are >2,000. The most commonly isolated salmonella sensitivity. Parenteral antibiosis in young goats may
serotype is Salmonella typhimurium, further classi- prevent other sequelae such as septic arthritis.
fied according to its phage type (an important factor Any investigation into an outbreak of salmonel-
in epidemiological investigations). A wide range of losis needs to be undertaken in depth to identify and
other serotypes have been identified as potentially hence eliminate the original source. Common routes
causing clinical signs in goats. of infection are:
Pathophysiology •• A purchased goat.

Following ingestion, organisms become established •• Other livestock species in direct contact.
in the gut, resulting in an inflammatory enteritis and •• Rodents or wild birds contaminating feed or
damage to enterocytes via potent endotoxins, result- water troughs.
ing in severe diarrhoea. As gut damage progresses, •• Infected slurry, sewage, bedding or litter (from any
organisms can gain access to the lymphatic system livestock species, including poultry, and humans).
and hence to the blood stream, resulting in multisys- •• Contaminated feed.
temic infection. Whether carrier status can develop •• Boots and clothing of farm personnel and
in goats is speculative. equipment.
Clinical presentation Pooled faecal samples are useful to establish mor-

Severe diarrhoea in goats of all ages is the most com- bidity and, together with environmental samples, to
mon clinical sign, often accompanied by the passage monitor successful control.
148 Chapter 5
Strict biosecurity aimed at keeping salmonello- spread to lymphatics leads to the characteristic
sis out of goat units and preventing spread between lymph node enlargement.
units is vital.
Salmonellosis vaccines are available for use in Clinical presentation
other species, with limited data on their effective use Although all ages of goat can potentially be infected,
in goats. most cases occur in goats <12 months old. In the
Suspicion or confirmation of salmonellosis enteric form (as opposed to abortion), diarrhoea is
should always trigger an emphasis of the potential the key feature, often with mucus. Incidents can be
zoonotic risks to those working with or handling transient and self-limiting or progressive, leading to
the goats, or consuming any unpasteurised milk weight loss, particularly when mesenteric lymphatics
or dairy product. Young children, the elderly and are involved.
those on immunosuppressive therapy are most at
risk. Some dairy herd contracts require the milk Differential diagnosis
buyer to be informed. Other causes of enteritis or diarrhoea.
Yersiniosis Diagnosis
Definition/overview Diagnosis in the live goat is by isolation of the
Yersiniosis has been reported in goats as a sporadic organism in faeces. Pathological changes include a
problem in many countries. It is most commonly characteristic enlargement of the mesenteric lymph
associated with enteritis and with internal abscess nodes with marked oedema. Gut changes may be
formation. It has also been linked to abortions and minimal, although focal areas of mucosal necrosis
mastitis. may be evident (Fig. 5.57).
Yersinia spp. are gram-negative, predominantly aero- Treatment with antibiotics is effective in the early
bic bacteria of the family Enterobacteriaceae. They stages, together with supportive fluid therapy.
are comparatively slow growing on blood agar, and Control is problematic as the organism is ubiq-
the resultant small colonies can be overgrown by uitous in the environment of many domestic and
other colonies and easily overlooked. The two organ- feral goats and most cases are sporadic. Keeping
isms associated with disease in goats are Y. pseudotu- feed stores bird- and rodent-proof is important, as
berculosis and Y. enterocolitica. It is a potential zoonotic is the need to keep stress factors such as handling
infection. Wild birds and rodents represent a reser- and transport to a minimum, including provision of
voir of infection, and have been linked to outbreaks shelter from inclement weather.
of disease via contamination of feed supplies.
Pathophysiology
Both organisms are widely distributed in the envi-
ronment, affecting a wide range of animals. It is
likely that many new infections contracted by goats
are eliminated with no evidence of clinical disease.
Clinical disease is often linked to exposure to
new infection and concurrent stress factors, such
as exposure to cold wet weather, transport, over-
crowding or excessive handling (particularly in
feral goats).
Infection is via the oral route, leading to multi- Fig. 5.57 Intestinal yersiniosis. Note the focal areas
plication in the gut and gut wall colonisation. Local of mucosal necrosis.
Clostridium perfringens occur and outbreaks to develop is most often associ-

(syn. enterotoxaemia) ated with dietary changes such as:
Definition/overview
Clostridium perfringens is one of the more important •• Sudden change in dietary constituents.
causes of diarrhoea (and death) in goats of all ages, •• Sudden increase in dietary intake.
although more prevalent in mature goats. •• Turnout to lush grazing.
•• Bringing in freshly cut green forage in zero-
Aetiology grazing systems.
Caused by C. perfringens, an anaerobic, gram-positive, •• Accidental access to feed stores and overeating of
rod-shaped, spore-forming bacterium. It produces grain, for example.
a number of potent exotoxins that characterise the
specific C. perfringens types (Table 5.2). A build-up of infection in the environment will
C. perfringens type D is by far the most common undoubtedly occur in outbreaks of disease in housed
cause of the condition referred to as enterotoxae- goats, and this may in turn increase the pathogen
mia. Types A and C have been occasionally linked load in the gut of susceptible goats, creating a cycli-
to clinical disease, but incidents have been reported cal problem.
only sporadically. This section will focus on disease Sporadic incidents are often more difficult to
associated with type D. explain, but may be linked to ill-defined stress fac-
The organism is a commensal in the intestinal tors such as:
tract of goats and other ruminants, is shed in
the faeces and can be found in bedding and soil •• Parturition and periparturient problems.
contaminated with the spores. It possesses the •• Environmental stresses such as excessive cold or
ability to multiply rapidly in gut content when heat.
stimulated. •• Concurrent illness such as severe foot lameness.
Pathophysiology The resulting increased level of epsilon toxin

Although goats can acquire infection from their appears to damage the gut wall, leading to increased
environment, most cases result from the sudden vascular permeability and hence absorption, result-
multiplication of harmless low levels of bacteria in ing in a gradually overwhelming toxaemia. The
the gut, overgrowing other bacterial flora and pro- toxin is necrotising and also acts as a potent neuro-
ducing high levels of its potent exotoxins. toxin, causing severe damage to the brain and other
Cases are more likely to develop in goats that are vital structures.
reared intensively or semi-intensively than those
kept extensively, and the condition is rarely encoun- Clinical presentation
tered in feral goats. The stimulus for overgrowth to Peracute cases commonly present as sudden death,
particularly in younger goats.
In older goats, there is a sudden acute depression,
Table 5.2 Exotoxins associated with different pyrexia and inappetence, coupled with visible signs
C. perfringens types. of abdominal discomfort such as arching of the back
and kicking at the flank. Watery diarrhoea quickly
CLOSTRIDIUM develops, often with blood and shredded mucous
PERFRINGENS TYPE ALPHA (α) BETA (β) EPSILON (ε) membranes (Fig. 5.58). There may be ill-defined
A + – – neurological signs, but affected goats can quickly
B + + + become comatose as death approaches, all within a
C + + – 12–24 hour time period.
D + – + In acute cases, the signs are less severe, and may
progress over 2–4 days. Diarrhoea is persistent and
150 Chapter 5
Fig. 5.58 Severe haemorrhagic diarrhoea in a Fig. 5.59 Ileal content (pure blood) and section of
confirmed enterotoxaemia case. colon wall showing ulceration in an enterotoxaemia case.
watery in consistency. Affected goats are often inap- finding. Impression smears of the intestinal mucosa
petent, but less frequently exhibit signs of abdomi- (in fresh carcases) may demonstrate high numbers of
nal discomfort. As the condition progresses, they gram-positive, rod-like organisms. The most useful
become dehydrated and acidotic. test confirms the presence of epsilon toxin in intes-
A chronic form has also been described: it is an tinal content or faeces using either an ELISA test
ill-defined presentation in which affected goats, usu- or a number of PCR tests – approximately 5 ml of
ally housed intensively, show progressive weight loss, gut content or faeces are submitted. The toxin is
reduced milk yield and soft pasty faeces. It is thought labile, however, and rapidly degrades as the carcase
to be related to heavy and constant environmental autolyses.
challenge causing low-grade gut damage due to
toxin release in vaccinated goats. Differential diagnosis
Peracute cases need to be differentiated from other
Diagnosis causes of sudden death such as plant or chemical
Diagnosis is based on a combination of clinical signs poisoning, acute listeriosis, anthrax or abdominal
and recent history. At PME, the most consistent catastrophies. For acute haemorrhagic diarrhoea,
finding is an enterocolitis. In severe cases, the gut salmonellosis is the main differential. Parasitic gas-
wall is intensely congested with pinpoint haemor- troenteritis (PGE) should be considered for acute,
rhages, ulceration, mucous membrane sloughing watery diarrhoea.
and content that may be pure blood (Fig. 5.59). In
less severe cases, gut wall changes may be fibrinous Treatment/management/control
and gut content often copious and liquid in consis- Treatment success is directly proportional to the
tency. Other features include pulmonary and mes- severity of the condition. Comatose goats and those
enteric lymph node oedema. The hydropericardium passing haemorrhagic diarrhoea carry a poor prog-
associated with pulpy kidney in sheep (also caused nosis. Supportive therapy is important, providing
by C. perfringens type D) is not a feature in goats. warmth and i/v or oral fluid therapy. Antibiotics may
Renal tubular necrosis has been described, and this reduce further bacterial proliferation in the gut, and
may lead to visible softening of the kidney cortex (in gut active astringents may be helpful, together with
fresh carcases). NSAIDs. If available, C. perfringens epsilon antitoxin
Being a commensal, the isolation of C. perfrin- may also be of benefit.
gens from gut content or faeces is not confirmatory, Because this is an unpredictable disease that
but the heavier the growth the more significant the develops when a gut commensal becomes overgrown
for a variety of often ill-defined reasons, the univer- from contaminated teats and udder while suckling.
sal advice is that all goats (particularly those kept Contamination of pooled colostrum can readily
intensively or semi-intensively) should be vaccinated transmit new infection to a group of susceptible
against the condition. It is preferable (unless other kids. There is also confirmed intrauterine infection
clostridial conditions are a known local problem) to of kids, from dams that are heavily infected in late
use vaccines that contain a minimal number of clos- pregnancy. Goats >6 months of age become pro-
tridial antigens, but ensuring that C. perfringens type gressively more resistant to new infection, although
D and C. tetani are covered. In most countries, sheep lateral spread even in adult goats may occur if the
vaccines have to be used in the absence of licensed environment becomes heavily infected.
goat products. The immune response to vaccina- Although susceptible to sunlight and desiccation,
tion is of a shorter duration than in other ruminants, MAP organisms can reportedly survive for up to
and the recommendation is to boost at least every 1 year on pasture (not forgetting potential mainte-
4–6 months following the primary course; even then nance in local wildlife).
the immunity imparted appears to be variable.
Booster doses should be given strategically Pathophysiology
3–4 weeks before perceived risks such as anticipated There is an extended incubation period during
feed changes or transport. Boosting pregnant does which infected goats will appear fit and healthy, but
4–6 weeks prior to kidding will enhance colostral may be shedding organisms in their faeces, thus add-
immunity for suckling kids. These should then ing to the environmental challenge.
receive their first dose of vaccine around 4–6 weeks Clinical signs may develop from 12 months of
of age, giving three doses for the primary course to age, but more commonly from around 2.5 years old.
account for any immaturity of their immune system The stimulus for infection to become clinical is still
and presence of maternally-derived antibodies. poorly understood, but may include stressful inci-
dents such as kidding, transportation, poor nutrition
Johne’s disease (syn. paratuberculosis) or concurrent disease such as endoparasitism.
Definition/overview After infection, MAP localises in the wall of
Johne’s disease is a worldwide problem causing clini- the ileum, lower jejunum and associated lymph
cal disease in intensively managed ruminants includ- nodes. This in turn stimulates a local macrophage
ing goats. Many wildlife species including rabbits are response, resulting in phagocytosis and a progressive
able to carry and thus maintain infections locally, t hickening of the gut wall and lymph node enlarge-
and can also spread the organism from unit to unit. ment. Depending on a number of host-to-pathogen
It is now recognised that there are specific cattle and factors, this infection may then be controlled with
sheep isolates, with most goat infections identified the goat becoming resistant to infection with no
as cattle strains. Goats will contract infection from further shedding or clinical disease, or the infection
other goats, from cattle (and more rarely sheep) kept may progress to intermittent shedding and subclini-
in close association or from faecal contamination of cal disease or become clinical with heavy shedding.
their environment. In an endemically infected herd, it is likely that all
three manifestations are present, thus further com-
Aetiology plicating its control.
The main causative organism of Johne’s disease in
goats is the cattle strain Mycobacterium avium subsp. Clinical presentation
paratuberculosis (MAP). Once introduced into a group Initial clinical signs may be subtle, including pro-
of goats, uncontrolled infection progressively becomes gressive weight loss and reduction in milk yield, with
established and can be very difficult to eradicate. appetite often unaffected. As the condition develops,
Infection is mainly transmitted to young kids anaemia and a lacklustre coat may become apparent
<6 months old by ingestion of faecally contami- together with submandibular oedema as a result of
nated feed or water supplies and also potentially the progressive hypoalbuminaemia. The diarrhoea
152 Chapter 5
associated with the disease in cattle is not a feature may give a positive result on one day, then a
of the condition in goats until the terminal stages. negative result when retested – these goats will
invariably retest as positive in time.
Diagnosis •• Infected goats in advanced clinical phase: sensitivity
There is no single reliable test that can be used to of all available tests increases, as the humoral
confirm infection because of the complex aetiopatho- response becomes stronger and faecal shedding
genesis and long period of latent infection in clinically increases.
healthy goats. The organism demonstrates typical acid •• Valuable or pet goats: laparotomy and
fastness when stained with ZN, either in the faeces histopathological examination of lymph node
of live goats or at PME in the lower bowel content or biopsy tissue has been described.
intestinal scrapes. Growth on culture is very slow, with
colonies often not visible for 6 weeks. Serum antibody At PME, the gut wall thickening evident in the
responses in infected goats prior to the development lower jejunum and ileum is more subtle (Fig. 5.60)
of clinical signs are poor, becoming stronger as clini- than that seen in cattle, in which ‘corrugation’ and
cal disease develops. Therefore, false-negative results apparent folding of the mucosal surface is evident.
are common with currently available commercial tests This sectional subtle thickening may be palpable
such as ELISA during the dormant period, with sen- when the unopened gut is passed between fin-
sitivity increasing as clinical disease develops. PCR ger and thumb. On opening, the affected mucosa
techniques have added to diagnostic tools. has a velvet appearance with mucosal fissures.
Mesenteric lymph nodes may be grossly enlarged
•• Clinically healthy goats: most available tests are and oedematous, with caseation and even calcifi-
ineffective during this phase of disease; there cation (Figs. 5.61, 5.62) being a feature of later
will be little if any humoral response detectable, stage infections.
and the sporadic shedding of organisms in faeces Histological examination of affected gut or asso-
may be below detectable limits. ciated lymph nodes reveals the acid-fast organisms
•• Infected goats in early clinical phase: humoral antibody within infected macrophages (Fig. 5.63). ZN smears
levels and shedding begin to rise, and faecal can be undertaken on intestinal mucosal scrapes,
examination, using ZN stains, culture and PCR content can be cultured or PCR techniques can be
techniques, begins to give fewer false-negative undertaken. An ELISA test can be performed on
results, but overall sensitivity remains low. Goats blood taken from fresh carcases.
Fig. 5.60 Thickening of the jejunal mucosa in Fig. 5.61 Enlarged mesenteric lymph nodes in
Johne’s disease (paratuberculosis). Johne’s disease (paratuberculosis).
Fig. 5.62 Section of lymph node showing caseation Fig. 5.63 Macrophages stained with ZN showing
and calcification in Johne’s disease (paratuberculosis). reddish–purple acid-fast mycobacteria.
Bulk milk monitoring is utilised widely in dairy •• Snatching kids at birth and rearing away from
cattle, and may in time be available when validated adults.
for dairy goat herds. •• Feeding colostrum from test-negative dams,
possibly combined with pasteurisation, and
Differential diagnosis avoiding the use of pooled colostrum.
Differential diagnoses for the combined signs of •• Culling kids born to does developing disease
weight loss, reduced milk yield and anaemia in the or becoming test positive in late pregnancy
absence of diarrhoea include fasciolosis and hae- (because of the risk of in-utero infection).
monchosis. At PME, lesions may appear similar to
tuberculosis. Control can also be achieved in endemically
infected herds by the use of vaccination, widely
Treatment/management/control available and licensed for use in goats in many
There is no known treatment for Johne’s disease. countries. Vaccination will result in far fewer clini-
Effective control is difficult to achieve, because of cal cases and increased productivity, but will not
the long subclinical incubation period, shedding by eradicate infection, effectively allowing a unit to
these subclinical goats and the low sensitivity of the continue in production. Vaccination may influ-
currently available tests. ence an animal’s response to intradermal tuber-
Eradication may be achieved over several years, culosis testing, and its use must be declared to,
but will need considerable commitment by the herd or approved by, the animal health organisation in
owner and attending veterinarian. It is based on some countries.
regular whole herd testing using serology and fae-
cal monitoring, with culling of test-positive goats. Parasitic gastroenteritis
Two consecutive negative herd tests are the ultimate Definition/overview
aim. An alternative to culling is to separate positive Abomasal and intestinal nematode infestation is one
and negative goats into a clean and dirty herd. of the most important diseases of goats worldwide,
Such a control programme must be supported by: particularly in those kept outdoors for all or part of
the time. Clinical signs may vary from weight loss
•• Prompt identification and removal of clinical cases. and reduced milk yield to marked disease and rapid
•• Minimising faecal contamination of feed and mortality. The biology and life cycle of these para-
bedding, particularly for young kids. sites is similar to that in other grazing ruminants,
154 Chapter 5
but there are a number of important and often subtle An understanding of the basics of nematode
differences in goats including: life cycles is important for treatment and control
attempts. The superfamily Trichostrongylidae,
•• An apparent inability to produce age-dependent which includes some of the genera above, has a direct
resistance (possibly because of their evolutionary life cycle, with adults in the alimentary tract pro-
development as ‘browsers’ with less pasture ducing eggs that are voided in faeces, thus contami-
exposure than ‘grazers’, resulting in a poor or nating the pasture (so-called ‘patent infestation’).
defective IgE response). Eggs hatch, then pass through two larval stages to
•• A poor understanding of the pharmacokinetics the infective third stage larvae (L3), which migrate
of many of the commonly used anthelmintics. onto surrounding herbage where they are ingested
•• A potential need to use anthelmintic dose rates by the grazing animal. The time period between
exceeding those recommended for use in sheep ingestion of L3 and the appearance of worm eggs in
and cattle. the faeces is typically between 16 and 21 days. The
developmental stages within the goat are fairly stan-
Many commercially reared goats such as those in dard, but those taking place outside the goat can be
the dairy sector will be housed continuously, thus very variable depending on environmental condi-
removing the disease and production risk that expo- tions. Under favourable conditions, hatching of the
sure to nematodes would pose (Fig. 5.64). eggs and development to L3 takes around 7–10 days.
However, this can be prolonged (and very unpre-
Aetiology dictable) in periods of drought or cold weather. Both
The species of nematodes affecting goats are iden- eggs and larvae are able to survive in pasture from
tical to those of both sheep and cattle with some one season to the next.
minor exceptions. The parasites that contribute
predominantly to clinical disease belong to the gen- Pathophysioloy
era Teladorsagia/Ostertagia, Cooperia, Nematodirus, As with all host–parasite relationships, the patho-
Oesophagostomum, Trichostrongylus, Strongyloides and genic effects of acquired worm burdens depend on:
Trichuris, and to Haemonchus contortus. There is varia-
tion between and within countries as to the locally •• The species of worms and stages of life cycle
significant nematode population, and the strategic present.
use of laboratory testing enables the establishment of •• The numbers of worms present.
prevalence patterns. This in turn facilitates the devel- •• The predilection site – abomasal worms are
opment of suitable control programmes. generally the more pathogenic.
•• The host’s age and immunity, which directly
affects the worm populations and pathogenicity.
Teladorsagia/Ostertagia nematodes present in the

abomasum cause symptoms and pathology similar
to those seen in cattle and sheep. Parasitised gastric
glands are hyperplastic and contain undifferentiated
cells leading to increased abomasal pH and leakage
of pepsinogen into the plasma. Macroscopically,
infected glands appear as raised nodules which, in
heavy infections, coalesce to produce a ‘morocco
leather’ effect, sometimes leading to mucosal necro-
sis and sloughing with oedema and hyperaemia pres-
Fig. 5.64 UK dairy goats kept indoors to control ent. The reduction in functional gastric mucosa
parasitic gastroenteritis. leads to impaired digestion and diarrhoea.
Infection with intestinal nematodes produces vil- Progressive faecal staining of the hind end is often
lous atrophy and crypt hyperplasia. Resultant rapid present. Heavy burdens of H. contortus can produce
cellular turnover of immature epithelial cells peracute anaemia (Fig. 5.66) and death; lighter burdens
mits loss of fluid and plasma proteins into the intes- may produce an iron deficiency anaemia and oedema,
tinal lumen, causing a protein-losing enteropathy. which may manifest as submandibular oedema, with
There is also a deficiency in brush border enzymes faecal consistency unchanged.
that affects nutrient absorption.
H. contortus is a blood sucking nematode (larvae Diagnosis
and adults) in the abomasum, causing anaemia. Traditionally based on faecal egg counts (FECs) in
live goats (Fig. 5.67), although this relies on the
Clinical presentation presence of a mature, egg-laying (patent) worm
Signs can be encountered in goats of any age, includ- burden, and can lead to false-negative results in
ing adults that may have been exposed regularly, prepatent burdens. Interpreting the significance of
because of the poor or variable immunity produced. FECs must take account of age of goat and clinical
Clinical signs will depend on the factors already signs present (e.g. there often is poor correlation
outlined, together with recent grazing history. With between FEC and actual worm burden in mature
the exception of H. contortus, these signs may vary goats). As a general guide, FECs in excess of 2,000
from weight loss/poor weight gain and reduced milk epg are usually clinically relevant. Counts of 500–
yield, to severe watery diarrhoea leading to hypo- 2,000 epg are suggestive of subclinical parasitism
albuminaemia, dehydration and death (Fig. 5.65). and subsequent reduced production.
In haemonchosis cases, haematology may con-
firm a clinical suspicion of anaemia coupled with low
serum albumin levels. An additional diagnostic aid is
the FAMACHA© system developed in South Africa,
initially for use in sheep, but also validated for use
in goats. It uses a laminated card with five different
colour shades representing the varying degrees of
anaemia evident in the conjunctival mucous mem-
brane (Fig. 5.68, Table 5.3).
At PME, pathological changes in the gut are
Fig. 5.65 Severe diarrhoea in a case of acute relatively non-specific, although some larger
parasitic gastroenteritis. nematodes may be clearly evident in gut content,
Fig. 5.67 Faecal egg counts are an important

part of the development of an anthelmintic control
programme.
Fig. 5.66 Severe anaemia in a case of haemonchosis.

156 Chapter 5
such as H. contortus in the abomasum (Fig. 5.69). burden. Owners should be encouraged to monitor
Investigation is based on identification of nematode faecal egg output regularly (Fig. 5.70) and only treat
burdens in the abomasum and intestinal tract fol- where there is clear clinical, FEC or post-mortem
lowing standard gut washing techniques, supported evidence of PGE. Criteria to identify goats for tar-
by FECs. geted selective treatment, based on production effi-
ciency, weight gain and diarrhoea score, are being
Differential diagnosis evaluated. Epidemiological studies in grazing dairy
Other causes of weight loss and diarrhoea such as herds show that within a herd, first lactation does
enterotoxaemia, salmonellosis and coccidiosis. For and high-yielders are most at risk of high worm bur-
haemonchosis, include Johne’s disease, fasciolosis, dens, and could be considered for targeted selective
other causes of anaemia or dependent oedema (see treatment.
Chapter 7). To prevent introduction of resistant nematodes
by incoming stock, the following protocol is recom-
Treatment/management/control mended: sequentially administer two different classes
Successful management and control requires a sound
knowledge of the life cycle of the parasites and the
Table 5.3 The FAMACHA© categories and
resultant host response. Several countries dissemi- corresponding parameters.
nate parasite forecasts, highlighting particular risk
periods. Nematodirus battus, with its mass hatching PACKED
in spring, is a good example where these forecasts CONJUNCTIVAL CELL
are invaluable, allowing pre-emptive management. MEMBRANE VOLUME TREATMENT
CATEGORY COLOUR (l/l) RECOMMENDED
Because of the many shared nematodes with grazing
sheep and cattle, any control programme on a mixed 1 Red ≥0.28 No
stock unit must be integrated. 2 Red-pink 0.23–0.27 No

Anthelmintic resistance is becoming a serious 3 Pink 0.18–0.22 Possibly
issue worldwide, thus anthelmintics must be used 4 Pink-white 0.13–0.17 Yes
appropriately and correctly, and always be combined 5 White ≤0.12 Yes
with pasture management steps to reduce pasture
Fig. 5.68 The FAMACHA© chart is a simple tool Fig. 5.69 Abomasal nematodes visible grossly.
to check for anaemia based on conjunctival mucous
membrane colour. It has proven effective for early
detection and selective anthelmintic treatment in the
control of haemonchosis.
Table 5.4 Comparison of suggested anthelmintic

dose rates in sheep and goats.
SHEEP GOATS
Group 1: benzimidazole 5 mg/kg 10 mg/kg
Group 2: levamisole 7.5 mg/kg 12 mg/kg
Group 3: ivermectin 0.2 mg/kg 0.3–0.4 mg/kg
Group 3: doramectin 0.2 mg/kg 0.2–0.4 mg/kg
Group 3: moxidectin 0.2 mg/kg 0.2–0.4 mg/kg
Group 4: monepantel 2.5 mg/kg 3.75 mg/kg
(see comment in text on its use)
Fig. 5.70 Regular faecal egg monitoring. Screw top

containers are preferable to plastic bags for sample
submission.
of anthelmintic, hold animals in a solid floored pen

for 2–3 days, incinerate faeces and any bedding, then
turn out onto ‘dirty’ pasture (i.e. already contami-
nated with nematode eggs). The two new classes of
anthelmintic (see below) may be used for this quar-
antine drenching.
Management by zero grazing is particularly suc-
cessful and practised by many large commercial units.
For haemonchosis, an additional control mea-
sure is the injectable vaccine Barbervax ®. It reduces
excretion, thus resulting in lower pasture contami- Fig. 5.71 Automatic dosing gun used for
nation and reduction in disease, and is reportedly anthelmintics. The angulation of the nozzle must be
effective against anthelmintic resistant strains. taken into account when placing it into the oral cavity.
Jointly developed by researchers in the UK and
Australia, it is currently being assessed for efficacy main anthelmintic groups in the goat, and it is now
in goats. recognised that using recommended sheep dose rates
Identifiying the genetic basis for individual goat may have resulted in underdosing, possibly increas-
resilience and resistance is being explored, and may ing the resistance risk.
offer selective breeding options in future. The three most widely available groups of
anthelmintics are all effective in goats, but at higher
Choice of product and route of administration dose rates: Table 5.4 is based on observations and
There are few, if any goat-specific anthelmintic recommendations cited worldwide. Oral products
products worldwide, and in many countries there provide more consistent results than injectable or
are no authorised or licenced products available. As topical products (Fig. 5.71). The benzimidazole
a result, in Europe, for example, products are used group is only available in oral forms. Both s/c and
under the veterinary prescribing cascade. oral levamisole will yield similar good efficacy,
One problem this lack of goat-specific products since the active ingredient is rapidly absorbed by
has led to is the paucity of information on efficacy, both routes. However, following s/c administra-
dose rates and pharmacokinetic properties of the tion absorption is extremely rapid, with higher
158 Chapter 5
peak plasma concentrations that are more likely common is owner error or inexperience (particularly
to cause toxic reactions. Oral absorption is slower, in the smallholding or pet/hobby sector). Reasons
producing a lower peak and thus greater safety. for possible failure, other than anthelmintic resis-
For macrocyclic lactones the oral route is the most tance, include:
effective since the worm has the greatest contact
with the product, even though studies show higher •• Dosing with insufficient anthelmintic:
bioavailability after s/c administration. In addi- • Incorrect dose rate.
tion, the period of residual subtherapeutic levels • Underestimation of the goat’s weight.
is reduced following oral administration, there- • Poorly maintained dosing equipment.
fore there is less selection for resistance. Any oral •• Failure to follow the manufacturer’s instructions:
anthelmintic should be administered at the back • Not storing the product correctly.
of the oral cavity to avoid spillage and potentially • Using products beyond their use-by date.
trigger a stronger oesophageal groove reflex. • Mixing anthelmintics with other products.
Group 1 products are broad spectrum and very • Administering via the wrong route.
effective against arrested hypobiotic larvae. They •• Rapid reinfection from heavily contaminated
are ovicidal and generally have a wide safety margin pastures.
(although teratogenic effects have been described
with use of albendazole in early pregnancy). If anthelmintic resistance is suspected, then post-
Group 2 products also have a broad spectrum, but dosing FEC (drench testing), FEC reduction testing
have no or only minimal effect on arrested larvae or in-vitro larval development and egg hatch assays
and are not ovicidal. They have a narrow margin can be undertaken.
of safety in goats, requiring accurate body weight
determination, and should not be used in severely Guidelines to limit anthelmintic resistance
debilitated animals. Several countries have developed guidelines because
Group 3 products are effective against nematodes of the concern over rising resistance to anthelmin-
and a range of ectoparasites. Persistence against tics in grazing animals. If not checked, this resis-
H. contortus has been recorded as 22 days for moxidec- tance could have a catastrophic impact on animal
tin and 14–25 days for doramectin. Eprinomectin as welfare and economic production worldwide. It is
a pour-on preparation has a product licence in some recognised that anthelmintics are a necessary part
countries for use in goats. The pharmacokinetics in of nematode control, but their use must be judicious
goats are relatively unknown, and results have often and effective. UK guidelines include SCOPS (sus-
been disappointing with suboptimal nematode kill tainable control of parasites in sheep) and COWS
rates. (control of worms sustainably). The principles can
Group 4 and 5 are two new classes of anthelmin- be applied to goats, and advice points veterinarians
tic, now available as ‘prescription only’ products in can apply include:
many countries (Group 4 AD: monepantel; Group
5 SI: derquantel). It is important that use of these Do:
new classes is kept under control, particularly as
isolated cases of nematode resistance to monepan- •• Encourage the development of farm health
tel have arisen in various countries including the planning including worming strategies.
Netherlands, New Zealand and Uruguay (associated •• Establish full grazing management
with a very high frequency of monepantel use on the programmes and regular FECs to reduce
premises). treatment needs.
•• Target the drug used to the parasite (and stage)
Apparent failure of efficacy to be treated.
Inherent problems of controlling nematodes in •• Leave proportion of group untreated to preserve
goats may contribute to apparent failure, but more susceptible worm population.
•• Emphasise and avoid the common reasons for a number of developmental stages involving the
underdosing: underestimation of body weight, intermediate host, before being available again to be
maladministration of the product or lack of ingested with herbage and complete the life cycle.
calibration of the dosing device. Following ingestion, the immature flukes migrate
•• Depending on the product used, do not move through the gut wall across the abdominal cavity
treated animals immediately onto clean pasture. to the liver, where they penetrate the liver capsule
•• Explain and emphasise the importance eventually ending up in the biliary system. In large
of quarantining incoming animals and give numbers severe parenchymatous damage and cap-
individual guidance on their treatment. sular haemorrhage can occur, resulting in acute fas-
•• Investigate suspected clinical cases of resistance ciolosis. Mature flukes may survive in the bile ducts
and advise on the selection of alternatives from and gallbladder for 3–4 years, and during this phase
other classes. result in chronic fasciolosis.
•• Report suspected cases of lack of efficacy to the
relevant authorities. Clinical presentation
The acute form can be encountered in goats
Do not: (Fig. 5.72), sometimes presenting as sudden death
from severe internal haemorrhage. More typi-
•• Treat unnecessarily or randomly. cally, affected goats show progressive weakness,
•• Blanket treat. anorexia and marked pallor of mucous membranes.
Respiratory rate may be markedly elevated in
(Note: The same anthelmintics and principles are response to anaemia. In the chronic form, depend-
applicable to the control of lungworm [see Chapter 6, ing on the degree of damage elicited, early signs
p. 173].) include weight loss, anorexia and drop in milk yield.
As the condition develops, weight loss can be dra-
Liver fluke (syns. fascioliasis, matic, with subcutaneous oedema secondary to
fasciolosis) hypoalbuminaemia most commonly manifesting as
Definition/overview submandibular oedema or ‘bottle jaw’. Faeces may
Liver fluke infection is a widely reported problem be unchanged initially, but in later stages diarrhoea
around the world. It is a parasite shared with other may develop.
ruminant species, and can be a major constraint on
production.
Aetiology
Disease is caused predominantly by the two trema-
tode parasites, Fasciola hepatica and Fasciola gigantica. F.
hepatica has the widest distribution, with F. gigantica
limited to the more tropical areas of Africa, Asia and
the Middle East.
Pathophysiology
The life cycle of both parasites is an indirect
one, involving a mud/water snail of the family
Lymnaeidae, of which many species have been iden-
tified. In the UK, for example, it is Galba truncatula
that maintains the fluke population in the local envi-
ronment. The mature flukes inhabit the gallbladder Fig. 5.72 Post-mortem specimen of liver (in situ)
and bile ducts. Eggs voided in faeces pass through showing acute fasciolosis in a lamb.
160 Chapter 5
Diagnosis any control programme should incorporate all co-

In the live goat FECs, taking the prepatent period grazing species.
into consideration (which can be as long as 8 weeks). Management is aimed either at removing the
Even a single fluke egg found on a FEC is notewor- developmental stages of the parasite from the liver of
thy. Most acute cases are diagnosed at PME. In early the goat, or at avoiding known parasite–intermediate
acute cases, local knowledge of the presence of flukes host interaction in the environment.
on a unit together with the known seasonality of the Several flukicides are marketed for the treatment
condition will lead to a tentative diagnosis, aided and control of flukes. If the product has no licence
by haematology and biochemistry (GLDH, AST) for use in goats, it is recommended to use the sheep
confirming anaemia and liver damage. In chronic dose (without increasing the dose rate, as for anthel-
cases, serum biochemistry will demonstrate a rise mintics, because of potential toxicity).
in gGT as a result of biliary damage, and typically Some flukicides can be used in all classes of
hypoalbuminaemia. Fluke serology tests confirming goat, others should not be used in lactating goats.
exposure, and PCR tests to identify fluke antigen Depending on the time of year it is to be used, atten-
in faeces, have been developed, but validation for tion must be paid to whether the product is e ffective
use in goats varies. At PME of chronic cases there in killing immature stages or only mature fluke.
is marked accentuation of the biliary tree by fibro- Products currently available include clorsulon, clo-
sis and, in long-term cases, by calcification. Mature santel, nitroxynil, oxyclozanide and triclabendazole.
fluke may be identified in the gallbladder and bile (Note: Resistance reported in the UK.) Albendazole
ducts (Fig. 5.73). may also be suitable (care in pregnant does).
Where possible, goats should be kept off known
Differential diagnosis snail habitats or these areas should be fenced off.
Includes Johne’s disease, haemonchosis, other gas- Snail supporting areas do not have to be constantly
tro-intestinal nematodes, and other causes of anae- wet. The area around a leaking water trough or
mia or dependent oedema (see Chapter 7). temporary puddles formed after a particularly rainy
period can form an excellent snail habitat.
Forecasts are issued in the UK, giving advance Small liver fluke (syn. lancet fluke)
warning of the likely risk periods and severity. As Dicrocoelium dendriticum is present in many European
the parasite is shared with both sheep and cattle, and other countries, and occasional cases are seen in
sheep in the UK. Inside the ruminant host, the para-
site migrates up, and lives in, the bile system. Because
there is no migration through the gut wall and liver
parenchyma, as in fasciolosis, infection is often sub-
clinical and only detected at slaughter or PME.
Sedimentation and McMaster FEC methods tend
to be insensitive for this parasite, with flotation using
a high specific gravity solution recommended. The
life cycle includes land snails and ants, making con-
trol via habitat management very difficult. Keeping
free-range poultry can reduce snail numbers to a
degree, and fencing off ant nests is recommended.
Tapeworms (cestodes)
Definition/overview
Fig. 5.73 Mature flukes (Fasciola hepatica) found in Intestinal tapeworms have been identified in
the gallbladder and bile ducts. goats worldwide, but rarely cause any significant
clinical disease. Owners may be disturbed by the as the bile duct. Control is based on breaking the
physical presence of tapeworm segments in faeces. life cycle, firstly by treating dogs in known endemic
areas for tapeworms on a regular basis, and sec-
Aetiology ondly by preventing access to ruminant carcases by
Moniezia spp. are the most common, and can achieve scavenging dogs. There is no specific treatment for
lengths of several metres, consisting of a head or hydatidosis in infected goats. Hydatidosis can be a
scolex, and many segments or proglottids. It is the significant zoonotic problem. Coenurus cysts (gid)
mature egg-containing proglottid that breaks off are discussed in Chapter 8.
and appears in the faeces.
Peste des petits ruminants
Pathophysiology (syn. goat plague)
Light infestations are generally asymptomatic. Very Definition/overview
heavy infestations may lead to competition for nutri- Peste des petits ruminants (PPR) affects small rumi-
ents in the gut, and can also cause partial or com- nants so far in almost 70 countries in Africa, the
plete intestinal obstruction, or even torsion. Middle East and parts of Asia. It is a highly conta-
gious disease, which causes massive economic losses
Clinical presentation each year in regions that are home to over 80% of
If clinical signs do develop, they are usually in the world’s sheep and goat populations and to more
younger goats, and can be very vague in nature, than 330 million of the world’s poorest people, many
including weight loss or poor weight gain. Large of whom depend on them for their livelihoods. The
burdens resulting in intestinal obstruction or torsion disease threatens food security and livelihoods, and
present with colic signs and reduced faecal output. prevents animal husbandry sectors from achiev-
ing their economic potential. Disease has been
Diagnosis spreading out from these traditional areas, hav-
Presence of segments in faeces. ing been endemic in Turkey since 2000 and now
common in North African countries bordering
Differential diagnosis the Mediterranean, both scenarios posing a risk to
Other conditions causing ill thrift in younger goats, Southern Europe. Goats appear to be more suscep-
including nematodes, coccidiosis, liver fluke and tible than sheep.
nutritional problems. PPR is a disease listed under the OIE Terrestrial
Animal Health Code and must be reported to the
Treatment/management/control World Organisation for Animal Health. There is
Treatment is not usually necessary as the condition currently a global strategy for the eradication of this
is relatively mild, although many anthelmintics are disease.
effective against intestinal cestodes.
Aetiology
Metacestode disease PPR is caused by a morbillivirus in the family
Metacestodes are the intermediate stages in the life Paramyxoviridae. In naive herds, the introduc-
cycle of cestodes and can occasionally be found in tion of PPR virus can result in devastatingly high
goats as intermediate hosts (with carnivores the morbidity and mortality figures of up to 100%.
definitive host). The most important species world- Recovered animals produce very strong and lasting
wide are hydatid cysts, the intermediate stage of the immunity. In an endemic area, the adults therefore
tapeworm Echinococcus granulosus. These cysts can be become naturally immune (or are immune follow-
found mainly in the liver and lungs, often presenting vaccination) and newborn kids are protected
ing at PME (as an incidental finding) or meat inspec- via colostral antibodies. Clinical disease is, there-
tion. Clinical signs may be encountered if the cyst fore, restricted to younger goats between 3 and
enlarges, causing pressure on vital structures such 12 months of age.
162 Chapter 5
Pathophysiology
The virus is secreted in ocular and nasal discharges,
saliva, sputum and faeces. Therefore, disease spread
is through close contact between goats and other
susceptible species, especially through inhalation of
aerosol droplets from coughing and sneezing. Water,
feed troughs and bedding can also be contaminated
with secretions and become additional sources of
infection; however, the virus does not survive for
long outside the body of a host animal. Since the
virus can be carried and shed before clinical signs
develop, PPR can be spread by movement of infected
but apparently healthy animals. Fig. 5.74 Peste des petits ruminants case showing
After a short incubation period of 2–6 days, the severe conjunctivitis and nasal discharge and crusting.
virus localises in the tonsils and pharyngeal and (Image courtesy Peter Roeder.)
mandibular lymph glands. This rapidly results in
viraemia and the virus colonising visceral lymph Progressive diarrhoea develops, with faeces
glands, spleen and bone marrow. Replication also becoming watery, malodorous and sometimes con-
occurs in the mucous membranes of both the respi- taining blood and pieces of intestinal tissue, leading
ratory and digestive systems, the latter leading to to marked dehydration and weight loss. Pneumonia
widespread erosions causing stomatitis and a severe is common in the later stages, and pregnant animals
watery diarrhoea. Immunity is compromised as a may abort. Clinical progression can be rapid, with
result of lymphoid tissue damage, and many deaths death within 5 days from onset, or peracute result-
are hastened by secondary bacterial infections such ing in sudden death. However, disease can also be
as pneumonia. mild or non-apparent, and circulate in an area caus-
ing little or no illness until susceptible goats are
Clinical presentation exposed.
Sudden onset pyrexia with severe depression, loss
of appetite and initially a clear nasal discharge. The Diagnosis
nasal discharge becomes thicker and yellow, often Tentative diagnosis is based on clinical signs. If sus-
becoming so profuse that it forms a crust that blocks pected, PPR is a notifiable disease in those countries
the nostrils, causing respiratory distress. Goats may in which it is not endemic, and the relevant authori-
sneeze persistently in an effort to clear the debris. ties should be contacted. In the live goat, blood and
Ocular involvement includes conjunctivitis, which tissue samples are submitted for virus isolation or
causes the eyelids to mat together with discharge antigen detection with PCR. Serum antibody can be
(Fig. 5.74). Gradual epithelial necrosis causes small detected in more long-standing cases, but is of no
pinpoint erosions leading to ulcers on the gums, den- value in acute disease.
tal pad, palate, lips, inner aspects of the cheeks and At PME, the carcass is usually emaciated, the hind-
dorsal surface of the tongue. These areas increase quarters soiled with soft or watery faeces, and dehy-
in number and size, eventually coalescing. In some dration is evident. The eyes and nose contain dried-up
cases, oral mucous membranes may be completely discharges. The mucosal changes described clinically
obscured by thick fibrino-necrotic material covering are evident in the mouth, often extending down the
the erosive changes beneath. Similar changes may oesophagus. There is often evidence of a secondary
also be seen in the mucous membranes of the nose, bacterial pneumonia. Both small and large intestine
the vulva and the vagina. The lips tend to swell and show marked congestion of the serosal surface, and
crack and become covered with scabs. congestion and erosive change of the mucosa.
Differential diagnosis Bluetongue

PPR is frequently confused with other diseases that Signs described include pyrexia, loss of appetite and
present with pyrexia and grossly similar clinical milk yield with hyperaemia and mild erosive damage
signs, especially when it is newly introduced. The to the oral mucosa. On occasion, more severe cases
epidemiological profile, including the often high may be encountered in which these oral changes
morbidity and mortality in the herd, is as important progress to ulcerative and necrotic changes to the
as the findings in a single goat or sheep. tongue, lips and gums, resulting in marked salivation.
Mouth lesions could be confused with foot and Diarrhoea may also develop. (See also Chapter 17.)
mouth disease, bluetongue or contagious pustu-
lar dermatitis (orf), the respiratory element with Miscellaneous conditions
pneumonic pasteurellosis or contagious caprine •• Adenovirus – adenovirus-associated diarrhoea
pleuropneumonia, and the diarrhoea with PGE, in young kids has been reported and should be
enterotoxaemia or coccidiosis. The combination of considered if other more common conditions
clinical signs, severity of disease and the geographi- have been eliminated.
cal location aids in achieving a diagnosis. •• Giardia – this protozoal parasite has been
reported as a potential cause of diarrhoea
Treatment/management/control and ill thrift in goats, but can also be found
In those countries in which PPR is not recognised, in the faeces of apparently healthy goats,
management is subject to outbreak measures to con- suggesting that its overall pathogenicity may be
trol and eradicate the disease. questionable. Of greater significance is its role as
In countries where the disease is endemic, control a zoonotic pathogen, and infection in goats may
is based very heavily on the use of strategic vaccina- well be identified as part of tracing to identify
tion, aimed most commonly at young goats in their the source of human infection.
first year of life after colostral antibody has waned. •• Caprine herpesvirus – can present as a number
Immunity following vaccination or recovery from nat- of clinical disorders, including diarrhoea in
ural infection is long-lived. Ring vaccination around young kids accompanied by pyrexia, weakness,
endemic areas is used to prevent further spread. abdominal pain and oral lesions. (See Chapter 2.)
CHAPTER 6
RESPIRATORY SYSTEM
165
NORMAL STRUCTURE AND FUNCTION
The goat’s nasal cavity mirrors the anatomy of other

ruminants. Clinically relevant aspects include:
•• The ventral meatus, being the widest, carries

most of the air flow and allows passage of an
endoscope or nasal tube.
•• Various recesses and bullae exist, which can only
be assessed using advanced imaging techniques.
•• Sinuses are connected rather than isolated
entities.
•• The lateral section of the frontal sinus connects
with the horn base. Fig. 6.1 Signs of poor ventilation. Cobwebs indicate
poor air circulation; rust on the metal roof and ‘tiger-
The cartilages of the tracheal rings are U-shaped stripes’ on the beams indicate frequent condensation.
in the goat, connected dorsally by a membranous
wall. The bifurcation into left and right main bron- on auscultation, percussion and observation of other
chus is at the level of the 4th to 6th intercostal space, abnormalities (e.g. type of nasal discharge, changes
with an additional bronchus just prior to the main in lung sounds).
bifurcation into the right cranial lung lobe. On the It is important to remember that several systemic
right, there are two additional smaller lung lobes, conditions can alter respiratory tract parameters
in addition to the main lobe. On the left, there is a (e.g. pain, excitement, ambient temperature and
smaller cranial lobe and the main lobe. The goat has humidity, rumen tympany, metabolic alkalosis and
a complete mediastinum. acidosis, septicaemia).
CLINICAL EXAMINATION OF Specific observations

THE RESPIRATORY SYSTEM The normal respiratory rate is 15–30 bpm in adults
and 20–40 bpm in kids, with a moderate abdomi-
General aspects nal effort to respiration. Nasal discharge is normally
Of particular interest for investigation of respira- clear and non-copious. A mucopurulent discharge
tory tract disease are: season, housing environment indicates inflammation (Fig. 6.4); haemorrhagic
(Figs. 6.1, 6.2), type of animal (e.g. goatling, first discharge indicates inflammation, bleeding disorder
lactation versus adult doe), recent animal move- or mucosal ulceration; and presence of feed or milk
ments (regrouping, return from show; Fig. 6.3), indicates a cleft palate, dysphagia or regurgitation.
individual versus group affected, vaccination sta- Air-hunger signs are abducted elbows, extended
tus, location of pathology (upper versus lower and lowered head and neck (Fig. 6.5) and, in severe
respiratory tract), likely type of pathology based cases, mouth breathing.
166 Chapter 6
(a) (b)
Fig. 6.2 Smoke-bomb test to check ventilation. The smoke rises well initially (a), but then fails to exit the
building (b). This suggests reasonable air inlet through the sides, but poor air outlet in the roof.
Fig. 6.3 Any recent animal movements are of Fig. 6.4 Nasal discharge suggests involvement of the
interest for disease investigation, including goats respiratory tract. The mucopurulent nature seen here
returning from shows. (Image courtesy Jenny Hull.) indicates an inflammatory pathology.
The goat should be observed for spontaneous

coughing and whether a cough can be elicited by
palpation of the larynx or trachea.
For auscultation, the lung field roughly extends
from the penultimate intercostal space in a straight
line towards the elbow, becoming inaccessible in the
shoulder area. The area around the thoracic inlet is
included in the auscultation for the cranial lobes.
Fig. 6.5 Air-hunger signs in a calf. Head and neck

are lowered and extended, and elbows abducted.
Also note the presence of epiphora: conjunctivitis
accompanies several respiratory diseases.
R e spi r at ory Sys t e m 167
Fig. 6.6 Congenital narrowing of the trachea at the

level of the shoulder in a lamb. Adventitious sounds
were loudest over the trachea in the distal neck area.
Where adventitious sounds are present, it is impor-

Fig. 6.7 Lateral chest radiograph showing a lung
tant to establish the point of maximum intensity of
abscess (arrows). Masses have to be at least 5 mm in
these sounds. This in part allows differentiation of
diameter to be detectable on x-ray. (Image courtesy
upper versus lower tract disease (Fig. 6.6). Equally,
Jenny Hull.)
it must be remembered that tracheal sounds may be
referred into the thorax.
culture and sensitivity; ensuring adequate hydration
Ancillary diagnostics status (to address fluid loss caused by tachypnoea and
These include endoscopy, tracheal wash or bronchoal- ensure optimum cilial function); well-ventilated but
veolar lavage for cytology and pathogen isolation, draught-free environment (pasture with shelter may
ultrasonography (e.g. to detect pleural effusion or lung be best); and maintaining feed intake.
tissue consolidation), faecal examination (for parasitic Antimicrobials with good penetration of lung
disease such as lungworm) and haematology (to estab- tissue include: trimethoprim-sulphonamides, tetra-
lish eosinophilia in parasitic lung disease or an inflam-cyclines, macrolides and florfenicol. Moderate con-
matory response). Thoracic radiography is of limited centrations are achieved with the penicillin group
value because of the fairly poor correlation between (ideally potentiated, e.g. amoxicillin and clavulanic
parenchyma pathology and radiographic appearance acid) and cephalosporin.
in ruminants. Lung masses (e.g. neoplasia, tubercu- Chronic pathology precludes complete cure and
losis nodules; Fig. 6.7) need to be at least 5 mm in return to normal production. Where fibrous tissue
diameter to become radiographically detectable. reaction is suspected, iodides may be beneficial (see
Post-mortem material is invaluable for establish- Chapter 5, Dental problems).
ing a definitive diagnosis, especially when a group-
affecting disease is suspected. Tracheotomy
Indication
TREATMENT PRINCIPLES Severe respiratory distress caused by obstruction of
the nasal passageways or larynx. Also to provide rest
General treatment principles include: isolation of to an inflamed and oedematous larynx.
affected animal(s); anti-inflammatory drugs (NSAIDs
or corticosteroids); antibiosis for primary bacterial Preparation and equipment
infections and possibly to control opportunistic sec- The ventral neck is clipped and surgically prepared.
ondary pathogens, with the choice ideally based on Equipment includes an uncuffed tracheotomy tube
168 Chapter 6
(e.g. Portex®; inner diameter of 5 mm for kid, 8 mm

for yearling, 10 mm for adult) and a small procedures
kit, ideally including a pair of Allis tissue forceps.
The distal end of a stomach tube can be used in an
emergency.
Where dyspnoea has led to cyanosis and severe
hypoxaemia, a 14–16 gauge hypodermic needle may
be placed into the distal trachea as an interim mea-
sure while the surgery is carried out (connected to
oxygen if available).
Restraint
Standing or in sternal recumbency, with the head
and neck held in extension. Local anaesthetic is infil-
trated in a rectangular fashion around, or as a line
over, the incision site.
Technical description
A 3 cm long, vertical skin incision is made in the Fig. 6.8 Tracheotomy (animal in sternal
midline of the ventral neck, one-third to one-half the recumbency). A vertical skin incision and blunt
way down. Blunt dissection is used to separate the dissection of the muscles expose the trachea, here
left- and right-hand side muscle bundles. The trachea manually pushed towards the incision. The annular
is manually pushed towards the incision and fixed ligament has been cut and a small section of cartilage
either manually or with the aid of Allis tissue forceps, removed out of each of the two adjacent tracheal rings
taking care not to cause too much compression. to create a circular opening.
Using a scalpel blade, the annular ligament
between two rings is cut over one-third to half of its
length/circumference (Fig. 6.8). In adults, it may be
possible to remove a crescent-shaped piece of car-
tilage out of the two adjacent rings. However, this
must not be done too aggressively, otherwise the tra-
chea may collapse once the tube is removed.
The tracheotomy tube is inserted and secured
with the supplied tapes around the neck (taking care
that the tape is not across the opening of the tube;
Fig. 6.9).
Aftercare
Prophylactic antibiosis and anti-inflammatory medi-
cation. The tube is changed twice a day and thor-
oughly cleaned each time (physical removal of debris,
followed by chlorhexidine then thorough rinsing with
tap water). Once the primary problem is deemed to
have resolved, the tube is removed for trial periods of
several hours.
The skin incision is allowed to heal by secondary Fig. 6.9 Tracheotomy tube (Portex®) in place and
intention. secured with tapes around the neck.
Potential complications used, possibly combined with iodides where actino-

Pneumonia, wound infection, fly strike. bacillosis is suspected. For fungal infections, drugs
from the azole group (e.g. itraconazole) may be
NON-INFECTIOUS DISEASES OF considered. With the patient under GA, the drug is
THE RESPIRATORY SYSTEM instilled into the nose and left in situ for 1 hour.
Sinusitis is addressed by surgical drainage (and
Conditions affecting the nasal tooth removal if involved in the aetiology) and
passages and sinuses repeated flushing, with concurrent antibiosis.
Overview
Various conditions may lead to narrowing of the Laryngeal problems
nasal passageways, resulting in dyspnoea. Overview
Laryngeal problems are occasionally seen in both
Aetiology adults and kids, typically affecting individuals
Obstruction of the nasal passages may be caused by only.
trauma, neoplasia, foreign bodies or infection of the
nostrils, turbinate bones or sinuses. Actinobacillus lig- Aetiology
nierisi infection occasionally occurs in the nasal mucosa, Damage to the laryngeal mucosa allows opportunis-
producing granulomatous lesions. Other infections tic pathogens such as Fusobacterium necrophorum to
include opportunist pathogens such as Trueperella pyo- establish a necrotic laryngitis or abscess (Fig. 6.10).
genes that gain entry following trauma or exposure of Drenching gun injury (see Chapter 5) is an example
the frontal sinuses after dehorning. The sheep (Oestrus of such trauma and should be considered if several
ovis) or deer bot fly can lead to nasal myiasis. Sinusitis animals are affected. An equivalent to the distinct
may occur secondary to maxillary tooth abscessation. disease of calf diphtheria is seldom recognised in
goats. A genetic predisposition to narrow upper
Clinical presentation airways, as in some cattle and sheep breeds, has not
Often noticeable are an abnormal nasal discharge, been reported in goats.
reduced or absent air flow through one or both nos- The laryngeal infection is often complicated by
trils, stertorous breathing in cases of partial obstruc- local oedema, which is self-perpetuating by forced
tion, unpleasant smell of exhaled breath and pain respiratory movements. Paralysis of the vocal folds
and dull resonance on percussion of the frontal or may also occur.
maxillary sinuses.
Diagnosis
Direct inspection is only possible in the most rostral
section. Useful imaging modalities are endoscopy,
radiography, CT and MRI. Culture and biopsy are
used to establish the aetiology.
Nasal discharge is also seen with some ocular abnor-
malities and with pathogens causing primarily tra-
cheitis and pneumonia. Stertor may be caused by
laryngeal disorders.
Anti-inflammatory therapy is indicated for most con- Fig. 6.10 Unilateral laryngeal abscess (post-mortem
ditions. For infectious causes, prolonged antibiosis is specimen, 2-week-old alpaca).
170 Chapter 6
Clinical presentation and suturing it to the skin opening, can also be used
An inspiratory stertor is evident and the goat com- in refractory cases.
monly adopts an air-hunger position. Astute owners
may report a change in the goat’s bleating. Aspiration pneumonia
Overview
Diagnosis Aspiration pneumonia affects individual animals,
Examination of the oropharynx by laryngoscope, and has a guarded prognosis.
speculum or endoscopy shows oedema and infec-
tious plaques of the arytenoid cartilages (Fig. 6.11). Aetiology
Common causes are regurgitation and inhalation of
Differential diagnosis rumen fluid during sedation or anaesthesia, oral med-
Enlarged retropharyngeal lymph nodes, partial nasal ication (e.g. propylene glycol) or milk or fluid therapy
obstruction or external pressure onto the trachea (e.g. administered via a stomach tube. It can also arise in
thymoma) cause a similar stertor. Ultrasonography animals with compromised swallowing (e.g. listeriosis
is useful to confirm these conditions. or rhododendron toxicity [see Chapter 16]).

Antibiosis for 7–14 days (e.g. oxytetracycline, ‘poten- Usually sudden onset of respiratory distress.
tiated’ penicillin). High-dose corticosteroid is given Opportunistic pathogens such as T. pyogenes soon
for severe laryngeal stertor to reduce the oedema become established with the development of a severe
and inflammation (e.g. starting dose of 0.5 mg/kg pneumonia, leading to ventral consolidation of the
on day 1, reducing to 0.25 mg/kg on days 2 and 3, lungs. Increased adventitious sounds, and decreased
then 0.15 mg/kg on days 4 and 5). Tracheostomy resonance on percussion of dependent parts of ante-
may be necessary in cases that do not respond to rior lobes, are found. Pyrexia is common.
steroid therapy. Occasionally, surgical drainage of
abscesses may be necessary. Creating a laryngeal Diagnosis
fistula, by splitting the cricoid cartilage length wise History will support clinical suspicion. Radiography
may be used to confirm the diagnosis.
Acute infectious pneumonia is the main differential
diagnosis. Traumatic causes, leading to haemothorax
or diaphragmatic hernia, are ruled out through his-
tory and imaging techniques.
Treatment consists of aggressive antibiosis (see
Treatment principles), NSAIDs and general nursing
care. Prevention relies on adequate starvation prior
to GA and the use of cuffed endotracheal tubes, and
proper technique when administering oral medica-
tion (see Chapter 1).
Pleural effusion
Fig. 6.11 Endoscopic view of bilateral necrotic Overview
laryngitis (calf). Note the thickened and ulcerated Pleural effusion is a potentially life-threatening con-
plaque on the arytenoid. dition, especially if severe and bilateral.
Aetiology Pneumothorax
Haemothorax caused by trauma. A pyothorax is very Overview
occasionally seen secondary to traumatic reticulo- Pneumothorax is a serious but, if unilateral, rarely
pericarditis or ruptured lung abscesses. Effusion life-threatening condition.
may be due to inflammatory processes (e.g. broncho-
pneumonia), hypoproteinaemia or severe uraemia. Aetiology
May result from trauma, including to neonates dur-
Clinical presentation ing the birthing process, or from ruptured emphy-
Dyspnoea, detection of a fluid line on percussion and sematous bullae.
signs of impaired venous return. If pleuritis is pres-
ent, signs of thoracic pain and friction sounds on aus- Clinical presentation
cultation. Additional signs depend on the cause, such Because of the complete mediastinum, collapse tends
as anaemia in cases of haemothorax or pain in the to be unilateral. A disparity in lung sounds between
anterior abdomen with traumatic reticuloperitonitis. left and right side is evident, with abnormal reso-
nance on percussion (which may be high pitched).
Diagnosis The goat displays inspiratory dyspnoea with marked
Confirmed with ultrasonography (Fig. 6.12), thora- abdominal effort, and possibly cyanosis. If traumatic
cocentesis and radiography. in origin, rib fractures may be present, with pain on
palpation evident. Subcutaneous emphysema is often
Differential diagnosis present.
Any other respiratory condition for dyspnoea. A fluid
line on percussion is practically pathognomonic. Diagnosis
Clinical signs are highly suggestive, with radiogra-
Treatment/management/control phy used to confirm the diagnosis.
Treatment needs to address the primary problem,
combined with drainage of the effusion. The latter Differential diagnosis
can be difficult in ruminants because of their ten- A diaphragmatic hernia may present similarly and is
dency to wall-off infection. Aggressive antibiosis ruled out using radiography.
(see Treatment principles) and NSAIDs.
Wound closure and care as required, and prophy-
lactic antibiosis if pneumothorax resulting from an
external puncture is suspected. If possible, the air
should be aspirated via thoracocentesis or via a tho-
racostomy tube. Otherwise, supportive therapy is
provided until the air in the thoracic cavity has been
absorbed.
Toxicities
Irritant gases or fumes
A variety of gases or fumes can cause an inflamma-
tory response in the respiratory tract. Of particu-
lar interest is nitrogen dioxide (NO2), generated
Fig. 6.12 Pleural effusion showing as dark in the first few days of silage fermentation. Crops
(echolucent) fluid on ultrasonography. The lung lobe of low dry matter or with high nitrate contents
can typically be seen ‘floating’ back and forth in line (e.g. rain close to harvest, late fertilisation) pro-
with respiration on a real-time scan. duce large amounts of the gas. It does not usually
172 Chapter 6
cause any problems in open, well-ventilated silage Aetiology

clamps, but cases of intoxication have occurred CCPP is caused by Mycoplasma capricolum subsp. cap-
where animal housing is close to a clamp with poor ripneumoniae, a very fragile organism that is not able
ventilation. NO2 is heavier than air and collects to exist for long in the external environment. On
around clamp walls. Once inhaled, it dissolves in average it survives outside the host for up to 3 days in
the moisture of the airways, forming a corrosive tropical areas and up to 2 weeks in temperate zones.
acid. It can be lethal to the animal, and is a work
place hazard. Pathophysiology
The incubation period under natural conditions
Snake bites is commonly 6–10 days, but may be prolonged
Snake bites commonly lead to pyrexia, tachypnoea (3–4 weeks). Some experimentally infected goats
and respiratory distress. Tracheotomy should be develop fever as soon as 3 days after inoculation and
considered in severely affected animals. Supportive respiratory signs as early as 5 days, but others do not
therapy includes corticosteroids and i/v fluids. become ill until up to 41 days after exposure. CCPP
Venom antiserum is given where the snake has been is highly contagious: disease is transmitted during
identified. close contact by the inhalation of respiratory droplets.
Chronic carriers may exist, but this remains unproven,
Neoplasia although there are reports of outbreaks developing in
In older goats metastatic tumour deposits may be endemic areas when apparently healthy goats were
identified in lung tissue, potentially compromis- introduced into clean herds. Outbreaks of the disease
ing lung function. Other clinical signs will vary often occur after heavy rains (e.g. after the monsoons
depending on the primary site and tissue affected. in India), after cold spells or after transportation over
One of the most common sites for neoplasia to long distances. This may be because recovered carrier
develop in older goats is the thymus gland. Some animals shed the infectious agent after the stress of
tumours are benign and usually well-differentiated/ sudden climatic or environmental changes.
encapsulated (thymoma), others are more diffuse
locally and may metastasise (thymic lymphosar- Clinical presentation
coma). Both can become very large and cause respi- Affected goats may simply be found dead. In acute
ratory distress. This is described in more detail in infection there is pyrexia (41–43°C), lethargy and
Chapter 7. anorexia, followed within 2–3 days by coughing and
laboured respiration (Fig. 6.13). Coughing becomes
INFECTIOUS DISEASES OF THE

RESPIRATORY SYSTEM
Contagious caprine
pleuropneumonia
Definition/overview
Contagious caprine pleuropneumonia (CCPP) is one
of the most severe diseases of goats worldwide. It
affects the respiratory tract and is extremely conta-
gious and frequently fatal. In naive herds, the mor-
bidity rate may reach 100% and the mortality rate
can be as high as 80%. CCPP causes major economic
losses in East Africa and the Middle East, where it is Fig. 6.13 Goat kid in the terminal stages of CCPP.
endemic. It is an OIE scheduled disease and is notifi- (© Crown Copyright 2017. Used with kind permission
able in many countries. of the Animal and Plant Health Agency.)
more frequent, violent and productive. In the final Differential diagnosis

stages of disease, the goat may not be able to move Diagnosis of CCPP can be complicated, particu-
and adopts a marked air-hunger position. Saliva can larly in those areas where it is endemic. The caus-
drip continuously from the mouth and the animal ative organism is readily contagious and fatal to
may grunt or bleat in pain. Frothy nasal discharge goats of all ages and both sexes, but rarely affects
and stringy saliva may be seen terminally. Pregnant sheep, and does not affect cattle where these are
goats may abort. co-grazed. The primary differential diagnoses
include:
Diagnosis
CCPP should be suspected in the field when a highly •• Peste des petits ruminants (PPR), to which sheep
contagious disease occurs in a herd characterised by are also susceptible.
pyrexia of 41°C or greater, severe respiratory distress, •• Pasteurellosis, which can be tentatively
high morbidity and mortality, and the characteristic differentiated at PME on the basis of the
gross pathology. At post-mortem examination (PME), distribution of gross lung lesions.
there is invariably a large amount of straw coloured fluid •• Contagious agalactia syndrome, in which the
within the chest cavity (Fig. 6.14), the result of a sero- pneumonia is accompanied by prominent lesions
fibrinous pleuritis (Fig. 6.15). There is marked consoli- in other organs, and is caused by another distinct
dation/hepatisation of whole lung lobes, which is often mycoplasma organism.
unilateral. Pea-sized, yellow nodules may be found in the
lungs, often surrounded by areas of congestion. Some Treatment/management/control
long-term survivors have chronic pleuropneumonia or As CCPP is an OIE scheduled disease, most control,
chronic pleuritis, with encapsulation of acute lesions and eradication, surveillance and reporting protocols are
numerous adhesions to the chest wall. regulated on a country by country basis.
A definitive diagnosis can be made by isolating
M. capripneumoniae from lung tissue or pleural fluid at Pasteurellosis
necropsy. Serology is considered to be of minimal value Definition/overview
due to the acute nature of the disease and problems Pasteurellosis occurs in goats worldwide as either a
related to cross-reaction with other Mycoplasma spp. primary or a secondary bronchopneumonia.
Fig. 6.14 Large quantity of clear fluid in the thoracic Fig. 6.15 Fibrinopurulent exudate covering the lung
cavity in a case with CCPP. (© Crown Copyright 2017. surface in a case with CCPP. (© Crown Copyright
Used with kind permission of the Animal and Plant 2017. Used with kind permission of the Animal and
Health Agency.) Plant Health Agency.)
174 Chapter 6
Aetiology can be cultured. Additional laboratory techniques

Caused predominantly by Mannheimia haemolytica or may identify concurrent exacerbating infections
Pasteurella multocida singly or in combination. such as mycoplasmosis (M. ovipneumoniae or M. argi-
nini) or lungworm.
Pathophysiology
Both organisms are commensal in the upper respi- Differential diagnosis
ratory tract of many goats, with disease occurring The most important differential diagnosis is CCPP.
following invasion of lung tissue. Although this
invasion may be the result of concurrent infection Treatment/management/control
with, for example, Mycoplasma spp., more com- In the face of an outbreak, attention should be
monly it occurs as a result of management induced paid to identifying the likely underlying stress
stress factors. The disease occurs most commonly in factors and addressing any management short-
young, intensively reared goats in which overcrowd- comings (e.g. reducing stocking rates, increasing
ing, poor ventilation and a dusty environment are all ventilation without making buildings too cold or
contributing factors. draughty, ensuring attention to dry bedding to
reduce condensation). Treatment of clinical cases
Clinical presentation is based on anti-inflammatory therapy and paren-
In peracute disease, affected goats can be found teral antibiosis.
dead. More commonly, there is a rapid onset of clini- There are Pasteurella/Mannheimia vaccines
cal signs including pyrexia, lethargy, a mucopurulent available and these are used widely in the sheep
nasal discharge, dyspnoea and coughing (Fig. 6.16). sector, often marketed as a multivalent clostridial/
pasteurellosis vaccine. In the UK, current advice
Diagnosis is to vaccinate against clostridial infection and
In the live goat, the clinical presentation is fairly pasteurellosis in two separate programmes, rather
characteristic. Ultrasonography may highlight the than to use these combined vaccines (due to the
marked consolidation and pleurisy of the cranioven- perceived poorer immune response to vaccination
tral lung lobes. Bacteriology of nasal swabs is of no in goats).
real value as the causative organisms are commen-
sal in this site. At PME, there is commonly a clearly Parasitic pneumonia
demarcated bilateral cranioventral lung consolida- Definition/overview
tion (Fig. 6.17), from which the causative organism Parasitic pneumonia occurs in goats worldwide.
Fig. 6.16 Goat kid showing profound depression and Fig. 6.17 Lungs showing severe cranioventral lung
respiratory distress. consolidation.
Aetiology asymptomatic and only identified as an incidental

The two most common parasites are Dictyocaulus finding at PME. In heavy infestations, respiratory
filaria and Muellerius capillaris. D. filaria has a direct signs may be very subtle and easily overlooked, but
life cycle: adults living in the airways produce 1st cases have been described in which exercise intol-
stage larvae (L1), which are coughed up, swallowed erance was a feature, with infected goats lagging
and appear in faeces on the pasture. Development behind others when driven.
continues to L3, and these can survive in a free-
living form on pasture, completing the lifecycle if Diagnosis
ingested. The life cycle of M. capillaris is an indirect In patent infections, larvae of both parasites can
one, involving a variety of slugs and snails acting as be readily identified in faeces by the Baermann
intermediate hosts for the infective larvae voided in technique. At PME, D. filaria parasites can be
faeces. identified in the airways (Fig. 6.18), and other
non-specific findings may include focal areas of
Pathophysiology consolidation near the caudal lung margins and
The physical presence of D. filaria in the airways emphysema. In heavy M. capillaris infestation, lar-
causes irritation to the lining of the airways. Heavy vae can be readily identified histologically in lung
infestation may lead to bronchitis/bronchiolitis and sections (Fig. 6.19).
pulmonary emphysema. M. capillaris by comparison
completes its life cycle in the deeper lung tissue at Differential diagnosis
alveolar level, where in heavy infestations the devel- Coughing due to D. filaria infestation needs to be
opmental stages can be identified histologically. differentiated from other causes, including pasteu-
rellosis, aspiration pneumonia, allergic pneumonitis
Clinical presentation and congestive heart failure.
Goats infected with D. filaria most commonly
cough due to tracheal and bronchial irritation, Treatment/management/control
which in heavy infestation leads to progressive The management, treatment and control of lung-
dyspnoea and weight loss, often in association worm in goats should be a component part of
with secondary bacterial infection. In compari- the control strategy for parasitic gastroenteritis
son, M. capillaris infestation in many goats may be (see Chapter 5, pp. 154–157).
Fig. 6.18 Dictyocaulus filaria parasites visible in the

airways on post-mortem examination. (Image courtesy
RVC-AHVLA Surveillance Centre.)
Fig. 6.19 Muellerius capillaris larvae evident histologi-
cally in lung tissue (in cross and longitudinal section).
176 Chapter 6
MISCELLANEOUS CONDITIONS Caseous lymphadenitis

Although caseous lymphadenitis typically presents as
Other Mycoplasma organisms abscesses causing enlargement of the superficial
Respiratory infection can be a feature of contagious lymph nodes, pulmonary abscesses and associated
agalactia (see Chapter 12). Mycoplasma ovipneumoniae lymph node enlargement can occur in housed goats
and Mycoplasma arginini can both cause relatively (Fig. 6.22) in which infection rates (and hence envi-
mild respiratory signs in isolation, but M. ovipneu- ronmental contamination with the causative organ-
moniae in particular is a common precursor to pneu- ism) can be high (see Chapter 7).
monic pasteurellosis.
Tuberculosis
Peste des petits ruminants Although tuberculosis is generally considered to
(syn. goat plague) be less of a problem in goats worldwide than in
PPR presents with a sudden onset pyrexia, with cattle, goats can become infected, predominantly
severe depression, loss of appetite and initially a with Mycobacterium bovis or Mycobacterium avium
clear nasal discharge. The nasal discharge becomes (see Chapter 17). Typical caseous or more liquid
thicker and yellow, often becoming so profuse pus-containing abscesses can develop in lung tis-
that it forms a crust that blocks the nostrils, caus- sue (Fig. 6.23) and associated lymph nodes. Heavy
ing respiratory distress, and goats may sneeze infection can lead to respiratory distress and cough-
persistently in an effort to clear the debris (see ing, but infection can also be subclinical.
Chapter 5).
Fungal pneumonia/
Caprine arthritis encephalitis allergic pneumonitis
One of the many manifestations of caprine Exposure to mouldy feed or bedding, particularly
arthritis encephalitis is an interstitial pneumo- in poorly ventilated buildings, can lead to inha-
nitis (Figs. 6.20, 6.21). This may be mild and non- lation of fungal spores (e.g. Aspergillus fumigatus),
apparent clinically and only identified on PME. resulting in a fungal pneumonia. This is most com-
However, it can cause clinical signs, including an monly confirmed at PME, when typical branching
increasing dyspnoea, exercise intolerance and a mild hyphae can be identified histologically colonising
cough, co-existing with other more typical signs (see lung tissue. One other sequela, more commonly
Chapter 9). identified in older goats following repetitive
Fig. 6.20 Cut section of lung with caprine arthritis Fig. 6.21 Caprine arthritis encephalitis pneumonitis
encephalitis pneumonitis. The lungs appear firm in showing mononuclear cell infiltrates in the alveolar
consistency. septae and the perivascular and peribronchial areas.
Fig. 6.22 Severe caseous lymphadenitis Fig. 6.23 Tuberculosis should be considered when
associated multifocal abscessation in lung tissue. presented with a caseous lung abscess.
Corynebacterium pseudotuberculosis was isolated.
exposure, is an allergic pneumonitis somewhat Vena cava thrombosis

analogous to the condition referred to as farmer’s In this condition, emboli pass to the lungs, resulting
lung in humans. This condition is worse during in abscessation, chronic pneumonia and lesions in
the winter housing period, but rapidly resolves the pulmonary arterioles. Less acute cases may pres-
when goats are turned out. It can vary from mild ent with a painful cough, pallor of the mucous mem-
coughing to more severe respiratory distress in branes, thoracic pain and increased lung sounds.
affected individuals. (See Chapter 7 for a full description.)
CHAPTER 7
CARDIOVASCULAR DISEASE AND DISORDERS

OF THE HAEMATOPOIETIC SYSTEM 179
NORMAL STRUCTURE AND FUNCTION Auscultation also aims to establish adventitious

sounds and, where present, their points of maxi-
The goat’s heart has a marked cone shape. It sits mum intensity (PMI). For this it is useful to know
upright in the thorax, at almost 90 degrees to the the location of the heart valves. On the left, the pul-
sternum, with five sevenths lying to the left of the monary valve is in the 3rd intercostal space and the
midline. It reaches from the 2nd to the 5th rib in atrial and mitral valves in the 4th intercostal space,
width, with a height equivalent to approximately half with the atrial valve dorsal to the mitral. The tricus-
the height of the thorax (the heart base is at the level pid valve is on the right in the 3rd intercostal space.
of the midpoint of the first rib). Part of the left-hand In young tachypnoeic goats, palpation of the chest
side is not covered by lung lobes. wall can be very useful to detect an abnormal car-
Of interest for post-mortem examination (PME) diac thrill inaudible on auscultation. The heart beat
are a normal reference weight of roughly 0.5% of the may be palpable in the 4th intercostal space on the
animal’s bodyweight and the typical patches of sub- left, although this becomes difficult in goats in good
endocardial fat tissue. body condition. A continuous rubbing sound could
indicate pericarditis. Percussion may highlight an
CLINICAL EXAMINATION OF THE enlarged heart shadow. It helps cardiac assessment if
CARDIOVASCULAR SYSTEM the front leg is pulled forward.
The jugular veins are assessed for efficiency of
Clinical assessment filling, speed of deflation and evidence of permanent
Examination of any patient should include actively distension. A jugular pulse half way up the neck is
looking for signs of cardiovascular (CV) disease. often present in the normal goat standing with a low-
General observations that may suggest a CV prob- ered head. The femoral artery is useful for assessing
lem include dependent oedema (especially the bris- pulse quality and possible deficits.
ket or mandible), dyspnoea, exercise intolerance or Normal mucous membrane colour is dark
changes of parameters during exercise, weight loss salmon pink and best assessed using the conjunc-
or poor weight gain, poor or fluctuating milk yield, tival membranes. Paleness suggests either anaemia
cold surface temperature or variable skin tempera- or poor perfusion. Cyanosis is seen with severe
ture between body areas, intermittent fever and pos- respiratory disease or left-sided heart failure.
tural abnormalities such as abducted elbows. Jaundice may be present with haemolytic anaemia.
For adults, a normal heart rate of 60–80 bpm is A capillary refill time of over 2 seconds suggests
commonly cited in the literature. However, several poor perfusion.
studies suggest a higher average resting heart rate of Typical signs of right-sided heart failure are
95 bpm, with a range of 70–120. The heart rate may caused by impaired venous return and venous s tasis,
increase during pregnancy. Reported rates in kids and include filling abnormalities of jugular veins,
are 200–220 bpm up to 1 month old, and 140 bpm brisket oedema, poor exercise tolerance and asci-
up to 6 months old. The two heart sounds S1 and S2 tes. Ascites is rare without signs of ventral oedema.
are typically heard. Respiratory sinus arrhythmia is An abdominal fluid thrill can be readily elicited in
common in goats. affected goats. Left-sided failure typically causes
180 Chapter 7
pulmonary oedema, dyspnoea, further exercise Pericardiocentesis

intolerance and cyanosis. Aspiration using a 5–10 cm long hypodermic needle
Clinical signs may not be evident until an through the skin and chest wall under local anaes-
advanced stage of disease, which is an important thesia is a simple procedure. Ultrasound guidance is
consideration for prognosis. useful. Colour and odour of fluid may suggest infec-
tion, and the sample may be submitted for cytology,
Ancillary diagnostics protein estimation and culture.
Ultrasonography
Ultrasonography is very useful for detecting valve Blood sampling and basic
anomalies, pericardial effusions, hypertrophy and in-house analysis
ascites. A linear array probe will allow some assess- Blood is most commonly collected from the jugu-
ment, but because of the narrow intercostal spaces, lar vein, but the cephalic or saphenous veins are also
a sector probe is preferable. Colour flow imaging suitable (following the same technique as in dogs).
using Doppler is useful for defects such as ventricu- For a jugular sample from an adult, an assistant
lar septal defect, patent ductus arteriosus (PDA) or stands astride over the goat just in front of its shoul-
valve insufficiency. ders, and with the goat’s backend against a wall or
corner. With one hand under the chin and the other
Electrocardiography on the poll, the assistant holds the head and neck in
Electrocardiography (ECG) can be used to establish extension and as straight along the longitudinal axis
rate, rhythm and some gross anomalies (Fig. 7.1). as possible. The thumb of the non-dominant hand is
The considerable variation between goats (in par- pressed into the readily identifiable jugular groove,
ticular in QRS pattern) means that further clinical about halfway down the neck, to raise the vein. In
application is limited. In addition, cardiac depolari- heavily coated goats (where clipping is undesired), it
sation is diffuse, therefore vectors are rarely used. can be useful to release and raise the vein a few times
Forestomach fill affects the heart axis. to identify its exact location. Surgical spirit is applied
A useful configuration is the base-apex lead sys- prior to needle insertion. A vacutainer or 5–20 ml
tem with RA over the heart base, LA over the apex syringe, with a 19–21 gauge, 2.5 cm (1 in) needle, is
and the N lead on the withers. The effect of position used.
of the goat during ECG on readings is minor, and
the pattern within an individual goat is quite con-
stant from reading to reading.
Dysrhythmia may be associated with metabolic
disease or septic foci, especially in the abdomen.
Atrial fibrillation – with its characteristic F waves –
is occasionally seen, and is almost always associated
with metabolic problems including hypochloraemia,
hypokalaemia and metabolic alkalosis.
Radiography
Some details of internal cardiac structures may be
detected, but typically radiography is only useful
for evaluating the overall size of the heart. A vena
cava thrombus is sometimes detectable, as are radi-
opaque foreign bodies associated with traumatic
reticulitis. Fig. 7.1 Smartphone technology allows capturing of
For positioning, it is important to pull the front an ECG trace and posting to a specialist for analysis, if
legs as far forward as possible, to limit any shadowing. desired (e.g. AliveCorTM ).
C a r diova sc u l a r D is e a s e a n d D isor de r s of t h e H a e m at op oi e t ic Sys t e m 181
With the exception of haematocrit and total pro- •• Heartwater (cowdriosis) is an infectious non-
tein, haematological and biochemical evaluation contagious tick-borne rickettsial disease of
rarely gives useful information without a thorough goats and other ruminants. Heartwater occurs
clinical examination (see Appendix: Laboratory in nearly all the sub-Saharan countries of
Reference Intervals). Blood culture may be attempted Africa and in the surrounding islands. The
in cases of suspected endocarditis, but bacteraemia is disease is also reported in the Caribbean,
often intermittent. Table 7.1 shows how interpreta- potentially posing a threat to the American
tion of haematocrit and total protein may be used to mainland.
broadly differentiate disorders.
Septal defects
CARDIOVASCULAR DISEASE Overview
Of the congenital defects affecting the heart, septal
There are few reports of primary heart disease in defects are the most common.
the goat worldwide, although cardiac failure and its
sequelae may be a secondary feature in many sys- Aetiology
temic infections. The non-athletic nature of the Ventricular defects are more common than atrial
species, and common group husbandry, may mask a defects. Aetiology frequently remains unestablished.
higher incidence. However, familial cases have been reported, suggest-
Specific CV conditions include: ing a genetic component in some instances.
•• Congenital cardiac abnormalities. Clinical presentation

•• Nutritional muscular dystrophy (white muscle Ill-thrift, poor growth (Fig. 7.2), lethargy and
disease). Can affect cardiac muscle, resulting in exercise intolerance may be noted, but a number of
sudden death (see Chapter 9). affected animals show no marked CV compromise.
•• Foot and mouth disease. During an outbreak, An atrial defect typically causes more severe and
kids may die suddenly as a result of a viral acute clinical signs. A palpable thrill is often present
myocarditis (see Chapter 17). over the thoracic wall, especially in kids.
•• Cardiotoxic plants. These can result in heart A pansystolic murmur is heard on both sides of the
failure and sudden death if ingested and include chest, but especially on the right (direction of blood
yew (Taxus baccata), foxglove (Digitalis purpurea) flow is from high pressure left ventricle to right).
and oleander (Nerium oleander). Plant poisoning The PMI is on the right, and the murmur is ‘diago-
is discussed in more detail in Chapter 16. nal’ with greatest intensity towards the caudal aspect
Table 7.1 Interpretation of haematocrit (Hct) in combination with total plasma protein (TP).
HCT TP INTERPRETATION
Normal Low Protein-losing enteropathy or nephropathy; severe liver disease; vasculitis
High Increased globulin production (e.g. chronic inflammation); anaemia masked by dehydration
Increased Low Combination of splenic contraction and protein loss
Normal Splenic contraction; erythrocytosis; hypoproteinaemia masked by dehydration
High Dehydration
Decreased Low Substantial acute blood loss (recent or ongoing); overhydration
Normal Increased destruction or reduced formation of erythrocytes; chronic blood loss
High Inflammatory processes; multiple myeloma; lymphoproliferative diseases
Source: Adapted from Meyer DJ, Harvey JW (2004) Veterinary Laboratory Medicine. Saunders, Philadephia.
182 Chapter 7
of the right side of the heart. Very occasionally there Diagnosis

is also a diastolic murmur due to aortic valve insuf- The character of the murmur is suggestive, and
ficiency (because of lack of support for the valve by ultrasonography is used to confirm the diagnosis
the defective septum). The degree of murmur varies (Fig. 7.3). Ventricular defects are often located very
depending on the size of the defect; in general, the dorsally and can go unnoticed without thorough
smaller the defect the more turbulence and friction examination. Small defects may be overlooked dur-
are caused and hence the louder the murmur. ing PME (Fig. 7.4).
Chronic changes include poor peripheral circula-
tion and overload of the right ventricle (leading to Differential diagnosis
hypertrophy) and pulmonary circulation. Fibrosis of Other causes of cardiac murmurs such as PDA (con-
pulmonary vessels can result, eventually leading to tinuous murmur of varying intensity [‘machinery-
a right-to-left shunt. Endocarditis may result from like’]), patent foramen ovale (closure may be delayed
turbulence. until 7–10 days old; loud murmur at level of heart
Concurrent congenital defects may be present base), endo- or pericarditis or more complex defects
and should be checked for. such as tetralogy of Fallot.
Animals with a relatively small defect may reach adult-
hood and can carry pregnancies and lactate success-
fully for several years. However, the owner should be
forewarned that sudden death is possible at any time.
Medical treatment is not effective and surgical
intervention rarely undertaken. Euthanasia is the
best option if severe compromise of cardiac function
is present.
Endocarditis
Overview
Fig. 7.2 Poor growth, as in the twin on the right, can Endocarditis is a common cardiac condition of adult
indicate a congenital cardiac defect. animals, typically carrying a guarded prognosis.
Fig. 7.3 Ultrasonography image showing a Fig. 7.4 Ventricular septal defect indicated by
ventricular septal defect (dotted line). a sampling tube inserted into the defect. (Image
courtesy Peter G.G. Jackson.)
Aetiology
Mostly bacterial, including Trueperella pyogenes,
Group D streptococci, staphylococci and Pasteurella
spp. The condition may arise from a septic focus
elsewhere in the body (e.g. udder, uterus, subcu-
taneous abscess) or from poor intravenous injec-
tion technique. Circulating bacteria from such foci
adhere to the endocardium, establishing infection.
Valves, especially the tricuspid, are colonised with
outgrowths developing and eventual compromise of X
valve function leading to cardiac failure. There is a
risk of emboli breaking off from affected areas, lead-
ing to bacterial colonisation and emboli elsewhere.
Early signs are not necessarily cardiac in nature. Fig. 7.5 Ultrasonographic cross-section through the
Intermittent or persistent episodes of pyrexia with heart (X), showing pericardial effusion (lines) in a case
few other signs are common in the early stage, with an with mitral valve insufficiency.
apparent response to antimicrobial therapy. Shifting
leg lameness is occasionally seen. Later signs include delay terminal heart failure. An affected goat
poor exercise tolerance, positive wither’s pinch test, is unfit for slaughter for human consumption,
heart murmur with the PMI over a particular valve because of recurrent bacteraemia.
and, occasionally, fluid sounds originating from
pericardial sac effusion. Terminally, there are signs Pericarditis
of right-sided heart failure (see earlier). Poor perfu- Overview
sion leads to compromised function of other organs Pericarditis typically affects adult goats and carries a
(e.g. kidneys), with associated signs. Anaemia may be poor prognosis.
seen because of red blood cell destruction by blood
turbulence around the affected valve. Aetiology
May arise sporadically from a focus of infection else-
Diagnosis where in the body or as part of traumatic reticuloperi-
History, clinical signs and ultrasonography. Where carditis. With the latter, infection may also involve
pericardial effusion is present (Fig. 7.5), a centesis local lung tissue or cause a pyothorax. Pathogens
will yield clear fluid with a low cell count. involved include T. pyogenes, Pasteurella spp., Histophilus
somni, staphylococci, streptococci and Mycoplasma
Differential diagnosis spp. After accumulation of infected fluid and debris,
Other causes of right-sided heart failure, especially fibrosis and adherence of the pericardium to the heart
pericarditis (cloudy fluid both on ultrasonography follow, leading to compression of the heart and com-
and centesis) and cardiomyopathies. promised cardiac function (Fig. 7.6). Toxaemia may
develop directly from the pericardial pathogens or
Treatment/management/control as a result of organ failure caused by poor perfusion.
May be too late by the time symptoms appear. Eventually, heart failure occurs.
Intense and prolonged antibiotic therapy can be
tried in early cases. Blood culture prior to com- Clinical presentation
mencing antibiosis is ideal, but intermittent shed- In cases of traumatic reticulopericarditis, premoni-
ding can lead to lack of pathogen growth. Diuretic tory signs include a short episode of pyrexia of
therapy may give short-term relief, but does not unknown origin, anorexia and rumen stasis (possibly
184 Chapter 7
Pleural effusion may also result in muffled heart
sounds and can be confirmed on ultrasonography.
Prognosis is poor, in particular once signs of heart
failure are present. High-dose antibiosis and drain-
age and flushing of the pericardium may give tem-
porary relief. Diuresis can result in temporary
relief and may be useful to support a dam to the
end of gestation. Surgical stripping of the pericar-
dium or fenestration carries a guarded prognosis.
An affected goat is unfit for slaughter for human
consumption.
Fig. 7.6 Pericarditis causing fibrosis and adhesions. Cardiomyopathies

The pericardium has been peeled back from the heart. Overview
Cardiomyopathies in young animals are associated
associated with the initial foreign body penetration). with tocopherol (vitamin E) and selenium deficiency.
The goat appears to respond to antibiosis, until the There are other rarer causes in adults.
pericarditis becomes fully established.
In general, clinical signs often vary and progress Aetiology
with changing pathology. Early signs include the Cardiac hypertrophy and myocardial degenera-
goat being uncomfortable and reluctant to move, tion in young animals is associated with tocopherol
with a fluctuating but marked pyrexia and reduced (v itamin E) and selenium deficiency (see Chapter 15).
rumen activity. Thoracic pain is evident through an A condition similar to dilated cardiomyopathy of
arched back, positive wither’s pinch test, grunting adult cattle has been described in goats. Ionophore
associated with breathing (especially when recum- (e.g. monensin) poisoning may result in coagulative
bent) and pain over the thoracic wall. Auscultation necrosis of cardiac muscle. Other reported toxins
often reveals a pericardial rub associated with heart include avocado leaves (Persea americana) and mem-
movements, or tinkling sounds from fluid trapped in bers of the Rubiaceae family causing ‘gousiekte’ in
the pericardium. Heart sounds themselves are muf- southern Africa.
fled. Later signs are associated with right-sided heart
failure (see earlier). May see signs of toxaemia or sep- Clinical presentation
ticaemia, and localised pleurisy and pneumonia. Exercise or excitement-induced sudden death with
tocopherol (vitamin E)/selenium deficiency.
Diagnosis Cardiomyopathy in adults is typically character-
Clinical signs are often highly suggestive. ised by signs of right-sided heart failure, often with
Pericardiocentesis yields an often malodorous fluid extensive and severe dependent oedema and body
with a high nucleated cell count; however, in advanced cavity effusions (hydrothorax, ascites). Cardiomegaly
cases free fluid may be absent. Although neutrophilia with ventricular dilation (Fig. 7.7) and hypertrophy
with a left shift and elevated fibrinogen are com- is common.
mon findings on haematology, these are not unique
for this condition. Ultrasonography often shows Diagnosis
echogenic pericardial contents and thickening of the See Chapter 15 for tocopherol (vitamin E)/selenium
pericardium. deficiency.
DISORDERS OF BLOOD VESSELS
Venous thrombosis
Overview
Venous thrombosis may affect any of the major
superficial veins and is often iatrogenic and there-
fore preventable.
Aetiology
LV
Local inflammation or infection, commonly after
RV intravenous injection or catheterisation leading
to trauma of vessel wall, irritation from injected
substances (e.g. calcium) or introduction of infec-
tion. May also result from external trauma of
veins (e.g. compression caused by poor restraint or
entrapment).
Obvious swelling over affected vessels. Initially
Fig. 7.7 Early stage right ventricular dilation in painful and warm, later becoming hard and fibrous.
a yearling animal resulting in thinning of the wall Complications may include tissue necrosis and
(RV = right ventrical; LV = left ventrical). sloughing, leaving the vein exposed. Proliferative
growth of a thrombus may arise if a jugular catheter
Right-sided heart failure is evident on clinical exam- is left in situ for too long, leading to sudden death
ination; however, PME is required to establish the because of occlusion of the right atrium.
cause. On PME there is commonly extensive myocyte Embolus formation (and pulmonary embolism)
degeneration, atrophy, hypertrophy and muscle tissue appears to be rare.
fibrosis and necrosis. The blood vessels of heart, lung,
kidney and lymph nodes may also show abnormalities. Diagnosis
Clinical signs or, in the case of sudden death, throm-
Differential diagnosis bus detected on PME.
Neurological problems for weak or collapsed ani-
mals. Endocarditis or pericarditis for right-sided Differential diagnosis
heart failure. Localised haematoma, foreign body reaction or
insect sting. History and ultrasonography is useful
Treatment/management/control to distinguish.
No rewarding treatment is known. Whether dilated
cardiomyopathy in the goat may be inherited, such as Treatment/management/control
in cattle, is not known. Animals are usually affected Warm water bathing may help speed up the heal-
as young adults, and therefore unlikely to success- ing process. Also consider local (e.g. topical cor-
fully produce offspring. ticosteroid in non-pregnant animals, dimethyl
sulfoxide) or systemic anti-inflammatories, possi-
Other conditions bly antibiotics.
Cor pulmonale has been reported secondary to After accidentally injecting an irritant substance
respiratory disease. Cardiac neoplasia appears to be perivascularly, dilute by injecting saline into the
very rare. perivascular tissue.
186 Chapter 7
If the vein has become exposed after tis- in the pulmonary arterioles. Arteritis and thrombo-
sue sloughing, healing mostly follows with rou- embolism occur and aneurysms may develop in the
tine wound care, and circulation is typically not pulmonary artery. These rupture, causing severe
compromised. haemorrhage into the alveoli and bronchial tubes.
Prevention includes good i/v injection tech- Organisms involved include Fusobacterium necropho-
nique, in particular where irritant solutions are rum and T. pyogenes.
involved: adequate restraint of patient, discarding
needle after drawing up the solution and insert- Clinical presentation
ing a new clean needle into the vein, and intermit- Sudden death in peracute cases, with blood appear-
tently drawing back to check that the needle is still ing at the mouth and nostrils. In less acute cases,
in the vessel. possible signs include a painful cough, haemoptysis,
For i/v catheter placement, attention is paid to pale mucous membranes, thoracic pain, increased
aseptic preparation and adhering to the maximum lung sounds and a haemic murmur. Some animals
dwell time for the type of catheter chosen (e.g. not may show signs of cardiac failure with liver enlarge-
more than 72 hours for short-stay catheters). ment and ascites.
Caudal vena cava thrombosis Diagnosis

Overview The sporadic and often peracute nature of the dis-
Caudal vena cava thrombosis is an occasional sequela ease prevents easy diagnosis, although haemoptysis
to ruminitis and liver abscessation. and anaemia are suggestive. The vena cava abscess
may be seen on radiographs (close to the diaphragm)
Aetiology or with ultrasonography.
The following sequence of events has been sug-
gested: rumenitis (e.g. caused by rumen acido- Differential diagnosis
sis; Fig. 7.8) leads to seeding of bacteria into the Anthrax for sudden death with bleeding. Other
liver and/or caudal vena cava (either direct diffu- causes of anaemia, thoracic pain or cardiac failure.
sion through rumen wall or via portal circulation).
Where initially just liver abscesses form, a result- Treatment/management/control
ing localised phlebitis in the hepatic portion of the Antibiosis is typically unrewarding, with prognosis
caudal vena cava creates abscessation in the vessel very poor especially where haemoptysis is evident.
(Fig. 7.9). From this, emboli pass to the lungs, pro- Others in the group on a similar diet are likely to have
ducing abscessation, chronic pneumonia and lesions suffered rumenitis and liver abscessation as well, and
Fig. 7.8 Signs of rumenitis: loss of papillae and Fig. 7.9 Vena cava thrombus and abscess (removed
scarring (post-mortem specimen). from vessel).
disposal in the near future should be considered. If Thymus

taken to slaughter, the owner should be prepared for The thoracic part of the thymus lies in the dorsal
carcase condemnation. mediastinum in front of the heart. Most of the cervi-
Control involves prevention of rumenitis, in par- cal part lies in the lower one-third of the neck, with
ticular rumen acidosis (see Chapter 5). bilateral limbs reaching all the way to the larynx.
Whether the thymus continues to grow in the kid
Other vascular abnormalities up to puberty, as in the lamb, is unknown. Although
Arterial thrombosis, or vasculitis resulting in the thymus does involute as the animal matures, a
occlusion of peripheral capillaries, may be seen with considerable thoracic remnant can still be found in
severe bacteraemia or septicaemia (e.g. salmonello- 5-year-old goats.
sis) and some toxins (e.g. ergot). This may lead to
necrosis of peripheral tissue, such as the ear tips, Lymph nodes
or the coronary band, resulting in loss of the horn Table 7.2 shows details of the main external lymph
capsule. A thrombus in the middle uterine artery nodes, plus a selection of internal lymph nodes that
is an occasional incidental finding and typically may be of interest during PME.
regresses slowly.
Trauma to superficial vessels may occur from Anaemia
fighting amongst animals, predator or dog attack, Overview
or sharp objects in the animal’s environment. The Anaemia is a common and potentially life-threaten-
mammary vein in the lactating doe is particularly ing condition, with a multitude of aetiologies.
vulnerable. Any severe haemorrhage is treated
accordingly, including blood transfusion where nec- Aetiology
essary. Resulting haematomata are best left alone. Common causes include endoparasites (blood suck-
Portosystemic shunts have been reported in a ing or blood losing such as Haemonchus contortus, liver
variety of breeds, in kids from 1 month to 1 year fluke [and other trematodes], coccidiosis), ectopara-
of age. Typical signs include poor growth and a sites (lice, ticks), blood parasites (babesiosis, ana-
hepatic encephalopathy resulting in neurological plasmosis), chronic inflammatory disease (including
signs. heavy endoparasite burden), haemolysis and haem-
Calcification of blood vessels can be caused by orrhage. Table 7.3 gives an overview of the more
toxicosis with calciferol (vitamin D) or golden oat common causes.
grass (Trisetum flavescens).
DISORDERS OF THE Pale to completely white mucous membranes are the
HAEMATOPOIETIC SYSTEM main clinical indicator (Fig. 7.10).
Normal structure and function Diagnosis

Blood forming organs Haematology will confirm anaemia. In cases of
Primary haematopoiesis (i.e. formation of the haemolytic anaemia, an animal-side urine sample
three lineages of blood cells, namely erythroid can be indicative (urine discolouration and abnor-
cells, lymphocytes and myelocytes) takes place in mal urine dipstick reactions). Where blood para-
the long bones in young animals and mainly in the sites are suspected, it is important to prepare an
pelvis, sternum and vertebrae in adults. Involved air-dried smear immediately after collecting the
in secondary, or extramedullary, formation are blood sample.
the spleen, thymus and lymph nodes (maturation Endoparasite burden should always be investi-
of cells, and activation and some proliferation of gated, bearing in mind that a faecal egg count (FEC)
lymphoid cells). In the fetus, the liver is important may give a false-negative result (e.g. larvae suck-
for haematopoiesis. ing blood in haemonchosis, severe pathology in the
188 Chapter 7
Table 7.2 The main external and selected internal lymph nodes of the goat.
NAME LOCATION SIZE (MM) PALPABLE?

Parotid Caudoventral to mandibular joint, covered by the 10–50 If enlarged
parotid gland
Mandibular Caudoventral mandibular ramus 15–35 Yes
Retropharyngeal (lateral) Below wing of atlas, 2–3 nodes each side 7–28, disc-shaped If enlarged
Prescapular At the cranial edge of the supraspinatus muscle, 35–60 Yes
two-thirds down the shoulder blade
Popliteal 2.5 cm deep between the semitendinosus and 10–25 If enlarged
glutaeobiceps muscles
Subiliac Cranial to quadriceps muscle, about halfway between 50 Yes
the tuber coxae and patella
Supramammary In female: two nodes at base of udder (near pudendal Bean-sized If enlarged
(superficial inguinal) vessels)
Caudal mediastinal Unpaired in midline between thoracic aorta and Small node: 10–30; Internal
oesophagus large node: 100–130
Jejunal In mesenterium, between jejunum and ascending Average 35 (range Internal
colon; typically about 12 nodes (2–25) 3–300)
Intestinal – other Associated with the various sections of small and Average 15–20 Internal
large intestine
Source: Compiled based on data from: Vollmerhaus B (2005) Lymphatisches System. In: Nickel, Schummer, Seiferle - Lehrbuch der Anatomie
der Haustiere, Band III, 4th edn. (eds K-H Habermehl, B Vollmerhaus, H Wilkens et al.) [Lymphatic system. In: Textbook of Anatomy of
Domestic Animals, Vol. III, 4th edn.] Parey Verlag, Stuttgart.
Table 7.3 Known or potential causes of anaemia in goats.
CAUSE COMMENTS
Inflammatory process In particular chronic processes. Blood protein levels often changed
Parasitism In particular Haemonchus contortus and liver fluke, but potentially any severe worm burden. Severe lice or
tick burden
Haemorrhage External (e.g. dog bite, accident) or internal (e.g. accident, obstetrical). (Note: Thick fleece may hide
external injuries.) Also extensive abomasal/duodenal ulceration
Iron deficiency Rare in grazing adults. Possibly microcytosis and hypochromia, especially in chronic cases
Blood parasites If suspected, prepare an air-dried smear immediately after taking blood sample. Examine with Giemsa stain
Haemolysis Nitrate/nitrite ingestion. Red maple leaves (presents with intravascular haemolysis and Heinz bodies).
Onions or brassica species. Haemolytic crisis in chronic copper toxicity
Copper deficiency
Bone marrow Neoplasia or functional abnormalities (e.g. myelodysplastic syndrome)
Coagulopathies Mycoplasma mycoides subsp. mycoides, inherited afibrinogenaemia (factor I deficiency in Saanen goats),
secondary to severe liver disease.
Also possibly snake venom, warfarin, mycotoxins or sweet vernal grass (Anthoxanthum odoratum) toxicosis
to thready character with anaemia), pulse defi-

cit, cold extremities and heart murmur (although
anaemia-induced murmurs can occur).
The primary cause is treated as appropriate, with
supportive nursing care including high-quality
nutrition.
A blood transfusion should be considered in
cases with either severe anaemia (PCV <0.12 l/l) or
rapid blood loss. It may also be of benefit outside
the emergency situation, in particular where there
are no signs of regeneration. Goats have at least
five major blood group systems with a substantial
degree of polymorphism, making exact matching of
Fig. 7.10 Pale mucous membranes (here conjunctiva) donor and recipient difficult. However, in the field
indicate either anaemia or poor perfusion. cross-reactions appear rare, especially during the
first transfusion. Suitable donor animals include
pre-patent period with coccidiosis and liver fluke, non-breeding males or non-pregnant females, at
less correlation between FEC and worm burden least 2 years of age, clinically healthy and ideally
in adult goats). Hypoproteinaemia may be present, from the same breed and herd. A human blood col-
especially with coccidiosis. lection set and its needle are suitable (see Fig. 4.11,
If anaemia is the result of inflammatory disease, p. 92). A 60 kg goat can easily donate 500 ml (from
finding the primary cause can be a challenge. A thor- the jugular vein; sedated if necessary). As a rule-of-
ough clinical examination, blood biochemistry and thumb, one litre of blood will increase the haema-
further diagnostic aids, such as ultrasonography, are tocrit of the recipient by 5%.
of immense value and may have to be repeated if a
diagnosis cannot be established first time round. Milk goitre/thymic enlargement
For prognosis and treatment, establishing whether Overview
the anaemia is regenerative or non-regenerative is of Milk goitre/thymic enlargement is a self-curing
interest. Signs of regeneration include anisocytosis, marked swelling of the cervical parts of the thy-
polychromasia, reticulocytosis and increased num- mus. Anglo-Nubian and Boer goats appear more
bers of metarubricytes. However, these are not con- susceptible.
sistently present and sometimes may be present in
clinically normal animals. In cases with a chronic, Aetiology
non-regenerative anaemia a bone-marrow biopsy is Unknown. Blood and dietary iodine levels are nor-
of value. Under local infiltration anaesthesia, a suit- mal. Investigated cases have been negative for a vari-
able biopsy needle is inserted into the thick part ety of pathogens.
of the sternum. Bone marrow is harvested by 2–4
strong pulls on a 10-ml syringe. A smear is prepared Clinical presentation
immediately. Additional sample material can be Large bilateral swelling just caudal to the mandibu-
stored in EDTA. lar ramus and sometimes underneath the lower jaw
as well. Swelling develops from about 1 week of age,
Differential diagnosis and typically starts regressing from 4–6 months of
The main one to consider is CV compromise, often age. If severe, discomfort and change in vocalisation
presenting with the following clinical findings: may be seen. The swelling must be differentiated
delayed capillary refill time, weak pulse (as opposed from thyroid enlargement.
190 Chapter 7
Diagnosis in goats. Aside from lymph nodes, almost all other

Clinical signs and PME. The cervical part of the tissues may be affected, including synovial mem-
thymus may reach around 200 g in weight. Histology branes and meninges. Sometimes associated with
is normal. bovine leukaemia virus, and occasionally there is
neoplastic involvement of the bone marrow.
Differential diagnosis The thoracic part of the thymus is retained well
Caseous lymphadenitis (CLA) is ruled out by culture. into adulthood, and thymoma is a common neoplasia
General abscessation is confirmed with ultrasonog- in mature goats.
raphy and aspirate. Severe upper respiratory tract
infection leading to reactive lymph node enlarge- Clinical presentation
ment will show associated clinical signs. Typically, a progressive debilitating presentation
in goats over 2 years old. Weight loss and increas-
Treatment/management/control ing weakness are common. Some goats are alert,
None. The apparent success of iodine supplemen- others depressed and inappetent. Depending
tation is highly ambiguous. In addition, forced on the lymph nodes involved, other signs may
reduction of the thymus may negatively influence include ataxia, dysphagia, abdominal pain, dys-
immunocompetence. pnoea, reduced milk yield, diarrhoea, exophthal-
mos, pyrexia and enlargement of superficial lymph
Neoplasia of lymph nodes or thymus nodes.
Overview For mediastinal lesions, tachypnoea and
Multicentric, sporadic or thymic lymphoma or lym- dyspnoea, tachycardia with uni- or bilaterally
phosarcoma (Fig. 7.11), and thymoma are recognised. muffled heart sounds, and pleural effusion are
common findings, as is a pronounced jugular
Aetiology pulse. However, a considerable number of goats
Sporadic forms of lymphoma/lymphosarcoma with thoracic thymomas show no obvious associ-
appear to be more common than multicentric ones ated signs.
Diagnosis
Imaging for internal lesions. Palpation and fine nee-
dle aspirate or biopsy for lesions of external lymph
nodes. Lymphocytosis may be evident on haematol-
ogy. Gross evidence of thymic enlargement is evi-
dent at PME (Fig. 7.12).
The main specific conditions to consider are:
Johne’s disease, CLA, dental disease and endo-
parasitism for progressive weight loss; CLA and
pneumonia for dyspnoea. In cases with ataxia, a
full neurological examination to locate the lesion is
indicated, and caprine arthritis-encephalitis should
be considered.
Fig. 7.11 Lymphosarcoma in a 7-year-old Anglo-
Nubian doe. Retropharyngeal and submandibular Treatment/management/control
lymph nodes were visibly enlarged (note swelling near Symptomatic treatment may be tried, but is often
throat). Internally, lesions were present in lung, liver without noticeable effect. Chemotherapy (cyclo-
and kidneys (and their associated lymph nodes). phosphamide) has been described in sheep.
Swelling disease to 5 kg of fluid accumulation reported. Affected

Overview animals may be lame and show signs of anaemia.
Swelling disease is recognised in multiple countries, Appetite often remains good and rectal temperature
including the UK, mainly affecting young animals typically within normal range. Goats usually recover
and fibre breeds. within 3–4 days, but recurrent episodes are possible.
Aetiology Diagnosis
Remains unestablished, with hypotheses including Clinical signs. Changes on haematology may
proteinaemia/hypoalbuminaemia, tocopherol (vita- include relative neutrophilia, basophilia and low
min E) or selenium deficiency, stress (like shearing) total protein or albumin or albumin:globulin
and vasoactive substances. ratio. Biochemistry parameters tend to be within
normal limits.
Oedema affecting the caudoventral abdomen Differential diagnosis
(Fig. 7.13a), limbs (Fig. 7.13b) and udder, with up For dependent oedema, consider chronic liver dis-
ease, cardiac problems, endoparasitism, Johne’s dis-
ease and plant poisoning.
For anaemia, see above.
Supportive only.
Caseous lymphadenitis
Definition/overview
CLA is a chronic bacterial infection affecting both
goats and sheep. It causes superficial and visceral
lymphadenopathy and has a worldwide distribution.
Fig. 7.12 A thymic lymphosarcoma at post-mortem It is a potential zoonotic pathogen.
examination (white arrow = heart; black arrow =
thymoma).
Fig. 7.13 Two

Angora goats
with swelling
disease showing
varying degrees
of oedema.
(a) Along the
ventral abdomen
up to the udder;
(a) (b)
(b) in the limbs.
192 Chapter 7
Aetiology
The causative agent in both species is Cory
nebacterium pseudotuberculosis, a facultative anaero-
bic organism.
Pathophysiology
The organisms gain access mainly through
wounds or small breaks in the skin and mucous
membrane, but occasionally in heavy infections
by inhalation into the lung tissue and associated
lymph nodes. They are carried to regional lymph
nodes, in which they can remain, resisting nor-
mal host immune mechanisms. The incubation
period from infection to superficial lymph node Fig. 7.14 A young Boer kid showing caseous
enlargement becoming apparent due to abscess lymphadenitis lesions in the parotid and prescapular
formation may be as long as 6 months, although lymph nodes.
2–3 months is more typical. Abscesses may rup-
ture and drain spontaneously or, if prominent, organs and lymph nodes are affected, and clinical
may rupture due to mechanical insult. This is signs will vary depending on the site of bacterial
usually followed by apparent resolution. In heavily multiplication.
infected herds, internal abscesses may develop in
a number of sites, particularly the bronchial and Diagnosis
mediastinal lymph nodes following inhalation, The presence of one or more superficial swell-
but have been reported in many other sites includ- ings anatomically linked to a lymph node should
ing renal and hepatic nodes. It is important to raise a strong suspicion of CLA. Culturing
emphasise that once infected, a goat will probably C. pseudotuberculosis will confirm the diagnosis.
never be free of infection, even if a lymph node If an abscess is burst, a swab inserted into the
has become enlarged, has ruptured and apparently abscess and rubbed over the abscess capsule is
healed. Disease can theoretically flare up at any ideal, although there is a greater chance of contam-
stage. inating bacterial overgrowth. If no burst abscesses
are available, then after shaving and sterilising the
Clinical presentation skin surface, a wide bore needle is inserted into
In many affected goats, there is little or no impact the abscess and pus aspirated, although this may
on their general health and productivity, because be very thick. It is important while waiting for
typically it is only the superficial lymph nodes that results that any goats with discharging abscesses,
are affected, although these are unsightly. The including any that were subjected to needle aspira-
most common superficial nodes are parotid, sub- tion, are isolated to minimise spread. Serological
mandibular and prescapular, reflecting the greater tests are available and are being used to manage
likelihood of superficial trauma in the areas to outbreaks, although false-negative results in early
which these nodes provide drainage (Fig. 7.14). infection can be problematic.
Infected lesions in the hind legs will lead to pop-
liteal lymph node enlargement, and damage to Differential diagnosis
the skin of the udder and teats may cause enlarge- The condition is fairly characteristic, but should be
ment of the supramammary node. However, differentiated from Morel’s disease, lymphosarcoma
if infection levels in the herd increase, abscess or bacterial abscesses due to other pathogens such as
formation becomes more widespread, internal Staphylococcus aureus or T. pyogenes.
Treatment/management/control There are commercial vaccines available in

Treatment of individual goats of economic or senti- some countries, and some success has also been
mental value can be attempted, but is of questionable reported following the use of autogenous vaccines.
value as a tool for control in infected herds. There Keeping new infection out of clean herds is of par-
are two approaches: either surgical or by the use of amount importance, but is problematic due to the
antibiotic (or a combination of the two). long incubation period when goats are outwardly
Surgical treatment involves either draining or healthy. All incoming goats should be examined
excising infected lymph nodes. Mature abscesses for evidence of enlarged lymph nodes while in
can be incised at a dependant point, and the contents quarantine, but an effective quarantine period
flushed out with a weak disinfectant solution. The for this disease should be 2–3 months. Serological
content is infectious and should be collected and dis- screening of incoming goats is a further tool,
posed of away from other livestock. The goat is then although false-negative results are a problem in
kept in isolation until the abscess has healed. Excision the early stages of disease. Where possible pur-
is a safer option for disease control, but care must be chases are made only from herds where no clinical
taken to avoid major blood vessels located near the disease has been recorded.
parotid gland in particular. The main problem with
the surgical approach is that only visibly enlarged Babesiosis
nodes are dealt with. Allowing the abscesses to mature Overview
and burst naturally is to be discouraged, as the leak- Babesiosis is caused by intraerythrocytic protozoan
ing pus can contaminate the building fixtures and fit- parasites of the genus Babesia. Transmitted by ticks,
tings (such as feed troughs) on which the organism babesiosis affects a wide range of domestic and wild
can survive for up to 10 weeks (and up to 6 months in animals worldwide. It is a particular problem in cat-
contaminated soil). Because of the potential zoonotic tle, but the disease has been described in goats.
risk, protective gloves should always be worn.
Antibiotic treatment of infected goats has been Aetiology
attempted, but can give disappointing results, mainly Goats can be infected by several species of Babesia.
because antibiotics cannot penetrate into the centre The two most important ones are B. ovis and
of abscesses where the organism resides. B. motasi, transmitted by the ticks Rhipicephalus bursa
Control in infected herds is based on identifica- and Haemaphysalis spp., respectively. Infection is of
tion of infected goats (by clinical evidence of abscess importance in the Middle East, southern Europe
formation, or positive serology) and a strict culling and some African and Asian countries.
policy. This approach has been reportedly success-
ful. Attention should be paid to possible environ- Clinical presentation
mental trauma predisposing to new infections, such Infection leads to erythrocyte destruction, often
as projecting nails, barbed wire or gate hinges. preceded by a non-specific pyrexia. This erythro-
Ectoparasitic infestations should be controlled – they cyte damage leads to inappetence, anaemia, jaundice,
will predispose to rubbing, potentially compromising weight loss and increased respiratory rate together
skin integrity, which may allow the causative bacteria with haemoglobinuria in the terminal stages.
to enter. Because the organism is so resistant in the
environment, control by segregating known infected Diagnosis
goats from ‘clean’ goats is difficult. Infection can be Diagnosis is based on the clinical signs, often with
readily transferred from one group to another on ticks still evident on the skin surface. Examination of
weigh crates, hurdles, feed troughs and in the milking Giemsa-stained, air-dried smears prepared immedi-
parlour. Thorough cleaning and disinfection with an ately after sampling from peripheral blood (e.g. ear) will
approved disinfectant should be undertaken regularly, demonstrate the dark staining intraerythrocytic inclu-
including shearing equipment in fibre herds. sions. Serological and PCR tests are being adapted for
194 Chapter 7
detection of disease in cattle, and these may be avail- Treatment/management/control

able and validated for use in goats in affected countries. Treatment commonly utilises the diamidine deriva-
At PME, splenomegaly is often a feature accompanied tives, with a single i/m dose of diminazine (3 mg/kg)
by evidence of jaundice and anaemia. or imidocarb (1–2 mg/kg). Control is aimed at tick
control. Vaccination using live, attenuated strains of
Differential diagnosis the parasites has been used successfully in a number
Other causes of haemoglobinuria (see Table 10.1). of countries.
CHAPTER 8
NERVOUS SYSTEM DISORDERS

195
CLINICAL EXAMINATION OF the important areas and functions of the central

THE NERVOUS SYSTEM nervous system (CNS). Severe impairment of vision
or hearing can lead to fear-induced behavioural
A good understanding of the nervous system and a abnormalities.
methodical approach to examination is essential to
pinpoint the lesion to a particular part of the system, Reflexes, upper motor neurons
thereby narrowing down the multitude of differen- and lower motor neurons
tial diagnoses. Exact location may remain elusive A simple reflex pathway triggers a motor response
in some patients because of overlap of neurological without CNS contribution. It is important that
function between areas or concurrent disorders. all components of the pathway are intact: sensory
receptor (e.g. a stretch receptor in the patella ten-
Consciousness, alertness don), corresponding sensory neuron in the dorsal
and behaviour ganglion, internuncial neuron (which effects muscle
For clinical cases, the following simplistic approach contraction via an efferent motor neuron), nerve
is usually sufficient. The fore- and midbrain and part endings, neuromuscular junction and muscle. A mal-
of the brainstem are responsible for mental state, function in any of these parts could be the reason for
behaviour and sensory functions. The hindbrain a reflex being absent. For example, an absent menace
(cerebellum) governs coordination. Table 8.1 details reflex in an animal with listeriosis is not necessarily
because it cannot see, but because it cannot blink due
to facial nerve paralysis.
Table 8.1 Central nervous system regions and
their associated functions. The motor neuron part in these reflexes is largely
alpha neurons, also called lower motor neurons
REGION FUNCTION (LMNs), located in the ventral grey matter of the
Frontal cortex Mentation, behaviour, fine spinal cord and brainstem. Signs of a LMN lesion
motor function include loss of reflexes, severe weakness and in par-
Parietal cortex Pain, proprioception ticular extensor muscle weakness, muscle atrophy,
Occipital cortex Vision
and flaccid paralysis (i.e. loss of voluntary move-
ment). The extensor weakness commonly results in
Temporal cortex Behaviour, hearing
a short stride length, with a bouncing or ‘bunny-
Hypothalamus and pituitary Autonomic and endocrine
hopping’ gait.
gland function
The upper motor neuron (UMN) system has the
Limbic system Inherent behaviour
following roles:
Cerebellum Coordination of voluntary
movements, subconscious
proprioception 1 It receives feedback from the sensory
input of the reflex arc on pain, touch and
Brainstem (reticular Consciousness, alertness
activating system) proprioception. It is important to observe
the animal for generic signs of pain, such as
196 Chapter 8
vocalisation, twitching, body movements or Normal limb reflexes include:

head jerk, particularly when conducting deep
pain tests, where a defect in the peripheral •• The patellar reflex, with the animal in
nerve or executing muscle may lead to absence lateral recumbency, is reasonably reliable.
of the expected localised response. Gastrocnemius, cranial tibial, biceps, or triceps
2 It controls voluntary movements, particularly reflexes show variable responses.
initiation of movement and flexor muscle •• The stoic nature of goats means that the
strength. Therefore, UMN lesions typically withdrawal reflex is very unreliable. Stimulation
manifest as slow onset of the swing phase, a long consists of pinching the interdigital space or
stride and decreased joint flexion (leading to coronary band. When present, an initial delay is
‘marching soldier’ gait in extreme cases). common.
3 Lastly, it has a calming effect on reflexes.
Therefore, a lesion cranial to a reflex arc will
result in an exaggerated response, potentially
to the point of spastic paresis. Ataxia, and
hypoalgesia in affected areas, may also be
Table 8.2 Guidelines on type of blindness and
seen. A small lesion often has a marked effect, likely location of lesion.
and depending on its location (e.g. off-centre,
unilateral, bilateral) signs are restricted to one REFLEX LOCATION OF LESION
side of the animal or not (e.g. hemiparesis versus PLR present ‘Higher’ lesion (i.e. CNS)
tetraparesis). In large animals, even marked Cases of cerebrocortical necrosis
lesions in the motor centres of the cerebral (CCN) or poisoning with sodium,
sulphur or lead
cortex do not appear to exert any severe or long-
term effect other than fine motor function. PLR lost Retinal, optic nerve or optic chiasm
Pupils dilated Optic nerve trauma, retinol (vitamin A)
Normal head/cranial nerve reflexes include: deficiency
Strabismus present Cranial nerves III, IV, VI (Fig. 8.1)
•• The response to noise is to look towards source.
PLR = pupillary light reflex.
A high-pitched sound is best to elicit a response.
•• Menace reflex is present, but is a learned
response and therefore may not be seen in
neonates. Care must be taken not to create
airflow towards the eye when testing the menace
reflex.
•• Palpebral and corneal reflexes are always present.
•• Facial sensation can be tested by tickling the
hairs on the muzzle or introducing a pen or
similar into the nostril.
•• Gag reflex can be elicited by palpating the
larynx, then observing the swallowing response.
•• Suck reflex is present in healthy kids.
•• Eyes follow nose when the head is moved.
•• Indirect and direct pupillary light reflexes
are present; however, the pupil rarely constricts
fully. Fig. 8.1 Strabismus (here in a cow) may be caused
•• Table 8.2 shows the connection between the type by lesions affecting cranial nerves III, IV or VI, or a
of blindness and location of lesion. space-occupying lesion in the orbit.
Ne rvous Sys t e m D isor de r s 197
Body region reflexes include:
•• The panniculus reflex is usually present, but may

be difficult to appreciate in thick coated goats.
•• The goat should dip its back in response to
stimulation of the withers region.
•• Anal/perineal reflex is variable. Stimulation of
the ventral vulva or base of penis may also be
tried.
Proprioception may be assessed by:
•• Asking the animal to move up and down a kerb, Fig. 8.2 Vestibular signs in a ewe with otitis media.
or over obstacles. Mild head tilt and facial nerve compromise shown by
•• Making the moving animal stop suddenly. a drooped left ear, lowered upper left eyelid and food
•• Pulling a foot away from the body with the aid impaction in the left cheek.
of a piece of paper, cardboard or towel placed
underneath (paper slide test). However, it is not Table 8.3 S
pinal cord lesions and their associated
uncommon to see considerable sideways movement clinical signs.
of the leg before the goat corrects the position
•• Knuckling reflex. Care must be taken not to REGION CLINICAL SIGNS
support the goat’s weight, otherwise a poor C1 to C5 All four legs affected, but spastic paresis often
response is likely. more pronounced in the hind legs compared with
•• 3-legged walking and hemi-walking should the front legs
result in hopping movements. Variable results C2 to T2 All four legs affected, but front legs worse than
hind legs. Front legs show reduced muscle
are more a function of logistics, with adults often
tone and reflexes (versus normal to increased in
resentful to handling and neonates collapsing in hind legs).
response. If both grey and white matter are affected, a ‘two
engine’ gait results: LMN component in front legs
resulting in short and/or bouncing stride; UMN
Vestibular syndrome
component in hind legs resulting in slow onset,
This is caused by lesions affecting the inner ear, long stride
cranial nerve VIII, the medulla oblongata or
T3 to S2 Trunk and hind legs affected. May see specific
parts of the cerebellum. Common causes are head peripheral nerves or muscles affected (e.g. lesion
trauma and otitis interna or media. Clinical signs at L4 resulting in femoral nerve deficits)
include head tilt (versus head aversion with fore- S1 to S5 Abnormal signs associated with rectum, anus,
brain lesions), strabismus, changes to the normal perineum and bladder function
nystagmus, leaning, falling, drifting sideways,
C = cervical vertebra; T = thoracic vertebra; S = sacral vertebra.
wide-based stance and deliberate movements.
There is a mild, regular irregular ataxia, but no
hypermetria. Blindfolding exacerbates signs. Spinal lesions
Bilateral lesions may present more like cerebel- Table 8.3 is a basic guide to pinpointing which part
lar signs. Because the facial nerve travels in part of the spinal cord is affected, depending on the
parallel to cranial nerve VIII, facial paralysis may signs seen.
also be present (Fig. 8.2). Neck pain (e.g. after
injection site reaction to an i/m injection) must Peripheral nerves
be ruled out as cause of apparent head aversion or Hyperflexion or hyperextension of particular joints
reluctance to bend the neck. typically allows identification of the compromised
198 Chapter 8
Table 8.4 Lesion location and associated gait and postural abnormalities.
CHARACTERISTIC FOR USUALLY PRESENT WITH USUALLY ABSENT

ABNORMALITY LESION OF LESION OF WITH LESION OF
Postural deficit Cerebrum, vestibular Brainstem, cerebellum, UMN,
LMN, spinal cord, peripheral
nerve
Paresis LMN, peripheral nerve Brainstem, UMN, spinal cord, Cerebrum, vestibular,
musculoskeletal cerebellum
Ataxia Cerebellum Brainstem, vestibular, UMN, Cerebrum, musculoskeletal
spinal cord
Hypometria Brainstem, vestibular, UMN, Cerebrum
spinal cord, some LMN
Hypermetria Cerebellum, some LMN Brainstem, UMN, spinal cord Cerebrum, vestibular,
musculoskeletal
LMN = lower motor neuron; UMN = upper motor neuron.

Source: Adapted from Mayhew J (2009) Large Animal Neurology, 2nd edn. Wiley-Blackwell, Ames.
peripheral nerve (see Table 8.5). To differentiate flight-path of the leg. If the goat is ataxic, it may
nerve malfunction from muscle malfunction, skin result in stepping on the other foot, crossing over or
sensation is tested (being absent if nerve is involved, circumduction etc.
Fig. 8.13). Close observation for muscle atrophy is Moving the animal backwards, or up and down
also useful to detect peripheral nerve disorders. an incline, highlights ataxia and may exacerbate
UMN signs (such as ‘marching soldier’ gait). A simi-
Specific assessment considerations lar result can be achieved by holding the goat’s head
Gait and posture high. This helps to detect UMN input, as several
Abnormalities in gait and posture may help to establish parameters are changed like the visual horizon.
what part of the nervous system is affected (Table 8.4) Pulling on the lead rope or tail is a good test
to detect extensor or flexor muscle weakness. If
Differentiating ataxia and weakness the goat can resist the pull while standing, but not
With ataxia, there is a lack of order or an inconsis- while circling, a UMN lesion is likely (e.g. a cervi-
tent order (i.e. proprioceptive dysfunction). This cal lesion in a wobbler case). In contrast, inability
results in irregular and unpredictable movements. to resist a pull while standing indicates an exten-
The ataxia is exaggerated by circling or moving sor muscle weakness (i.e. likely a LMN lesion
backwards or on an incline. [e.g. resistance to a tail pull is poor in a lesion at
Weakness, or paresis, presents with consistently lumbar vertebrae 3–5]). The pull should be applied
changed movements. Lifting one leg will often make in a constant manner, not a sharp jerk, and with
the weakness worse, inducing muscle tremors on the force appropriate for the goat’s size.
contralateral leg. The swing phase is shortened or
delayed, and the animal cannot resist a tail pull. Blindfolding
This is a useful technique to accentuate abnormal-
Using challenging movements ities arising from the brain or inner ear lesions (in
Forcing the animal to make unusual movements particular vestibular syndrome). It is also useful
can highlight ataxia or any unilateral character of a to establish unilateral blindness. It should be per-
deficit, and is useful to differentiate lameness from formed on soft ground or with an assistant ready
a neurological disorder. Circling and weaving dur- to prevent falling. The left and right eye are blind-
ing the swing phase forces a change to the normal folded in turn, followed by complete blindfolding.
The recumbent patient

Neurological assessment of the recumbent goat
is often difficult. Unless a fracture is suspected,
every effort should be made to lift up the animal,
or encourage it to stand, to facilitate examination.
Flaccid attempts to take its own weight after lifting
suggest a LMN lesion or severe depression. Spastic
attempts suggest UMN involvement.
If the goat can get into a dog-sitting position
and is using its front legs well, including extending
the legs, in an attempt to stand, it likely has a lesion
caudal to T2. Otherwise, the lesion is cranial to T2.
If the goat is lifting its head, but not the neck, the
location is in the cranial cervical cord.
Spinal reflexes can be tested quite well in the
recumbent patient. However, it must be remembered
that muscle tone and reflexes are often poor in the
limb the goat has been resting on. Flaccid muscle Fig. 8.3 Limp, flaccid ‘rag-doll’ presentation in a
tone suggests an LMN lesion. neonatal alpaca with a brain lesion.
For progress monitoring of a patient undergo-
ing treatment, the tail, anal and perineal reflexes
should be checked regularly. Contusion and oedema Cerebrospinal fluid
of the lower spinal cord often result from prolonged collection and analysis
recumbency, dog-sitting posture or suspension in a Indication
sling. Cerebrospinal fluid (CSF) collection and analysis is
useful in most cases with neurological signs or sus-
The neonatal goat pected spinal trauma. Collection from the lumbo-
Mentation and sensory function adjust within sacral space (as described here) can be safely carried
24 hours post partum in the neonate, and out in the field. Collection from the cisterna magna
behaviour within 2–7 days. A mild wide-based
requires general anaesthesia and carries a higher risk
stance (see Fig. 4.9, p. 91) and somewhat jerky of adverse reaction.
movements or mild hypermetria are normal in
neonates. They usually have a dominant extensor Preparation and equipment
tendon strength, and this may result in hyperre- The lumbosacral area is clipped and surgically
flexia. As mentioned earlier, the menace reflex is prepared. A hypodermic or spinal needle, 19 or 20
a learned response and is typically absent in kids gauge, 2.5 cm (1 in) for kids, 3.75–5 cm (1.5–2 in) for
less than 1 week old. A neurological neonate may adults, plain and EDTA sampling pots, a 5–10 ml
demonstrate sham-chewing, lip curling, star gaz- syringe and surgical gloves are required.
ing, yawning and ‘rag-doll’ limpness (Fig. 8.3).
Common non-neurological disorders may pres- Restraint
ent with a similar clinical picture to nervous system Conscious, possibly lightly sedated goat in sternal
disorders. In particular, tendon hyperextension or recumbency. An assistant kneels facing backwards
contraction, septicaemia, hypothermia, hypoglycae- over the withers of the goat, with the goat’s head
mia and parturition-induced anoxia. These common and neck between their legs (taking care not to exert
conditions should always be ruled out. Particular too much pressure onto the withers). The assistant
attention should be paid to ensuring passive transfer grasps a hind leg in each hand, pulling them forwards
in a neurological neonate. so that they come to lie along either side of the goat’s
200 Chapter 8
abdomen. This results in downward tilting of the flavum (slight ‘pop’) followed by entering the epi-
spine and opens the lumbosacral space (Fig. 8.4). dural space, then dura mater (another slight ‘pop’)
Local anaesthetic (1 ml in a kid or 2–3 ml in an to enter the subarachnoid space. Placing a drop of
adult of 2% lidocaine HCl or 5% procaine HCl) is local anaesthetic into the needle hub once the skin
injected subcutaneously and into the muscle. has been penetrated is useful to establish that the
epidural space has been entered. After entering the
Technical description subarachnoid space just a little deeper to this, CSF
The lumbosacral space can be felt just caudal will typically well up after about 10 seconds and can
(1–2 finger-widths) to an imaginary line connecting be collected free-flow or with a syringe (break seal
the tuber coxae (Fig. 8.5). When placing the index of syringe plunger before connecting). It is impor-
finger onto the dorsal spinous processes just cranial tant to not advance the needle too deeply, as pen-
to this line, and then drawing it caudally with some etration of the conus medullaris will elicit a pain
pressure, the finger will ‘fall’ into the space. response (Fig. 8.6). If two attempts (using a fresh
Kneeling behind the animal, the surgeon intro- needle) fail, the procedure should be abandoned.
duces the needle precisely midline into the space One to 2 ml is placed into an EDTA and a sterile
at an angle of 75 degrees to the skin (i.e. slightly sample pot. A rough assessment can be undertaken
off perpendicular with the hub angled caudally). on farm: orange discolouration suggests haemor-
With the wrist resting on the animal, the needle rhage into the spinal canal. Vigorous shaking of the
is steadily advanced while appreciating the layers sample may lead to precipitation if the protein con-
it penetrates, namely: skin, subcutaneous tissue tents is increased. (Note: Precipitation renders the
and muscle, interarcuate ligament and ligamentum sample unsuitable for running through an analyser.)
Normal values for common CSF parameters in
ruminants are: protein, <0.4 g/l; nucleated cells,
0–8/µl; red blood cells, none; bacteria, none.
Aftercare
The penetration site should be protected from
contamination.
Fig. 8.4 Restraint for CSF collection. The animal is Fig. 8.5 The person’s index finger rests on the
held in sternal recumbency, with an assistant pulling lumbosacral space, which is 1–2 finger-widths caudal
both hind legs forward alongside the body. to a line between the tuber coxae (indicated by
person’s thumb and middle finger).
Fig. 8.6 The needle has been advanced at 75 degrees Fig. 8.7 Vertebral fracture in the lumbar region,
to the skin and, after entering the subarachnoid space, obvious on a plain radiograph (arrow).
a syringe attached to collect the CSF.
take into account normal variations and incidental

findings.
Myelography (Fig. 8.8) has largely been super-
seded by CT and MRI. MRI is the most useful
imaging modality for nervous tissue abnormalities,
otitis and brain lesions. Electromyography (EMG)
is useful to further investigate peripheral nerve
deficits. The brainstem auditory evoked response
(BAER) test aids diagnosis of deafness and cranial
nerve VIII deficits.
NON-INFECTIOUS DISEASES
Fig. 8.8 Myelogram highlighting a space-occupying
cervical spine lesion. The contrast material does not Central nervous system
progress caudally (arrows indicate its end point).
Disbudding injury
Because of the thin skull in kids, prolonged (over
Potential complications 3–4 seconds at a time) application of a disbudding
Haemodilution of sample if needle is placed laterally. iron may lead to thermal insult of the meninges
Pain response if needle is placed too deep. Mild to (Fig. 8.9). Clinical signs typical of encephalitis
moderate haemorrhage at site if goat moves during develop within 2–3 days of disbudding, usually fol-
procedure. Spinal abscess or meningitis if asepsis is lowed by death. Treatment with anti-inflammatory
not observed. or intracranial pressure reducing drugs may be tried
but is unrewarding.
Imaging and further diagnostics
Radiography is useful to detect fractures, osteomy- Acquired storage disease
elitis and bone malformations in the spinal column Overview
(Fig. 8.7). It may also highlight parasite-induced Acquired mannosidosis is reported from several
pathology (e.g. coenurosis or calcification in mus- regions around the world, but in particular South
cles caused by sarcocystosis). Interpretation must America.
202 Chapter 8
and atrophy of Purkinje cells, with lectin binding typi-

cal of alpha-mannosidosis or other glycoproteins.
Other cerebellar or brainstem disorders.
There is no specific treatment other than remov-
ing goats from affected pastures. Goats may recover
if ingestion was over a relatively short period
(3–4 weeks), but about one quarter of those retain
some abnormalities such as head tremors and a stag-
gering gait. Euthanasia is often required.
Goats have been observed to develop compulsive
eating of Ipomoea plants. Long-term control relies on
eradication of the plant.
Fig. 8.9 Circular thermal trauma to the brain Inherited central nervous
following disbudding. The affected kid died within system disorders
15 minutes of the procedure. Few reports on neurogenetic disorders exist in the
goat. However, beta-mannosidosis (see Chapter 4)
Aetiology and cerebellar abiotrophy have been identified.
Plants containing swainsonine (so called locoweeds), Abiotrophy leads to ataxia, wide-based stance
such as Ipomoea spp., Astragalus spp., Oxytropis spp., and hypermetria in affected kids. Head tremors and
Delphinium spp. and also Solanum spp,. have been asso- nystagmus are common. Thinning of the cerebellar
ciated with these poison-induced neurological disor- vermis may be detected on MRI. Other cerebellar
ders. Ingestion of both fresh and dried plant material disorders need to be considered as differential diag-
appears poisonous. Feeding 0.8 mg/kg swainsonine noses. There are no treatment options.
(equivalent to 4 g/kg of dried I. verbascoidea leaves)
for 40–55 days leads to irreparable damage. Swayback (syn. enzootic ataxia)
Pathology consists of vacuolation of Purkinje cells See Copper deficiency (Chapter 15).
in the CNS, but also cells in the pancreas, liver, kid-
ney, thyroid gland and lymphoid organs. Polioencephalomalacia
(syn. cerebrocortical necrosis)
Clinical presentation Definition/overview
The first clinical signs appear after about 3 weeks of Polioencephalomalacia (PEM), also referred to as
ingestion. General signs include weight loss and inap- cerebrocortical necrosis (CCN), is a sporadic condi-
petence. Neurological signs include ataxia, dysmetria, tion affecting growing ruminants worldwide includ-
intention tremors, head tremors and postural abnor- ing goats. It is most often encountered on units in
malities including a wide-based stance. Handling, which young goats are being intensively reared.
moving or other stimuli may trigger pronounced
signs and lead to the goat falling over. Aetiology
PEM is a descriptive term for the pathology encoun-
Diagnosis tered, which is essentially softening or necrosis of
Anaemia is often present, and depending on the organs the grey matter of the cerebral cortex. Although
involved, other biochemistry parameters may be ele- there are a number of causes for this condition, the
vated (e.g. AST). Histopathology shows vacuolation term is most closely linked and most commonly
associated with disturbances to thiamine (vitamin most often seen is one of acute onset, although clini-
B1) metabolism. In healthy goats, thiamine is pro- cal signs may be more protracted over 24–48 hours
duced in the rumen by microbial activity, providing following an initial period of depression and inap-
the daily requirements without the need for ration petence. Affected goats become excitable, staring
supplementation. Dietary factors resulting in rumen upwards (‘star-gazing’), and they begin to wander
acidosis will result in a change in the rumen micro- aimlessly, often in circles (Fig. 8.10). Teeth grinding
flora. Under this type of change, PEM is thought and blindness may also be features before collapse
to result from a reduction in thiamine produc- into lateral recumbency with profound opisthoto-
ing bacteria, coupled with an overgrowth of other nus. In these later stages, affected goats become
bacteria that produce a thiaminase enzyme, fur- hyperaesthetic, develop extensor muscle rigidity of
ther degrading available thiamine and resulting in the limbs and can convulse violently. If untreated,
deficiency. Other reported causes of the condition affected goats will die in 24–48 hours.
include sulphur toxicity and water deprivation or
salt poisoning, although these mechanisms and bio- Diagnosis
chemical pathways remain poorly understood. The The clinical signs, age of the goat and past history of
condition can often be encountered sporadically a dietary change are all highly suggestive of PEM. In
alongside an outbreak of enterotoxaemia, both con- the early stages, a response to i/v thiamine therapy
ditions essentially precipitated by dietary imbalance. may give further support to the diagnosis. The acute
nature of the disease means that laboratory tests are
Pathophysiology of limited value overall, although measurement of
Thiamine is an important co-enzyme (as thiamine blood erythrocyte transketolase (an indirect mea-
pyrophosphate) in a number of important biochemi- sure of thiamine activity) may be offered by some
cal pathways related to brain function. The degener- laboratories. At post-mortem examination (PME),
ative change in brain tissue results most likely from lesions are confined to the brain, which shows flat-
accumulation of sodium in the cerebrocortical cells, tening of the cerebral gyri, with areas of yellowish
leading to water ingress, cell swelling and cell death. discolouration. Examination of the sagittally sec-
tioned brain in a darkened room under UV light can
Clinical presentation show very clearly delineated areas of tissue necrosis
The clinical condition is seen most frequently in (Fig. 8.11). Histological examination confirms lami-
growing goats and young adults. The presentation nar necrosis.
Fig. 8.10 Evidence of circling can be seen in the Fig. 8.11 Polioencephalomalacia showing
straw bedding in this goat’s pen. autofluorescence under UV light in a dark room.
204 Chapter 8
Differential diagnosis the neonate. Brachial plexus compromise may result

Includes listeriosis, enterotoxaemia and bacterial from a goat becoming trapped over a gate or bar with
meningitis in the early stages. As the condition pro- its front leg. Unstable leg fractures can cause second-
gresses, the limb rigidity often exhibited can be con- ary nerve damage, as can casting a leg or pressure
fused for tetanus. The convulsive stages need to be during prolonged anaesthesia. Other causes include
differentiated from rabies, Aujeszky’s disease (pseu- localised abscess formation, injection site reaction,
dorabies) and chemical poisoning. neoplasia or haematoma. Space-occupying lesions in
the spinal cord at the level of the nerve roots may
Treatment/management/control also occur. In the case of spinal canal abscessation, a
Rapid and decisive treatment with intravenous secondary pathological fracture can lead to further
thiamine (10–15 mg/kg thiamine hydrochloride nerve insult (Fig. 8.12).
every 4–6 hours) can be very effective in the early
stages, and should be repeated twice daily for the Clinical presentation
next 48 hours. Multivitamin preparations can be The immediate effect is an abnormal leg angula-
used, but with the dosage calculated based on the tion. Table 8.5 shows the normal action of the main
thiamine content of the product. Nursing is vital to peripheral nerves. Where nerve compromise is pres-
prevent injuries while convulsing and in prolonged ent, the opposite would be observed (e.g. flexion or
lateral recumbency. Any other concurrent problem knuckling of the fetlock with peroneal paralysis).
(such as rumen acidosis, enterotoxaemia) should also Skin sensation over the nerve’s sensory supply areas
be treated. is absent (Fig. 8.13). Longer term, atrophy of the
Prevention is problematic due to the sporadic muscles that receive motor supply from the affected
nature of the condition, but is best aimed at ensur- nerve is seen.
ing that any dietary changes are made gradually,
particularly at weaning. It is important to ensure Diagnosis
that all goats can feed on concentrate or grain simul- Clinical signs are highly suggestive. CSF analysis
taneously (to avoid individual goats engorging), and and imaging where a spinal disorder is suspected as
ensuring that feed stores are goat proof. Although its the cause. EMG to confirm.
role is poorly understood, the overall sulphur con-
tent of the ration may need to be explored if an out-
break continues.
Floppy kid syndrome

See Chapter 4.
Peripheral nervous system
Peripheral nerve paralysis

Overview
Paralysis of various peripheral nerves is occasionally
observed.
Aetiology
Trauma anywhere along the nerve’s path is the most
common cause. For example, obturator or peroneal
nerve paralysis may be a sequela to dystocia caused
by feto-maternal disproportion. In dystocia cases, Fig. 8.12 This spinal abscess at the lumbosacral joint
excessive traction may also result in nerve damage in in a cow led to bilateral tibial nerve paralysis.
Table 8.5 Major peripheral nerves of the front and hind legs, and their main action.
MAIN MUSCLES RECEIVING MAIN ABNORMALITY SEEN

MOTOR SUPPLY JOINT ACTION WHEN COMPROMISED
Front leg nerves

Suprascapular Supraspinatus, infraspinatus Shoulder extension and lateral Shortened stride, abduction of leg
stabilisation
Axillary Deltoideus, teres major and minor Shoulder flexion
Musculocutaneous Biceps, proximal end of brachial Elbow flexion
Median and ulnar Carpal and digital flexors Carpus and digit flexion ‘Goose-stepping’, hyperextension
of carpus and fetlock
Radial Triceps, distal end of brachial, Elbow, carpus and digit extension Dropped elbow, inability to extend
digital extensors lower limb, dragging of leg
Hind leg nerves

Obturator Adductors Limb adduction Recumbent, ‘frog-leg position’
Femoral Quadriceps Hip flexion, stifle extension Dropped stifle resulting in vertical
line of upper limb, often unable to
support weight (Fig. 8.14)
Tibial Gastrocnemius, digital flexors Hock extension, digit flexion Dropped hock, hock has more acute
angle than normal (Fig. 8.14)
Peroneal Cranial tibial, digital extensors Hock flexion, digit extension ‘Knuckling’ of fetlock
Femoral
Tibial Tibial Ulnar
Median Musculocutaneous
Peroneal
Fig. 8.13 Autonomous zones of skin innervation.

(Adapted from: Mayhew J (2009) Large Animal
Neurology, 2nd edn. Wiley-Blackwell, Ames.)
Abnormal angulation caused by muscular, tendon or Fig. 8.14 Stance showing moderate femoral and
ligament disorders, dislocations or fractures. Skin sen- tibial nerve compromise in a goat with a suspected
sation will be intact and often there is localised swelling thoracolumbar lesion. The upper limb is straighter
(although this may also be present with nerve damage). and the hock more flexed than usual, resulting in the
Crepitus is present in fractures and dislocations. hind feet being placed deeper underneath the body.
206 Chapter 8
Treatment/management/control the environment and can be found in the faeces of

Anti-inflammatory therapy is often successful if wild animals and birds (potentially contaminating
instigated early. Corticosteroids (e.g. starting dose of feeds), soil and other organic matter, thereby being a
methylprednisolone at 30 mg/kg or dexamethasone potential risk factor in the process of silage making.
at 2 mg/kg) may be more effective in nerve damage
cases than NSAIDs (providing they are not contra- Pathophysiology
indicated [e.g. a pregnant doe]). Spinal lesions carry Clinical disease in goats can often be initiated by
a poor prognosis. stressful insults such as sudden changes in weather
Control relies on using caesarean section for conditions or by overcrowding coupled with keep-
feto-maternal disproportion, providing a safe envi- ing them in a dirty contaminated environment. The
ronment for goats, good i/m injection technique introduction of a feedstuff (particularly silage) con-
(appropriate needle length, correct insertion angle taminated with Listeria organisms is a significant risk
and site) and casting technique, adequate positioning factor, particularly in intensively managed herds.
and padding during anaesthesia, and good nursing Goats kept on overgrazed pasture may inadvertently
care of recumbent animals. ingest contaminated soil. Sporadic incidents will
occur, however, even in the absence of any of these
INFECTIOUS DISEASES risk factors. As an example, one author encountered
encephalitic listeriosis in two of three goats that had
Listerial encephalitis been eating brambles growing over a stacked heap of
Definition/overview horse manure and bedding.
Listeriosis is an important neurological disease of In the encephalitic form of the disease, the organ-
goats worldwide, and can also be associated with ism gains entry to nerve endings in the mouth via
other clinical syndromes including septicaemia and breaks in the oral mucosa (e.g. abrasions caused
abortion. There are potential human health implica- by coarse feed [brambles, thistles or browsings]),
tions associated with the production and sale of dairy dental or gum abnormalities, or teeth loss or
products, particularly soft cheeses. Septicaemic goats change. Infection ascends along the cranial nerves
may excrete the organism in milk, and infected to the brain, resulting in focal microabscess for-
vaginal discharge following abortion may contami- mation. The incubation period may be as long as
nate the udder, teats and hands of the milker, and 3–4 weeks. The onset of septicaemic listeriosis is
hence the milk. Milk excretion is less likely to occur more rapid, with an incubation period as short as
in the encephalitic form of the disease, but has been 1–2 days, probably resulting from organisms gain-
reported in latent carriers, that can be found paring access to the blood stream via a damaged gut
ticularly in endemically infected herds. Even a small mucosa. If pregnant, septicaemic goats may abort.
inoculum in unpasteurised milk may rapidly prolifer- Ocular listeriosis may result from contaminated feed
ate when the milk and resulting dairy products are (principally silage) falling into the eyes as goats feed
stored at fridge temperatures. from raised containers.
Aetiology Clinical presentation

Listeria monocytogenes is a small, gram-positive, aero- Outbreaks of clinical disease tend to feature only
bic and facultative anaerobic rod-like organism. It one manifestation of the infection, although there
grows at a wide range of temperatures from 3°C to are reports of encephalitis, septicaemia and abor-
45°C, with active proliferation at fridge temperatures tions all occurring in the same incident.
(a useful technique when isolating the organism in a The encephalitic form tends to develop slowly,
laboratory). It can be subclassified into a number of with initial signs confined to depression, anorexia
serotypes (and subtypes), with serotypes 1/2a, 1/2b, and reduced milk yield. Incoordination then
4b and 5 (Listeria ivanovii) most commonly associated develops, with stumbling and an increasing ten-
with disease in goats. The organism is ubiquitous in dency to lean, move or fall in the same direction.
Other characteristic signs include a drooped ear, Diagnosis

ptosis, nystagmus, protruding tongue, flaccid buccal The clinical signs in encephalitis cases are fairly
muscles and an increasing inability to prehend food typical. Bacteriological and cytological examina-
and to swallow (Fig. 8.15). Weakness, progressive tion of CSF may be of benefit, but haematology is of
dehydration and recumbency (Fig. 8.16) follow, and limited value due to the localisation of the infection.
if untreated the mortality rate can be high. Available serological tests are of limited value in
The initial presentation in the septicaemic form clinical cases due to cross reaction with other gram-
is similar, but progression is rapid and neurologi- positive organisms, but may be of benefit for herd
cal signs are usually not a feature. Diarrhoea, often screening exercises.
haemorrhagic, is a common finding and affected At PME there are few gross lesions evident.
goats deteriorate rapidly over a few days. If pregnant, Confirmation of infection is based on the labora-
septicaemic goats may abort, but not all goats that tory isolation of the organism from brain tissue of
abort show other clinical signs. In the ocular form, encephalitic cases and from multiple sites in septi-
both keratoconjunctivitis and anterior uveitis (silage caemic carcases. Histological examination of brain
eye) have been reported (see Chapter 13). tissue will demonstrate focal microabscessation and
perivascular lymphoid cuffing as the primary fea-
tures (Fig. 8.17).
Differential diagnoses for the encephalitic signs
include bacterial meningitis, brain abscesses,
PEM, coenurosis and early rabies. For septicae-
mic cases presenting with haemorrhagic diar-
rhoea consider enterotoxaemia, salmonellosis and
yersiniosis.
Fig. 8.15 Saanen doe with encephalitic listeriosis To be successful, treatment must be instigated rap-
showing drooping of the ear and eyelids and idly and decisively. High doses of antibiotic admin-
hypersalivation. Marked nystagmus was also evident. istered i/v for the first 24 hours should be followed
Fig. 8.16 Lateral recumbency in a case of advanced

Fig. 8.17 Encephalitic listeriosis showing
encephalitic listeriosis.
perivascular cuffing with mononuclear cells and focal
microabscessation histologically.
208 Chapter 8
by i/m antibiosis for 3–7 days. Suitable antibiotics The development of a brain or pituitary abscess is
include penicillin, tetracycline and potentiated sul- most likely the result of haematogenous spread from
phonamide. Supportive therapy includes NSAIDs a cutaneous, visceral or foot septic focus or following
and fluid therapy (orally or i/v) to combat both middle ear infection.
dehydration and rumen acidosis resulting from the
inability to swallow saliva and the loss of its rumen Clinical presentation
buffering capacity. Nursing, particularly of recum- Affected kids may exhibit depression, incoordination,
bent goats, is essential. ataxia, teeth grinding, hyperaesthesia and blindness,
In an outbreak, attention is directed at identi- leading to recumbency often with opisthotonus and
fying the source of infection and likely risk fac- extensor rigidity, although the front legs are usually
tors identified for future herd control measures. If flexed. Signs related to umbilical infection may be
contaminated silage or other feed is suspected, this evident including umbilical inflammation and joint
should be removed and replaced. For prevention, effusion and pain. Clinical signs related to brain
uneaten silage should routinely be discarded after abscess formation will vary depending on the size
24 hours. If silage is the source, the production pro- and location of the abscess, but may include pro-
cess is reviewed: excessive soil contamination must gressive incoordination, aimless wandering (often in
be avoided during the ensiling process (mole hills one particular direction), head pressing, blindness,
are commonly incriminated, and cutting blades are abnormal pupillary responses and dysphagia.
often set too low). Ensure the silage clamp or bags/
wraps are airtight. Silage pH should be around Diagnosis
3.8–4.3. Silage with a pH of 5 or greater will be of Diagnosis is based predominantly on the spectrum
high risk. Avoid feeding wet bales of either hay or of clinical signs in young kids, combined with CSF
pea straw, and avoid the use of wet bales for bedding. analysis. Brain abscess diagnosis is almost always
Vaccines are available in some countries. presumptive and confirmed at PME or with diag-
nostic imaging such as MRI or CT.
Bacterial meningitis/encephalitis
Definition/overview Differential diagnosis
This condition is seen most commonly in young One of the main differentials is thermal damage
kids as part of a spectrum also including septicae- and resulting infection following disbudding injury
mia and joint ill resulting from umbilical infection (Figs. 8.9, 8.18). Brain abscesses need to be differ-
and/or concurrent hypogammaglobulinaemia (see entiated from other space-occupying lesions such as
Chapters 4, 5 and 9). In mature goats, there are those caused by trauma or parasitic cysts, and from
occasional reports of brain abscesses and specifi- CCN, listeriosis, neurological signs of C. perfrin-
cally abscesses of the pituitary gland. gens enterotoxaemia or lead poisoning. Tetanus may
cause a similar picture of recumbency with extensor
Aetiology rigidity affecting all four legs.
Escherichia coli is the most common isolate, although
other possible (essentially environmental) patho- Treatment/management/control
gens include Streptococcus dysgalactiae, S. zooepidemicus, Treatment of affected kids is most successful in
Pseudomonas aeruginosa, Trueperella pyogenes and early cases, with more advanced cases carrying a
Corynebacterium pseudotuberculosis. poor prognosis. The use of broad-spectrum antibi-
otics, or those with activity against gram-negative
Pathophysiology organisms, capable of crossing the blood–brain bar-
In young kids infection will most often develop fol- rier, such as potentiated sulphonamide, ampicillin
lowing a bacterial septicaemia and localisation of or cephalosporin at high dose rates i/v, has been
infection within the meninges, predominantly over- advocated. Supportive therapy with NSAIDs and/
lying the brain and, more rarely, the spinal cord. or agents reducing intracranial pressure should be
spinal cord, leading to sustained discharge of motor

neurons, resulting in the clinical signs of tetany.
In addition to accidental wounds or injuries, infec-
tion can also be acquired as a result of a variety
of managemental procedures such as disbudding,
dehorning, castration (both surgical and via an elas-
trator ring), ear tagging and obstetrical procedures.
It occasionally results from i/m injection of certain
drugs (e.g. prostaglandin-F2-alpha).
Clinical signs are highly variable, depending on the
location of the primary focus of proliferation and
the size of the goat (both influencing the distance
toxin must travel along peripheral nerves). Onset
Fig. 8.18 Trauma, necrosis and suppuration of signs may vary from days to several weeks. An
(penetrating into brain tissue) as a result of a early sign may be mild unexplained rumen tym-
disbudding injury. pany. Affected goats become reluctant to move,
developing both front and hind leg rigidity, and
given, and affected kids kept in a well-bedded dimly major muscle groups may feel firm. The ears are
lit hospital pen, and turned frequently if recumbent held high and may not move in response to a noise.
to avoid pressure sores and hypostatic lung conges- The third eyelid becomes more prominent and
tion Force feeding may be required. Treatment of hyperaesthesia develops, with an exaggerated reac-
brain or pituitary abscesses is rarely successful. tion to sounds. Constipation may be present. The
Neonatal problems in general can be prevented by disease progresses to convulsions, recumbency and
reviewing overall management (see Chapter 4). death usually from respiratory failure.
Tetanus Diagnosis
Definition/overview There are no laboratory tests in the live goat and no
Tetanus is a well-documented condition affecting specific post-mortem signs. Bacteriology is of limited
many animal species and humans worldwide, caus- value as the organism remains at the site of entry, but
ing tetanic muscular spasms, convulsions and death. the typical ‘drumstick’ morphology of the organism
It is easily preventable by strategic vaccination. may be evident in Gram-stained smears taken from
the primary lesion.
Aetiology
Caused by Clostridium tetani, a highly resistant gram- Differential diagnosis
positive, anaerobic, spore-forming organism found The disease is fairly characteristic in the later stages.
widely in animal faeces and soil. In the early stages, stiffness could mimic either lami-
nitis or muscular dystrophy, and other causes of rumen
Pathophysiology tympany must be ruled out. Hypomagnesaemia
As the organism proliferates at the site of entry, it causes hyperaesthesia, but does not result in continu-
produces and releases a potent neurotoxin. This can ous muscle spasm.
occur, for example, when spores are introduced from
the environment into a deep penetrating wound or Treatment/management/control
necrotic lesion encouraged by the localised anaero- Treatment of clinical cases is usually disappointing
bic environment within the lesion itself. Neurotoxin unless detected early. Crystalline penicillin given
tracks up the local peripheral nerve trunks to the i/v has a rapid mode of action, and may be followed
210 Chapter 8
by procaine penicillin (30,000–40,000 IU/kg i/m

q12h for 2–3 days). Tetanus antitoxin, where avail-
able, is given i/v or intrathecally. Persistent rumen
bloat is addressed by placing a trocar or surgically
creating a rumen fistula (see Chapter 5). The lat-
ter also facilitates instilling feed and water into the
rumen if swallowing is impaired. Sedatives when
convulsing are useful, as is analgesia to counteract
the marked pain caused by muscle spasm (prefer-
ably opioids, with NSAIDs or acepromazine having
some effect). Euthanasia on welfare grounds should
be considered if cases do not improve. Prevention
is based on a sound tetanus vaccination regime (e.g.
a multivalent clostridial vaccine providing cover for
both tetanus and enterotoxaemia), good techniques
for routine procedures and prompt attention to
wounds.
Enterotoxaemia
C. perfringens toxins can lead to CNS signs as a result
of focal symmetrical encephalomalacia changes
in the brainstem and cerebral oedema (Fig. 8.19).
These changes can result in profound neurological
signs including ataxia, blindness, opisthotonus, con- Fig. 8.19 Cerebral oedema. Note the cerebellar
vulsions and death, in addition to the more typical herniation through the occipital condyles.
signs described in Chapter 5.
writing, no further natural cases of BSE have been
Scrapie and bovine spongiform identified in goats, and the BSE epidemic itself is
encephalopathy undoubtedly on the decline.
Definition/overview Scrapie is still endemic in goats (and sheep) in
Scrapie is one of the transmissible spongiform the UK and other countries in Europe, in Iceland,
encephalopathies or prion diseases that can affect and in the USA and Canada, although many of
sheep and goats. Although scrapie has been reported these countries are developing successful control
in sheep for over 200 years, the first case of natural and monitoring programmes. Cases have also been
scrapie in a goat was only confirmed in 1975. The reported in many other countries, but most often
emergence of bovine spongiform encephalopathy with links to sheep imports from the UK. Australia
(BSE) in the UK in 1986, and in particular the sub- and New Zealand have subsequently both eradi-
sequent links to human health, resulted in a world- cated the disease.
wide interest in this group of diseases. Extensive
monitoring of cattle, sheep and goat brain mate- Aetiology
rial followed across Europe, focussing on healthy It is generally accepted that scrapie and BSE are
animals entering the food chain and on stock that caused by the expression of an abnormal form of
died on farm. Initially, BSE was confined to cattle the naturally occurring cellular protein referred to
brain and scrapie to sheep and goat brain, but in as prion protein (PrP), found throughout the body
2002, BSE was confirmed in the brain tissue of a but being of clinical relevance in the nervous system.
goat in France, and a second case was subsequently Disease appears to be associated with replication
identified in a goat from Scotland. At the time of of this abnormal protein, although this is only one
factor in what is a highly complex and still incom- Diagnosis

pletely understood process. Most cases of natural A presumptive diagnosis in the live goat is based on
scrapie in goats occur as a result of lateral spread the clinical signs described. There is no detectable
between sheep and goats, although the rate of goat immune response. A number of experimental tests
to goat transmission has been reported to be high in are now being used diagnostically in live sheep
intensively housed animals in the UK. and goats, such as the rectoanal mucosa-associ-
ated lymphoid tissue (RAMALT) test, in which
Pathophysiology a biopsy specimen is taken from the rectum and
The infective PrP agent present in the placenta subjected to immunohistochemical testing. There
and uterine fluids of either goats or sheep (and a are no gross lesions on PME. Definitive diagnosis
risk if co-located) appears to be the primary source is based on histological examination of brain obex
of new infection for newborn kids, although other tissue (in which vacuolar/spongiform change is
minor transmission routes may also exist. As goats evident; Fig. 8.20) or by brain immunohistochem-
are fastidious about clearing up and consuming the istry or immunoblotting. These latter techniques
placenta after kidding, this behavioural trait may in will also distinguish between scrapie and BSE.
part explain the rapid spread among housed goats
once infection is present in the cohort. Differential diagnosis
The agent is notoriously resistant in the envi- The slow rate of development of clinical signs is
ronment, and thorough cleaning and disinfection highly typical of scrapie. Other causes of progressive
of buildings in which infected goats have been ataxia include space-occupying lesions in the brain
housed is important, particularly after kidding or or spinal cord.
lambing has taken place. Following oral ingestion,
it is thought that the infectious agent enters via Treatment/management/control
Peyer’s patches, then colonises the lymphoreticu- There is no treatment. Scrapie and BSE are both on
lar system and other body tissues including the the OIE list of notifiable diseases, and any suspicion
brain, where further replication occurs. The incu- should be reported to the relevant national author-
bation period is variable, but usually 12 months or ity, which in turn will initiate a full epidemiologi-
more. cal investigation and instigate their own national
control and advisory plan. In the sheep sector, the
Clinical presentation use of genetic selection of scrapie resistant breed-
Clinical signs will not usually develop until infected ing stock has become a well-established disease con-
goats are at least 18 months old, and even then trol option in scrapie-affected flocks and has been
progress very slowly over a period of several weeks.
Early signs are easily overlooked, but may include
subtle changes in behaviour towards other goats or
their owners such as lack of interest/recognition
or increased irritability. This is followed by pro-
gressive ataxia, difficulties in leg placement and
stumbling when moved forward, particularly when
made to deviate their course. Although pruritus is
a common presentation in sheep, it is more rarely
reported in goats. The ears and tail are often held
aloft. Reaction to sound and other stimuli is often
exaggerated. A gradual decline in body condition
is followed by eventual recumbency, by which time
most goats will have been destroyed on humane Fig. 8.20 Neuronal vacuolation histologically in a
grounds. confirmed scrapie case.
212 Chapter 8
highly successful. The genetics of scrapie resis- in known rabies areas resulting from elimination of
tance in sheep, however, are significantly different other potential causes.
to that of goats. Collaborative work within the EU
is ongoing to establish genetic resistance in goats, Differential diagnosis
although this has been hampered somewhat by the Includes listeriosis, tetanus, brain abscess, scrapie,
wide genetic variation within goat breeds. Aujeszky’s disease (pseudorabies), lead poisoning and
some plant poisonings.
Rabies
Definition/overview Treatment/management/control
Rabies is a viral disease that can infect all warm There is no treatment for rabies. It is on the OIE list
blooded mammals, including on very rare occasions of notifiable diseases, and any suspicion should be
goats. In those countries in which rabies is present, reported to the relevant national authority, which in
it should be considered as a differential diagnosis in turn will initiate a full epidemiological investigation
neurological cases. It also has important zoonotic and instigate their own national control and advi-
implications. sory plan.
Aetiology Aujeszky’s disease

Rabies is caused by a neurotropic rhabdovirus, (syn. pseudorabies)
which is excreted in saliva and transmitted by the Definition/overview
bite of a rabid animal such as a dog. Goats are Aujeszky’s disease is primarily a condition of pigs
effectively end hosts and rarely transmit the dis- that can pass to goats kept in close contact. Individual
ease when infected, although there is always the cases are invariably sporadic, but morbidity and sub-
possibility of infected saliva gaining access to cuts sequent mortality within outbreaks may be high.
and abrasions on the hands and arms of human
handlers – hence its potential importance as a zoo- Aetiology
notic infection, although there appear to be no Caused by a herpesvirus that is excreted in saliva and
reports of human infection acquired from goats. nasal droplets and can remain active in a damp warm
environment for several months. Indirect transfer
Pathophysiology has been reported via transport vehicles previously
After a bite, the virus replicates at the site of the used for pigs.
lesion, before tracking along peripheral nerves to
the CNS. The distance of the bite from the CNS Pathophysiology
dictates the incubation period, with bites on the face Goats that become infected are almost always housed
resulting in clinical disease developing more rapidly with or close to pigs in which infection is established.
than one on the distal limb. The virus continues to Virus is picked up either via aerosol inhalation or
replicate within the CNS, resulting in the expres- contamination of skin abrasions. The incubation
sion of clinical disease. period is very short (less than 5 days), after which
the virus has a predilection for CNS tissue.
Clinical disease is rare, but signs have included an Clinical presentation
increase in aggressive behaviour, excessive vocalisa- Severe pruritus is a very common finding, with
tion, salivation, ataxia and recumbency. intense rubbing, scratching and licking leading
to self-inflicted trauma. In acute infection goats
Diagnosis may simply be found dead or show marked pyrexia
Diagnosis is problematic due to the often vague ini- and profound depression, leading to recumbency,
tial presenting signs, with a presumptive diagnosis rumen tympany and death with or without pruritus.
Diagnosis Aetiology
The clinical presentation of acute disease, pruritus
The metacestode stage found in the CNS of an
and contact with pigs all lead to a presumptive diag-
infected goat is Coenurus cerebralis, the intermediate
nosis. Serology is of limited value as goats rarely live
stage of the carnivore tapeworm Taenia multiceps.
long enough to mount an immune response. There
are no gross lesions at PME, and confirmation is
Pathophysiology
based on the typical histological picture of a severe
The tapeworm segments are passed in the faeces
focal non-suppurative encephalitis and myelitis and
of the dog or fox. If these are ingested by a grazing
subsequent immunohistochemistry.
goat, the Taenia eggs are released and penetrate the
gut wall, entering the blood stream. Those meta-
cestode stages that reach the brain begin to develop
Cases in which pruritus is a feature need to be dif-
and increase in size, although it is usually only one
ferentiated from skin disease (see Chapter 11), and
that outgrows the remainder over a period of several
scrapie and rabies, which can both cause neurogenic
weeks, developing into a thin-walled, fluid-filled cys-
pruritus. Acute cases need to be differentiated from
tic structure in which the developmental scolices may
CCN, acute listeriosis and poisoning.
be seen within the cyst wall (Fig. 8.21). If the goat
Treatment/management/control dies or is slaughtered, and its head is eaten by carni-
There is no treatment. Control is based on avoiding vores thus consuming the cystic structure, a new wave
keeping goats near potentially infected pigs. Many of T. multiceps will develop to complete the life cycle.
countries have control and eradication measures in
place for the disease in pigs, which has a direct effect Clinical presentation
on reducing the risks to goats. The clinical presentation depends on the size of the
cyst and its location. In the early stages, signs may be
Caprine arthritis encephalitis very vague, including dullness, apathy, inappetence
See Chapter 9. and an unsteady gait. As the cyst grows, the intra-
cranial pressure will increase, with signs determined
Louping ill by its location. A cyst found in the cerebellum tends
Louping ill is caused by a tick-borne flavivirus, most to produce the most dramatic signs, including opis-
commonly seen in sheep in the UK, but capable thotonus and a severe loss of balance. Cysts in the
of causing clinical disease in goats. It is character- cerebral cortex can be quite large, even destroying
ised by an initial febrile viraemic stage, which may
be accompanied by depression and anorexia, fol-
lowed in susceptible animals by neurological signs.
In goats with encephalitis, the clinical signs may
include muscle tremors and/or rigidity, incoordina-
tion, ataxia, hypersensitivity, salivation and nervous
nibbling, progressing in some cases to head pressing,
posterior paralysis, recumbency, convulsions and/or
coma. It is a differential diagnosis for other neuro-
logical conditions such as scrapie.
Coenurosis
(syn. gid)
Definition/overview
Coenurosis is a space-occupying lesion in the brain Fig. 8.21 Coenurus (gid) cyst in caudal cerebellar
(and occasionally in the spinal cord) of ruminants tissue. Note the scolices (arrows) evident on the cyst
caused by a metacestode parasitic cyst. wall between the occipital condyles.
214 Chapter 8
(by pressure necrosis) 50% or more of the total cor- elsewhere carry a poor prognosis. Surgery is most
tex, with only minimal signs. If the cyst is present on successful when there is obvious thinning of the skull
one side of the cortex, the goat will tend to move or overlying the cyst. The goat is sedated or anaesthe-
circle to that side, with blindness in the opposite eye. tised, and an incision is made down to the bone over
In established cases, softening of the skull overly- the cyst location. Using a bone trephine, a circular
ing the cyst may be apparent, and gentle downward hole is created. If the cyst has been correctly located,
pressure may exacerbate the clinical signs. Cysts it should be seen beneath the dura mater and will
developing in the spinal cord will result in gradual begin to protrude when the dura is cut. Using blunt
leg weakness (depending on location) and progres- forceps, the cyst wall is grasped (Fig. 8.23), with its
sive paresis. removal facilitated by holding the goat’s head upside
down. The skin is closed over the incision.
Diagnosis Prevention is based on ensuring that dead sheep
Diagnosis is based on the clinical signs, and the and goats are not left in the open for carnivores to
knowledge that the pathogen is present in the local- consume, and that goat and sheep offal (particularly
ity. There are no reliable laboratory tests, but MRI or the head) is not fed. If gid is a known problem, then
CT scans are useful in valuable animals (Fig. 8.22). regular worming of all dogs in the locality against
At PME, thin-walled cystic structures can be clearly tapeworms should be encouraged.
identified within the CNS tissue.
Cerebrospinal nematodiasis
Differential diagnosis (syn. meningeal worm)
Once established, the condition needs to be differ- Cerebrospinal nematodiasis is reported in goats in
entiated from other space-occupying lesions such as Switzerland, occurring mainly in winter. Goats
brain abscesses, the pituitary abscess syndrome and present with progressive ataxia in the hind legs and
trauma. proprioceptive deficits, circling, vestibular syndrome
and eventually recumbency, but with normal appe-
Treatment/management/control tite. CSF may contain eosinophils. Elaphostrongylus
There is no medical treatment for the condition. cervi and Parelaphostrongylus tenuis are nematodes
A thorough neurological assessment enables identi- suspected to be involved. P. tenuis has occurred in
fication of the location of the cyst. If located in the llamas in the UK. Treatment with albendazole may
cerebral cortex, it can be removed quite success- be tried. Monthly ivermectin treatment is used for
fully. Cysts present in the cerebellum, spinal cord or prevention in camelids in the US.
2 1
LOSSY (Q=95)
Fig. 8.22 MRI showing a cerebral coenurus (gid) Fig. 8.23 Surgical treatment of gid. The cyst wall is
cyst in a ram (1 = cyst; 2 = nasal septum; 3 = tongue). grasped and the cyst removed.
CHAPTER 9
MUSCULOSKELETAL DISEASE
INCLUDING FOOT DISORDERS 215
CLINICAL EXAMINATION OF THE Gait and posture

MUSCULOSKELETAL SYSTEM The goat is assessed while walking. A weight-bearing
lameness presents with a shortened stride of the nor-
Clinical assessment mal leg, and lesions tend to affect the lower limb or
History and environment involve fractures or joint infection. At the point of
Speed of onset can give an indication as to the likely weight-bearing, the head is lifted up if a front leg is
cause; for example, slow onset in degenerative joint involved or dipped down if a hind leg is involved.
conditions as opposed to sudden onset in fracture A swinging leg lameness presents with a shortened
cases. Establishing current environment (Fig. 9.1) stride of the affected leg, and usually indicates an
as well as recent management procedures, and upper limb problem. The degree of lameness (on a
observation of animal behaviour is important for scale of 1 to 5 or 1 to 10) gives an indication of likely
prevention of further cases (handling, transport, pathology, and should be recorded in case notes to
oestrus etc.; Fig. 9.2). Diet analysis is important allow monitoring of progression.
where metabolic bone or cartilage disease is sus- Resting of one particular leg may be obvious
pected. For infectious causes, potential breaches when the goat stands still (Fig. 9.3). Limb angula-
in biosecurity and disease prevention should be tion and position are judged for normal appearance.
investigated. Noting any asymmetry between the left and right
Fig. 9.1 A rubber mat on the ramp into the milking Fig. 9.2 Goats rushing to exit the parlour increases
parlour provides good grip, thereby reducing the risk the risk of musculoskeletal trauma. The green
of slipping. gate swung into the goats’ path poses an additional
injury risk.
216 Chapter 9
placing a companion animal at a distance may encour-

age the patient to trot away from the observer.
Imaging
Radiography is useful to establish bone integrity and
position and the presence of joint effusion or degen-
erative changes, as well as soft tissue swelling and
integrity (e.g. gas shadows in open fractures). A view
of the contralateral leg is invaluable if one is unsure
about normal radiographic anatomy or appearance
(e.g. open growth plates in young goats; Fig. 9.4).
Ultrasonography is useful for tendon injuries
and investigation of swellings (e.g. differentiating
Fig. 9.3 Non-weight-bearing lameness caused by a an abscess from a haematoma). It can also be used
foot abscess in the right hind leg. successfully to demonstrate an interruption in bone
outline (e.g. in a pelvic fracture).
body sections is very useful and indicates muscle Other imaging modalities include MRI, CT,
atrophy or tissue swelling. arthroscopy, thermography and scintigraphy.
Palpation Arthrocentesis
Ideally, the goat should be in lateral recumbency This is easiest performed with the goat in lateral
for further assessment (using sedation if neces- recumbency. The site is clipped and thoroughly sur-
sary). Attention is paid to any hair loss, skin abra- gically prepared. Asepsis must be strictly maintained
sions, soiled areas or discharge. Palpation establishes throughout. A 20 or 21 gauge needle (3.75 cm [1.5 in]
excessive or reduced range of movement, heat or long for stifle, 1.8–2.5 cm [3/4 to 1 in] long for other
coldness, pain, crepitus and any swelling. Joints are joints) is inserted into the joint cavity. Having broken
assessed for effusion. If pain is detected, care must be the seal, a 2 or 5 ml syringe is attached and joint fluid
taken to manipulate the leg very gently and to move aspirated. The synovial fluid is transferred into EDTA
one joint at a time, so that the affected region can and plain sample containers and assessed for nucleated
be accurately determined. Auscultation while mov- cells and protein, plus bacterial culture where required.
ing the leg can be useful in heavily muscled animals When interpreting results, communications between
to detect any crepitus in the shoulder or hip region. joint compartments must be taken into account.
Average values for normal synovial fluid of the
General assessment goat are 20 g/l protein and a nucleated cell count of
Some infectious causes affect additional body sys- 50/µl, of which most are lymphocytes or monocytes.
tems or vital signs. Where a traumatic aetiology is
suspected, the patient is examined for systemic prob- Nerve and joint blocks
lems, such as ABC (airway, breathing, circulation), To allow accurate interpretation, lameness must be
hypo- or hyperthermia, shock or hypovolaemia, and shown consistently. The blocks are carried out in a
haemorrhage. distal to proximal sequence along the leg. Thorough
surgical preparation of the injection site and aseptic
Ancillary diagnostics technique throughout are absolutely essential. Using
Flexion tests a 23–25 gauge, 1.8 cm (3/4 in) long needle, 1–2 ml
Applying maximum flexion to a joint can exacerbate of lidocaine or mepivicaine is injected either over
lameness. Starting with the most distal joint, flexion the nerve or into the joint. To maintain asepsis, a
is held for 2 minutes, followed by the animal mov- new bottle of local is used for each joint block. Loss
ing off at a trot. For goats that are not halter trained, of skin sensation confirms the onset of a successful
Musc u l os k e l e ta l D is e a s e I nc lu di ng Fo o t D isor de r s 217
(a) (b)

Fig. 9.4 Lateral (a) and dorsoplantar (b) radiographs of the stifle of a 1-month-old lamb showing open growth
plates and the secondary centre of ossification of the tibia (X). Osteomyelitis is present in the lateral condyle of
the femur.
nerve block. Deep pain, mechanical lameness or Aetiology

learned behaviour may lead to unsuccessful isolation The condition is classically linked to calciferol (vita-
of the affected region or joint. If blocks are conducted min D) deficiency, but has also been linked to long-
in multiple legs, care must be taken not to reach the term deficiencies of calcium or phosphorus when
toxic dose for local anaesthetic (see Chapter 18), and calciferol levels have been considered adequate.
the animal may be ataxic for a few hours.
Pathophysiology
NON-INFECTIOUS DISEASES Inadequate mineralisation results in a structural
weakness of bone tissue, which is most apparent in
Nutritional muscular dystrophy/ the long bones, resulting in visible distortion and
white muscle disease ‘bowing’ of legs and prominent end plates.
Selenium/tocopherol (vitamin E) deficiency (see
Chapter 15). Clinical presentation
Affected goats initially develop a stiff gait and are
Rickets reluctant to move. When viewed from the front,
Definition/overview there is visible ‘bowing’ of the front legs (angular
Rickets is a disease of young growing goats limb deformity [ALD]; Fig. 9.5) and swelling of the
(mainly those kept indoors) associated with a fail- carpi. Palpation of the epiphysis often elicits pain,
ure of bone mineralisation in the epiphyses of the and palpable enlargement of the costochondral
long bones. junctions may also be apparent. Within an affected
218 Chapter 9
Osteodystrophy of mature bone

Overview
Metabolic bone diseases occur with reasonable fre-
quency in young adult or mature goats.
Aetiology
A deficiency or imbalance of the minerals calcium,
phosphorus and copper, and the calciferols (vita-
min D). Calcification, and bone tissue and cartilage
formation, are impaired. In the mature bone, this may
lead to poor mineralisation of the trabecular structure
at the ends of weight-bearing bone (osteomalacia) or
bone cortices (osteoporosis). Enzootic calcinosis is
also recognised in goats, typically caused by plant
poisoning or by excessive calcium intake or cholecal-
Fig. 9.5 Angular limb deformity affecting all four ciferol (vitamin D3) supplementation. Little infor-
legs in a lamb. This may be congenital, but rickets mation is available on renal failure-induced mineral
should be ruled out. imbalance causing osteodystrophy in the goat.
cohort, there may be goats showing severe abnor- Clinical presentation

malities alongside others with subclinical disease. Stiffness, increased periods of recumbency, reluc-
tance to move or rise and increased incidence of long
Diagnosis bone fractures are common signs. Milk yield and
Diagnosis is based on clinical signs and a review of body condition are often reduced. Where vertebrae
feeding and management practices. Elevated serum are affected, lordosis and kyphosis are seen. Swelling
alkaline phosphatase (SAP) is a consistent finding. of joints (especially hock) and epiphyses (especially
There may also be a reduction in serum calcium and with copper deficiency) is reported.
phosphorus and other minerals such as copper and
zinc. Radiographic examination may confirm poor Diagnosis
bone density in long bones, with widening of the Most useful for a definitive diagnosis are post-mor-
growth plates. tem findings including histopathology and bone ash
concentration. Serum calcium may be low and SAP is
Differential diagnosis often elevated because of bone pathology. Thinning
The clinical presentation is quite characteristic. of cortices may be seen on radiographs. Ration anal-
Congenital ALD or a poorly aligned healed fracture ysis is important to establish the cause. Typically,
should be considered. several animals are affected over a period of time.

Severely affected goats may need to be culled on Other causes of fractures such as trauma, disco-
humane grounds. Those less severely affected may spondylitis for spinal presentation, septic arthritis
respond to management changes aiming to correct for joint swelling (with associated increased cellu-
the mineral imbalance and allowing access to day- lar content of joint fluid), other infectious causes of
light if this has been deprived. This approach will musculoskeletal problems.
also prevent further cases developing. Calciferol
(vitamin D) administration at 1,000–2,000 IU/kg Treatment/management/control
given twice (1 month apart as injection or 2 weeks Euthanasia in severely affected animals, otherwise
apart as oral paste) is beneficial in some cases. there is usually a good response to a balanced diet,
with recovery over 2–3 weeks. Control relies on

adequate mineral and vitamin supplementation, in
particular on farms using home grown cereal based
diets (cereals have a high phosphorus:calcium ratio).
Fractures
Overview
Fractures comprise one of the more common mus-
culoskeletal disorders associated with marked pain.
Aetiology Fig. 9.6 Follow-up

Trauma is the most common cause of fractures in radiography (taken
livestock. However, spontaneous fractures may through the cast)
occur, especially as a sequela to osteodystrophy. showing poor callus
A cluster of long-bone fractures in a group of animals formation at a
should prompt assessment of the diet for mineral metatarsal fracture in
imbalances (e.g. hypophosphataemia). Pathological a lamb. Insufficient
fractures may occur in bone weakened by infection stabilisation, poor
or necrosis. blood supply or
infection of the
Clinical presentation fracture are the main
Typically, acute onset non-weight-bearing lameness. considerations.
Muscle tone in the affected leg is lost and the leg
may hang limply, possibly showing abnormal angu- Differential diagnosis
lation. Unusual and abnormal movement of adjacent Decreased weight bearing and gait abnormalities
parts of the leg may be present. There may be severe may be caused by septic arthritis, joint dislocation,
soft tissue swelling in upper leg fractures, caused tendon or ligament rupture and neurological deficits.
by haematoma formation. Crepitus is evident when Tendon, ligament or neurological problems should
the leg is moved (this should be performed very also be considered for abnormal angulation (see
gently). Pain on manipulation is not always present. Fig. 8.14) or excessive movement in the limb.
Superficial soft tissue damage may be present, and in
open fractures a bone fragment may protrude from Treatment/management/control
the wound. First aid is important to prevent further displacement
and soft tissue trauma. The patient’s movements are
Diagnosis restricted (e.g. tying up, hurdles). If transport is nec-
Even though the diagnosis is usually obvious based essary, a Robert-Jones bandage or splinting is imper-
on clinical findings, radiographs should be taken ative (Table 9.1), and the patient is placed with two
whenever possible. Assessment of alignment, fracture sound legs forward in the vehicle (which is padded
direction (straight, spiral etc.), and joint involvement out to limit movement). Failure of passive transfer
is important for choice of treatment and prognosis. needs to be considered in neonatal fracture patients.
Gas shadows in the tissues surrounding the site sug- Treatment is governed by the type of fracture,
gest an open or infected fracture. Follow-up radio- expertise and available equipment, as well as costs
graphs will demonstrate callus formation, union or and future purpose of the patient. Techniques used
complications such as osteomyelitis (Fig. 9.6). In in companion animal orthopaedics can generally be
young animals with open growth plates, comparative applied in the goat. In brief, options include:
views of the unaffected contralateral leg are often •• Box rest. For fractures involving the humerus or
helpful for interpretation. femur. Box rest may only be considered if there
220 Chapter 9
Table 9.1 Splint positioning in relation to fracture site.
FRACTURE REGION SPLINT DETAILS

Front leg
Foot up to and including carpus One splint each on the lateral and palmar aspect of the leg, reaching from the foot to the elbow
Proximal carpus up to and Single splint on the lateral aspect of the leg, reaching from the foot to the top of the shoulder
including the elbow blade (with the holding bandage extending as high into the axilla as possible)
Above the elbow No splint. A Velpeau sling may be appropriate in some cases
Hind leg
Foot to proximal metatarsus One splint each on the lateral and plantar aspects of the leg, reaching from the foot to mid-tibia
Between and including the hock Single splint on the lateral aspect of the leg, reaching from the foot to the hip joint (with the
and stifle holding bandage extending as high into the groin as possible)
Above stifle No splint. An Ehmer sling may be appropriate in some cases
of the fracture, and therefore is only suitable

for lower limb fractures up to the level of the
carpus or proximal metatarsus (Fig. 9.7). Deep
sedation and analgesia must be provided to allow
pain-free manipulation of the limb in order to
achieve good alignment and prevent movement
during cast setting. In growing animals, the foot
Fig. 9.7 A cast used is not included in a cast and the support replaced
to stabilise a metatarsal after 10–14 days.
fracture. Elastic bandage •• Hanging pin casts (also called transfixation pin
has been applied at the casts) are an intermediary between coaptation
proximal end to stop and external skeletal fixation. It is a useful
bedding getting between technique for comminuted fractures with many
cast and leg. Note that or small fragments, or where the distal fragment
deep straw bedding is very small or close to a joint.
can make it difficult •• External skeletal fixation (ESF) is useful for
for a goat with a cast to comminuted and open fractures (Fig. 9.8).
move freely. General anaesthesia is required to allow proper
placement of the pins. While a technique readily
is no displacement, no joint involvement and the achievable in private practice, it requires familiarity
animal is ambulatory. Because a good degree of with the art and science behind it. ESF does have
muscle mass is required to stabilise the fracture, the disadvantage of creating some motion at the
it is rarely suitable for goats. Appropriate bone–pin interface, creating pain. Compared with
analgesia must be provided. internal fixation, less reduction and anatomical
•• Amputation may be considered in open or alignment of the fracture is achieved.
severely comminuted fractures. Goats are •• Intramedullary pins are suitable for some
nimble and lightweight and cope well with an types of fractures, such as simple mid-shaft
amputated leg. The technique is the same as for upper limb ones. They do not provide much
companion animals. stability against rotational forces and the pin is
•• External coaptation involves the application a potential tract for infection. They sometimes
of a cast, splint or Robert-Jones bandage. can be used successfully in combination with
The support must include the joints either side cerclage wires for comminuted fractures.
(a) (b)
Fig. 9.8 (a) External skeletal fixation for an open metacarpal fracture in an alpaca cria, allowing ongoing
wound care. (b) The corresponding radiograph showing pin placement in relation to the fracture site and
adjacent joints.
•• Internal fixation in the form of ASIF plates and Aetiology

screws requires special equipment and expertise. The typical cause is trauma to the leg and is the
Neonates can pose a special problem, with their reason why the metacarpus and metatarsus are
thin bone cortices offering little holding power most often affected (with little ‘soft tissue pad-
to screws. ding’ over these particular bones). However, hae-
matogenous spread of infection is also recognised
Good nursing care is essential. Especially, young as a cause, potentially leading to several sequestra
animals require help in standing up for the first few (Fig. 9.9). Where a haematogenous aetiology is
days. Malodour, increased heat in the limb, pyrexia
or a period of weight-bearing followed by protect-
ing the leg indicates a problem, and should prompt
re-assessment. Disuse atrophy after extended immo-
bilisation is commonly seen, and it is important to
provide support of decreasing strength after cast/
fixation removal, such as a Robert-Jones bandage or
splint, or removing ESF pins gradually.
Complications include nerve damage, non-
union, osteomyelitis, abnormal bone growth and
nursing complications. Blood supply to the portion
distal to the fracture may also be compromised.
Prognosis is generally better in young animals (less
body weight, better bone healing, better mobility),
distal limb versus proximal limb, closed versus open
and simple versus comminuted fractures. Quite
often there is a delay in presenting goat patients,
reducing prognosis.
Bone sequestrum
Overview
A bone sequestrum results from the loss of periosteal Fig. 9.9 Multiple areas of osteomyelitis in the right
or cortical blood supply to a small section of long metatarsus of a lamb. Similar lesions were also present
bone, with concurrent infection. Surgical treatment in the left metatarsus and tibia and both metacarpi,
is indicated to achieve long-term resolution. suggesting a haematogenous aetiology.
222 Chapter 9
suspected, other potential abscessation sites, such over the area in question, with lysis around the dead
as liver or heart valves, need to be examined. The piece of bone and diffuse new bone formation in the
pathogens involved tend to reflect those in the ani- area. To aid later surgical approach, it is of great help
mal’s environment. to position 2–3 three radiodense markers (e.g. skin
staples or drawing pins secured with clear adhesive
Clinical presentation tape) onto landmarks such as a discharging tract or
A bone sequestrum should be suspected in non- particular anatomical feature (Fig. 9.10b).
healing wounds of the lower limb (Fig. 9.10a), recur-
rence of discharge through a fistula or recurrent Differential diagnosis
lameness with pain on palpation over a small area of For a discharging fistula, foreign body embedment
one of the long bones. The degree of lameness can or soft tissue abscess. For pain on palpation, fracture
vary from mild to severe. (acute or non-union) or ostitis/periostitis.
Diagnosis Treatment/management/control
Confirmative diagnosis is via radiography. No radio- Surgical removal of the sequestrum gives the best
graphic changes will be seen for the first few weeks long-term prognosis. A temporary resolution of
after the insult. Then, the cortices appear disrupted any discharge may be achieved with antibiosis,
(a)
(c) (b)
Fig. 9.10 (a) Chronic discharging fistula at the level of the radius. (b) Corresponding radiograph showing
a bone sequestrum. Two skin staples (arrows) were placed either side of the fistula to aid orientation.
(c) The sequestrum (arrow) in the process of being removed. Note the circumcision of the fistulous opening.
but invariably the foreign body nature of the seques- shows abnormal distances. Radiography with flexed,
trum will lead to a flare up. In addition, the loss of extended and skyline views is used to confirm.
blood supply leads to poor drug penetration of the
area. Prognosis for surgical resolution is about 80% Differential diagnosis
in cattle (no figure known for goats). Fracture of the affected joint or nearest long bone
Surgery may be carried out under general anaesthe- (e.g. femoral fracture in hip dislocation), confirmed
sia or sedation and i/v regional anaesthesia (although by radiography.
the latter was found to carry a lower prognosis in
cattle). A longitudinal skin incision is made over Treatment/management/control
the sequestrum. Where this coincides with any dis- Best prognosis is achieved when the patient is
charging tract, the fistulous opening is circumcised. attended to within 12 hours. Closed or open reduc-
Exploration follows to locate a loose edge of the seques- tion is suitable for hip, shoulder and elbow disloca-
trum. Occasionally, a bone chisel is required to loosen tions. A Velpeau (front leg) or Ehmer (hind leg) sling
the piece of dead bone (Fig. 9.10c). After removal, any is applied prior to recovery from sedation or general
remaining abnormal soft bone in the area is removed anaesthesia for several days to provide stability fol-
with a curette. The skin incision is closed in a rou- lowing reduction. The goat should receive suitable
tine fashion. Leg support is necessary for 2–4 weeks; analgesia and box rest for several weeks.
a Robert-Jones bandage, cast or splint are all suitable. For patellar luxation and ruptured cruciate
ligament, surgical techniques used in the dog are
Joint dislocation suitable.
Overview
Dislocation typically affects the upper limb joints: Tendon injuries
hip, stifle, shoulder or elbow. Patellar luxation has Overview
also been described in the goat. Flexor tendon injuries appear to be most common.
Aetiology Aetiology
Joint dislocation usually occurs as a result of exces- A traumatic insult is common in farmed livestock.
sive rotational force caused, for example, by the Spontaneous rupture may result from excessive rota-
leg becoming trapped, inaccurate handling or dis- tional or weight-bearing force. Occasionally, prior
mounting in the male. The female appears to be at infection leads to weakening of a tendon. The role
particular risk of hip dislocation in the periparturi- of hypophosphataemia or compartment syndrome
ent period and during oestrus. Patellar luxation, in is not known in the goat. Multiple tendons may be
particular bilateral medial, may be congenital. involved.
Clinical presentation Clinical presentation

Severe, acute-onset, swinging leg lameness with A physical, external insult (e.g. from farm machin-
markedly reduced anterior phase. With hip disloca- ery) typically results in a wound. Rupture as a result
tion in a craniodorsal direction, the animal usually of excessive force (e.g. involving the gastrocnemius
remains ambulatory, whereas dislocation in a cau- tendon) may be ‘closed’, with the overlying skin
doventral direction results in recumbency. Pain on intact. The angulation of the leg is changed, with
palpation, increased joint movement, swelling in the overextension of the immediately affected joint,
joint area and crepitus are commonly present. resulting in overflexion of other joints. Swelling may
be present over the rupture site.
Diagnosis
Comparison of angulation, position and joint space Diagnosis
with the contralateral, unaffected leg shows dis- Clinical signs such as visible trauma to the tendon
symmetry; comparison with anatomical landmarks or abnormal limb angulation are usually diagnostic.
224 Chapter 9
Changed joint angulation caused by peripheral nerve
deficiency will show loss of skin sensation over the area
innervated by the relevant nerve (see Fig. 8.13).
First aid consists of stabilising the leg in a flexed posi-
tion (using a splint or Robert-Jones bandage). Where
a wound is present, this is treated in the standard way
using lavage, debridement and bandaging, combined
with antibiosis (systemic, i/v regional or intraosseus)
and anti-inflammatory therapy. Depending on the site
of the wound, joint involvement must be ruled out.
Options for stabilising the tendon include splint-
ing, casting (once tissue infection is under control, or
using a fenestrated cast), tenorrhaphy or a combina-
tion of these. Prognosis for traumatic ruptures in the Fig. 9.11 Severe erosion of the femoral head
lower limb is good, but convalescence may be several cartilage, presumed secondary to hip dysplasia (alpaca
months. Chronic lameness and digit hyperextension specimen).
are the most common complications. Upper limb
tendon ruptures carry a guarded prognosis. to be bilateral. Lameness may not be o bvious until
osteochondrosis dissecans is present.
Cartilage disorders DJD is a severe, progressive arthropathy, typi-
Overview cally affecting the fetlock and carpal joints.
Hip dysplasia, osteochondrosis (OC) and degenera-
tive joint disease (DJD) fall into this category. Diagnosis
Radiography is a useful first-line imaging modal-
Aetiology ity, followed by ultrasonography, MRI or CT if
In goats, factors such as age (young adult for OC required. DJD lesions may appear aggressive and
and DJD), gender (males) or breed disposition, as septic on radiography, but tend to be focal, and there
recognised in other species, are not established. Fast is usually little joint effusion. Joint fluid analysis is
growth and excessive body weight are likely to play either within normal limits or shows mild inflamma-
a role. OC is a complex arthropathy. Its aetiology is tion and mildly increased protein levels.
still poorly understood, but a heritable component
is present in other species and it may be a precursor Differential diagnosis
for DJD. Septic arthritis results in joint effusion and joint
fluid with marked cellularity and high protein.
Clinical presentation Osteoarthritis is a differential to DJD, but typically
Animals with hip dysplasia present with a shortened affects older animals.
stride and pain on palpation and extension of the hip
joint. While usually a bilateral condition, one leg is Treatment/management/control
often affected worse. When looking from behind, For hip dysplasia, the conservative and surgi-
the stifle and fetlock are rotated outwards and the cal options used in the dog may be considered.
hock inwards. The dorsal acetabulum and femoral Conservative treatment of OC includes box rest
head are affected in hip dysplasia (Fig. 9.11). for 3–6 months, combined with NSAIDs and pos-
OC commonly affects the atlanto-occipital and sibly intra-articular hyaluronic acid or polysul-
femoropatellar joints, but also the hip joint, and tends fated glycosaminglycan. Surgical options include
debridement and forage or microfracture. Prognosis because of close contact. Feeding pooled colostrum
is poor if radiographic signs of DJD are pres- and milk (Fig. 9.12) in dairy herds can also lead
ent at the commencement of treatment. For DJD, to increased infection rates as one infected doe can
arthroscopic debridement, lavage and NSAID ther- infect the pool, and hence potentially a large num-
apy may be tried, but is likely to result in temporary ber of kids.
relief only. In general, because high motion joints The development of any clinical disease after
are involved, arthrodesis is not feasible for these car- infection will be slow and protracted, and as
tilage disorders. such is associated with a high prevalence of latent
Affected goats should be removed from the breed- inapparent infection, in which goats remain fit,
ing pool, in particular males. healthy and productive. The incubation period
between infection and the development of clini-
INFECTIOUS DISEASES cal signs can be very variable. Infection induces
a strong humoral response, but the antibody pro-
Caprine arthritis encephalitis duced is not protective, and an infected goat is
Definition/overview essentially both virus and antibody positive. The
Caprine arthritis encephalitis (CAE) is a viral disease colostrum from infected dams will contain both
caused by CAE virus (CAEV). It is an important dis- virus and antibody, the latter affording no mater-
ease of goats worldwide, causing a spectrum of clini- nal protection.
cal presentations and was only identified in the early After infection is acquired by whatever route, the
1970s. Many countries have instigated voluntary or virus quickly enters the reticuloendothelial system,
compulsory control and eradication programmes. carrying virus to target tissues such as the synovial
membrane, lung, choroid plexus and udder where
Aetiology virus replication and lymphoproliferation continues.
A lentivirus in the family Retroviridae, a genus caus-
ing a group of slowly developing insidious conditions Clinical presentation
such as CAE and maedi visna (MV) of sheep, the two After initial infection, goats may be asymptomatic
diseases often referred to collectively as SRLV (small for many months or even years before clinical dis-
ruminant lentivirus). Although the two viruses cause ease is seen. There are a number of different clinical
different clinical presentations in their respective presentations that may be encountered either singly
host species, cross-species infection can occur and or in combination.
is an important factor in CAE control programmes.
Pathophysiology
CAE is transmitted predominantly via the ingestion
of infected colostrum or milk from infected does.
There are, however, many other important routes
of infection such as via nose to nose contact and
aerosol transfer, via ‘infected milk impacts’ at the
teat end in the milking parlour, or through shared
use of equipment such as drenching guns or tattoo-
ing equipment. Transplacental infection can occur
but is thought to be at low levels, and although both
embryo transfer and artificial insemination may
pose only a minimal risk of transferring infection,
both practices need to be risk managed if eradica-
tion is being attempted. Increased infection rates Fig. 9.12 Feeding pooled colostrum, a major risk
will occur in housed and intensively managed goats factor for CAE transfer in infected herds.
226 Chapter 9
Arthritis manifestations of CAE in the individual or herd.

Seen most commonly in mature goats aged 12 months Secondary bacterial infection may be a sequela.
and older. The onset may be acute or more slowly
developing. All leg joints are susceptible, as is the Mastitis
atlanto-occipital joint. The carpal joint appears to be Referred to colloquially as ‘hard udder’, CAE infec-
the most common site (Fig. 9.13), followed by the tar- tion has been linked to the development of an indu-
sal, stifle and fetlock joints. Single or multiple joints rative mastitis in which the udder tissue becomes
may be affected. Most affected joints are enlarged, firm and shrunken and milk production from the
often visibly, but not always painful. Signs will include affected half progressively ceases. The condition is
obvious lameness, unwillingness to move, increased usually insidious in onset. Mastitis is also discussed
recumbency with inappetence and reduced milk pro- in Chapter 12.
duction in lactating goats.
Progressive weight loss
Leucoencephalomyelitis May occur in goats in which other manifestations of
A slowly developing presentation confined to young the disease are apparent, but CAE-seropositive ill-
kids mainly from 1–6 months of age. Early signs thriving goats in which no other more typical signs
include incoordination and poor leg placement are present can also be identified in herd investiga-
progressing to paresis, with the hind legs most tions into CAE.
commonly affected. They may manage to drag
themselves around, and remain relatively bright and Diagnosis
alert in the early stages. Other CNS signs described Diagnosis is based on the clinical signs, a previous
include blindness, nystagmus and abnormal head indication of CAE in the herd and positive CAE
carriage. serology. The possibility of new infection should be
considered when investigating any group of goats
Interstitial pneumonitis with an increased incidence of ill thrift, particu-
A slowly developing condition that may initially larly if there is evidence of increased lameness due
only cause exercise intolerance progressing to dys- to swollen joints, reduced milk yields and udder
pnoea and weight loss, although often with other induration. For serological diagnosis of CAE it is
recommend targeting up to 10 older goats exhib-
iting clinical signs, as infection is usually well
established when clinical signs become evident.
At post-mortem examination (PME), findings
may include lesions within the joints such as vis-
ible thickening of the joint capsule, and in more
chronic cases calcification of the tendon sheaths,
joint capsules and bursae can occur. There may also
be evidence of an indurative mastitis and enlarged
supramammary lymph nodes. Less commonly,
there may be lung pathology and the lungs may be
heavy and swollen. A diagnosis at PME can be made
by histopathological examination of tissues in com-
bination with serological testing.
Depends on the clinical presentation: arthritis
Fig. 9.13 Swollen carpal joint in a CAE-seropositive in mature goats needs to be differentiated from
goat from a herd with a high prevalence of infection. degenerative arthritis or from trauma in more
acute conditions. Nervous signs need to be differen- For this approach to work successfully the two
tiated from swayback and spinal trauma. The signs groups have to be managed completely separately and
of indurative mastitis are fairly typical and distinct strict biosecurity measures put in place. Equipment
from other causes of mastitis. should not be shared, which can be more difficult in
the dairy situation. In a dairy herd the semi-clean
Treatment/management/control group should be milked first and the dirty group sec-
There is no treatment for CAE and no commer- ond. Ideally, the equipment is disinfected between
cial vaccines are available at the time of writing. milkings. At parturition, the clean group should be
Control is therefore based predominantly on kidded separately. Kids from the ‘dirty’ group could
developing a test and cull policy. Determination be snatched at birth before they have been licked or
of the disease prevalence is the first step. Ideally, suckled, but as intrauterine transmission can occur
all mature goats in the herd over 12 months of age in a small proportion of infected dams, further
should be tested using a validated CAE serological screening of these kids as they get older would be
test. If this is not financially viable, a proportion required.
of the herd could be tested ensuring that goats Heat treating or pasteurising has reportedly been
of all age groups (over 12 months) are included. a useful supportive measure: milk or colostrum is
Once the level of infection is established, an eradi- held at 56°C for 60 minutes. Commercial pasteuris-
cation or control programme can be instigated. ers are available.
If the infection is ignored and no control meth- There is evidence of natural cross infection
ods are put in place, it is likely with time that between goats and sheep with CAE and MV,
the infection will lead to significant production respectively. The most likely risk factors are
losses. ingestion of virus-contaminated ovine colostrum
Culling of seropositive animals with or without and milk by goats and vice versa, as well as close
their progeny has been used successfully to reduce contact between the species in overstocked hous-
herd prevalence. This approach involves blood testing. It is unclear at what rate these viruses spread
ing all goats over 12 months at regular intervals within the ‘heterologous’ host population, but
(every 3–6 months) and removing all seropositive there is consensus that SRLV infection across the
animals at each test. After two tests six months apart, species barrier must be taken into account in any
where no antibody positive animals are identified, control programme. Any control programme in
the herd can be classed as free of CAE, providing goats that ignores sheep kept in close contact may
sensible biosecurity procedures have been followed not be successful.
and no goats of unknown health status have been
purchased. Bacterial arthritis (syn. joint ill)
If the prevalence of disease is high in a herd Definition/overview
(or the affected goats are not being kept commer- A condition most commonly encountered in young
cially) and culling of the seropositive a nimals is not kids, referred to as ‘joint ill’, and encountered world-
possible, the herd can be separated into two groups wide, particularly where goats are reared intensively.
(one ‘dirty’ containing seropositive animals and It most commonly results from rearing in unsani-
one ‘semi-clean’ containing seronegative animals). tary conditions, allowing bacterial colonisation of
Seronegative animals cannot be guaranteed to be the umbilicus and resulting septicaemia, especially if
uninfected as some could be in the early stages of combined with failure of passive transfer.
infection. The ‘semi-clean’ group should therefore
be tested on a 6–12 monthly basis and any sero- Aetiology
converted animals moved to the ‘dirty’ group. Any A wide variety of organisms have been incriminated,
animals showing clinical signs of CAE should be most commonly Escherichia coli, Streptococcus dysgalac-
culled as they are likely to be excreting high levels tiae, Trueperella pyogenes, Erysipelothrix rhusiopathiae,
of CAEV. Pasteurella spp. and Klebsiella spp.
228 Chapter 9
Pathophysiology Aetiology
Most infections arise following intensification, with Our understanding of Mycoplasma spp. is dynamic;
few cases seen in kids born outdoors. A combination new species are being identified and known species
of overcrowding, environmental pathogen build-up, reclassified and often renamed. They are quite dis-
lack of umbilical hygiene at birth and hypogamma- tinct from bacteria, do not possess a cell wall and
globulinaemia are all contributing factors. Infection are difficult to grow in the laboratory. Isolation rates
gains entry most commonly via the umbilicus, caus- have been improved by new molecular techniques
ing septicaemia with organisms settling in a number such as denaturing gradient gel electrophoresis
of predilection sites such as joints. (DGGE). The primary species involved in polyar-
thritis are M. capricolum subsp capricolum, M. mycoides
Clinical presentation subsp capri, M. agalactia, M. arginini and M. mycoides
Swollen painful joints in young kids, often with a subsp mycoides, and the distribution of each of these
thickened necrotic umbilicus. The carpus and stifle organisms varies from country to country.
are most commonly affected, followed by the hock
and fetlock. Pathophysiology
Mycoplasma arthritis most commonly occurs in
Diagnosis multiple joints because of localisation of infection
Clinical signs and presenting history are typi- from an initial septicaemia.
cal. Joint aspirates taken aseptically (or at PME)
may appear turbid and will show elevated protein Clinical presentation
and nucleated cell counts. Bacterial culture of Although arthritis can occur at any age (particularly
joint fluid is useful, but false-negative results are with the more virulent Mycoplasma spp. organisms),
common. it is encountered more commonly in kids and young
immature goats. Joint involvement is most often
Differential diagnosis seen in association with other clinical signs within
Joint ill should be differentiated from mycoplasma the spectrum of mycoplasma-associated disease
infection and tick pyaemia and from joint trauma. in the herd, including pneumonia, ocular infections,
mastitis, abortion and agalactia. Carpal, tarsal and
Treatment/management/control stifle joints are most commonly affected and become
Treatment can be disappointing unless instigated at swollen, painful and often warm to the touch, caus-
an early stage by use of broad-spectrum parenteral ing marked lameness and reluctance to move.
antibiosis at a high dose rate. Joint lavage is benefi-
cial in valuable or pet goats, but should be considered Diagnosis
early on in the disease process for best prognosis. Clinical signs are fairly characteristic. Joint aspirates
Control centres on good neonatal kid care (see can be subjected to laboratory testing for mycoplasma
Chapter 4). by culture or DGGE. Affected and recovered goats
may demonstrate seroconversion. At PME, joint fluid
Mycoplasma arthritis is initially clear before becoming turbid and blood
Definition/overview tinged (Fig. 9.14), and there is evidence of a necrotis-
Mycoplasma spp. organisms are responsible for a ing synovitis histologically.
variety of conditions in goats. Contagious caprine
pleuropneumonia is described in Chapter 6 and con- Differential diagnosis
tagious agalactia in Chapter 12. Mycoplasma arthri- Joint ill and tick pyaemia are the main differen-
tis can occur in isolation as a result of localisation in tials. Mycoplasma spp. infection should always be
joints of a septicaemic infection, but it can also be suspected if polyarthritis and joint enlargement are
one of the clinical presentations in a multisystemic seen in association with pyrexia and other clinical
infection such as contagious agalactia. signs within a group of goats.
recorded, goats affected with blackleg may simply be

found dead. Those with malignant oedema usually
present with a localised tissue swelling, often at the
site of a wound or injury. In both conditions, gas accu-
mulates under the skin in the affected areas, causing
crepitus. Disease is confirmed most often at PME in
which typical gas-gangrenous change to muscle tissue
and associated oedema are features. If seen alive, very
high doses of i/v penicillin (20,000 iu/kg q12h) should
be administered, with multiple incisions into affected
tissue to allow aeration and drainage. Prevention is by
the implementation of a multivalent clostridial vac-
cine regime.
Fig. 9.14 Turbid and blood-tinged joint fluid in
infectious arthritis. Arbovirus infection (Akabane,
Schmallenberg)
Treatment/management/control These viruses can cause leg and joint abnormalities
Treatment can be disappointing, particularly if in newborn and neonatal kids (see Chapter 2).
joint lesions are advanced or there are other accom-
panying systemic signs. Prolonged courses (5 days FOOT DISORDERS
m inimum) of, for example, tetracyclines (15 mg/kg)
or tylosin (20–40 mg/kg) have been recommended. Laminitis
Control should be aimed initially at keeping Definition/overview
the important Mycoplasma spp. infections out, by Laminitis is an aseptic inflammation of the sensi-
applying strict biosecurity with quarantine and tive laminae beneath the foot horn. It can present
laboratory testing of incoming goats. Contagious as an acute attack causing severe lameness or can
agalactia, if confirmed, will be controlled by the be chronic causing long-term damage to the foot
imposition of statutory control measures as a architecture.
reportable OIE disease. Vaccines are available in
some countries, and should be used alongside man- Aetiology
agement procedures to minimise spread of infec- The causes of laminitis have been investigated in
tion if confirmed. If infection is widespread, a strict many livestock species, including goats, and opin-
culling policy of infected groups of goats may be ions still vary as to the exact aetiological basis. Cases
beneficial, as infection is seldom restricted to indi- tend to occur predominantly in intensively man-
vidual goats within a cohort. aged herds or in goats kept as pets with excessive
or unsuitable supplementary feeding (e.g. biscuits).
Clostridial myositis Any sudden change in the ration, particularly exces-
Blackleg and malignant oedema caused by the pro- sive feeding of cereal grain (or inadvertent access
liferation of Clostridium chauvoei, Clostridium septicum, to stored grain), can lead to lactic acidosis and to
Clostridium novyi and Clostridium sordellii in muscle tis- laminitis change. It can also occur following an epi-
sue singly or in combination is relatively common in sode of acute toxaemia resulting from, for example,
cattle and sheep worldwide, but relatively uncommon metritis, retained placenta or mastitis.
in goats. Its absence as a cause of disease in the UK,
for example, is the reason ‘4 in 1’ clostridial vaccine Pathophysiology
is generally advised (as opposed to more multivalent The principle lesion appears to be an engorgement
vaccines). In those countries in which it is occasionally of the vessels in the sensitive corium, resulting in
230 Chapter 9
intense pain in the foot in acute cases and insidious show horizontal grooves. If the third phalanx has
changes to the foot architecture in mild (and pos- rotated, horn overgrowth may result in ‘slipper foot’
sibly asymptomatic) cases leading to more long-term formation. Chronic laminitis can be a particular
chronic change. These changes include rotation of problem in geriatric goats.
the third phalanx and progressive distortion of new
horn growth. Diagnosis
Diagnosis is based on the clinical signs described
Clinical presentation and the history suggesting sudden diet change or
In acute cases, affected goats will either stand toxaemia.
motionless unwilling to move or be recumbent and
unwilling to stand, and there may be other signs of Differential diagnosis
illness related to the primary insult. The condition Other causes of lameness need to be eliminated, but
is almost always bilateral, and front feet tend to be laminitis should always be suspected if more than
affected more than hind feet, but all four feet may one foot is affected.
be affected at the same time. The digits feel warm,
particularly around the coronary band, and any Treatment/management/control
pressure applied to this area is resented. Lameness In acute laminitis, any potential underlying fac-
may only be obvious if one individual foot is painful, tors should be identified and managed. Treatment
otherwise a change in gait and stance is more appar- is aimed predominantly at controlling the pain
ent. Frequent weight-shifting may be seen, and goats and discomfort by the use of analgesics and
may walk on their knees (Fig. 9.15) or shuffle along NSAIDs. If a dietary cause has been identified,
lifting affected front feet in an exaggerated manner. rapidly fermentable carbohydrates should be
When hind feet are affected, these are placed for- removed from the diet (or reduced as much as pos-
ward of their natural position. Chronic cases tend sible in lactating does) and replaced by good qual-
to follow a series of earlier laminitic episodes, which ity hay or other forage. In chronic cases, attention
may or may not have been apparent. The claws in should be directed to identifying and removing
chronic laminitis progressively become ‘box shaped’, any underlying causes, and to regular foot trim-
and the horn becomes abnormally hard and may ming to address overgrowth and re-establish the
correct foot shape. Analgesics and NSAIDs are
used if required, with culling on humane grounds
in elderly goats in which there is no improvement.
Prevention is focused on avoiding any sudden
dietary changes.
Scald and footrot

Definition/overview
Footrot is a potentially severe and highly conta-
gious foot disorder affecting both goats and sheep
worldwide, with cross infection and spread between
species. The condition is more prevalent in tem-
perate climates, particularly if goats are kept out-
doors with warm wet conditions underfoot. Severe
outbreaks have also been described in goats kept
Fig. 9.15 Lame goats will often adopt this attitude, indoors on deep litter, when rapid transfer from
and may even move around on their knees, although goat to goat can occur. Scald or interdigital derma-
some goats may naturally feed like this and develop titis is generally classified as a milder form of the
superficial abrasive lesions as a result. condition (Fig. 9.16).
Aetiology compacting with soil and faecal debris and becomes

The primary pathogen of both these conditions is detached, causing underrunning of the wall. This
Dichelobacter nodosus, with Fusobacterium necrophorum often results in the affected claw being shed, a process
as a co-existing secondary pathogen in footrot cases. referred to as ‘thimbling’ (Fig. 9.17).
D. nodosus is an obligate anaerobe, easily adapted to
foot tissue, and was originally thought not to sur- Clinical presentation
vive in the environment for long. Recent work in the This will vary depending on the severity of the
sheep sector, however, has indicated that D. nodosus condition and the number of feet affected. In scald,
can survive for up to 14 days at 5°C in soil, and at when damage may be mild, there may be little or
least 24 days when hoof material is present, depend- no lameness. In established footrot cases, lameness
ing on ambient weather conditions. This factor is becomes more apparent with affected goats reluc-
important when developing any footrot and scald tant to move. If both front legs are affected, goats
control programme. may move around and feed on their knees or remain
recumbent. Other sequelae include loss of condition
Pathophysiology and reduced milk yield.
Weaker strains of D. nodosus are now thought to be
involved in the development of the interdigital lesions Diagnosis
typical of scald and more virulent strains with footrot, Initial diagnosis is based on localisation of any lame-
although these pathogens are often found in associa- ness to the foot, followed by differentiation from
tion with F. necrophorum, an environmental organism other causes of foot lameness. The changes described
that is able to colonise damaged foot epithelial tissue. above are fairly typical in both conditions.
D. nodosus strains possess varying degrees of kerato-
lytic enzyme activity which, in the development of Differential diagnosis
footrot lesions, effectively erodes the thin keratin lay- When a number of goats suddenly become lame,
ers, beginning at the horn–skin junction in the inter- foot and mouth disease, bluetongue and laminitis
digital space and heels and extending to involve large should be considered.
areas of the hoof matrix. Because the sensitive lamina
and its network of capillaries are destroyed by the Treatment/management/control
infection, the hoof wall’s corium loses its blood supply As the condition is contagious, the primary aim is
and anchorage to the underlying tissue, progressively to keep infection out by examining the feet of any
Fig. 9.16 Scald, evident in the interdigital cleft of Fig. 9.17 Severe footrot in a goat housed all year on
the foot of this sheep. deep litter.
232 Chapter 9
purchased goat on arrival and taking swift action Footrot vaccines are available, but should be part
if footrot is suspected. Once identified in a group, of an overall foot health programme; they cannot
the first step is to isolate any affected goats imme- replace it. Culling of any goat that does not respond
diately to prevent further spread of infection, while to treatment, or whose welfare is severely compro-
monitoring the remainder of the group for develop- mised, is recommended.
ing infection. Treatments for footrot in sheep are
constantly under review and undoubtedly influence Treponeme-associated foot disease
the current approaches used in goats. Treatment of Definition/overview
individual cases with systemic antibiosis has proved CODD is a highly contagious foot disorder first
successful in sheep, but is unproven in goats, with identified in sheep and reported in the UK (by one
the added problems of milk withhold for dairy goats. of the authors [DH]) in 1997. Although the char-
Although paring away the infected and underrun tis- acteristic clinical signs identified in sheep have not
sue has been a traditional approach to treatment, this been encountered in goats, a virulent and apparently
is now being challenged in the sheep sector as being contagious presentation with a similar mixed aetiol-
counterproductive. Proprietary antibiotic sprays are ogy has been reported in dairy goats by veterinary
used widely, but have only a short duration of action researchers in the UK at both the University of
and are probably ineffective in deep-rooted infec- Liverpool and the University of Bristol.
tion. Footbathing is an extremely useful approach
for both affected and in-contact goats, and footbaths Aetiology
can be easily installed in race exits from milking par- Consistent isolates have been species of Treponema
lours or buildings. organisms, which have also been incriminated in
Footbathing is only effective if carried out correctly: CODD and in digital dermatitis of cattle. Outbreaks
have been associated with three cultivatable digi-
1 Feet must be clean before entering the footbath tal dermatitis treponeme phylogroups: Treponema
(ideally sprayed with water). medium, Treponema phagedenis and Treponema pedis. It
2 Zinc sulphate 10% is the treatment of is still not known whether the treponeme bacteria
choice, although there are a number of other are the only cause of the disease in goats, or whether
commercial products available worldwide. there are other factors as yet unidentified.
3 Goats must stand in the solution and not run
straight through. Pathophysiology
4 Traditionally, formalin has been used in Treponema organisms can survive in faeces and con-
footbaths, but this product is painful on open taminated bedding, thus facilitating spread between
foot lesions, it poses safety risks to the operator goats. Histopathological examination of early lesions
and disposal is difficult. confirms a morphological diagnosis of chronic lympho-
5 Antibiotic footbaths should only be used where plasmacytic, suppurative and ulcerated pododermatitis.
there is a specific clinical indication such as
contagious ovine digital dermatitis (CODD). Clinical presentation
An appropriate milk withdrawal period must be To date there is no single consistent description of
observed. the disease presentation; however, a common finding
6 Footbath content should be replaced regularly. appears to be severe, non-healing toe, wall or sole
7 Goats must stand on a dry, hard surface (ideally ulcers (Figs. 9.18, 9.19).
concrete) after footbathing until the feet are dry.
8 Animals should be moved to clean pasture, or Diagnosis
cleaned and disinfected pens, after treatment. Diagnosis is currently based on the clinical signs iden-
9 A sponge mat soaked in footbath solution on tified, the sudden emergence within a group of goats
the base of the bath can be an effective way of and its rapid spread within that group. There are cur-
ensuring that all the feet are immersed. rently no commercially available diagnostic tests.
Fig. 9.18 Treponeme-associated solar ulcer. (Image

courtesy Hayley E. Crosby-Durrani.) Fig. 9.19 Radiograph of a chronic lesion suspected to
be associated with Treponema spp. (leg on left). Note
Differential diagnosis the severe bone reaction around, and partial destruction
The condition needs to be differentiated from other of, P3. Of note in the control foot (leg on right) is the
causes of foot lameness, specifically sporadic toe normal club-shape and almost plantigrade position of P3.
ulcers. (Image courtesy Hayley E. Crosby-Durrani.)
Treatment and control is currently extrapolated
from measures developed to control both CODD in
sheep and digital dermatitis in cattle. These include:
•• The rapid identification and isolation of affected

goats.
•• Topical and/or parenteral antibiotic or antibiotic
foot bathing.
•• Improved underfoot hygiene (keeping deep litter
yards clean and dry).
•• A review of foot trimming practices – ensuring
extra care is taken with routine hoof trimming, Fig. 9.20 Foot trimming equipment must be
never over trimming feet and never causing disinfected between animals and herds, particularly
bleeding and hoof damage. where infectious conditions are present.
•• Cleaning and disinfecting hoof clippers between
goats (Fig. 9.20) and handling area after a move around. Under normal circumstances, feet are
trimming session to avoid spread between goats worn down by contact abrasion with the walking
and premises. surface. The problem can be controlled by regular
monitoring of claw length and shape, with foot trim-
Overgrown claws ming undertaken where necessary.
Overgrown claws can be a particular problem
in intensively managed goats kept on deep litter Routine foot trimming
(Fig. 9.21). Wall growth rates can be as high as This is a skilful procedure and should only be under-
6 mm per month. If left untreated, they can lead taken by trained personnel – in untrained hands
to abnormal stresses on joints and other soft tissue overtrimming can have disastrous results. Foot exami-
structures, leading to pain and an unwillingness to nations should be carried out regularly on at least
234 Chapter 9
Fig. 9.21 Foot overgrowth. Note the excessively Fig. 9.22 Goat restrained for foot trimming. Such a
elongated claws. (Image courtesy Kathy Anzuino.) device is useful on large units. (Image courtesy Kathy
Anzuino.)
Fig. 9.23 Trimming of an overgrown hoof wall. Fig. 9.24 Blood must never be drawn on purpose
Note that the wall of the left claw has been trimmed during foot trimming.
back more severely than is ideal in this goat.
a proportion of the herd. However, there is no set fre- Otherwise, using a pair of sheep foot shears, the wall
quency of trimming. If required at all, this will vary horn is trimmed to a level just above the sole surface
from goat to goat and from unit to unit depending on itself (Fig. 9.23). Trimming should be as minimal as
both genetics and environment. In intensively housed possible, and blood must never be drawn on purpose
goats on deep litter, this may be 3–4 times a year (Fig. 9.24). Foot trimming equipment is disinfected
(Fig. 9.22), whereas goats kept in drier climates out- between animals.
doors may never need to have their feet trimmed unless
there is a hereditary abnormality of horn growth. White line disease
Mild to moderate horn overgrowth does White line disease is a condition affecting the junc-
not require trimming if the goat is not lame. tion between the wall and sole horn on the abaxial
Fig. 9.25 Swollen foot due to a well-established foot Fig. 9.26 Burst foot abscess, with a tract that leads
abscess. directly to pedal bone.
solar surface of the foot, whereby the structure

becomes weakened and the junction begins to open
allowing dirt and gravel to become trapped, caus-
ing further separation and eventual pressure on the
sensitive laminae causing lameness. The condition is
most commonly identified on routine examination
and rectified by remedial foot trimming. The con-
dition is more common when the feet are soft and
goats are walking along muddy gravel tracks.
Pedal joint abscess

Outbreaks of pedal joint abscess have been encoun-
tered in goats, presenting as a sudden onset severe
lameness most commonly affecting only one foot
(Fig. 9.3). The condition presents initially as visible Fig. 9.27 Amputated digit showing suppuration of
swelling around the top of the hoof, becoming more the pedal joint.
apparent until the whole foot is affected (Fig. 9.25),
eventually bursting, leaving a tract into the pedal
joint (Fig. 9.26). Various treatment regimes have Foreign bodies and foot lameness
been tried with varying success, and are dependent These include penetration of the sole by sharp pieces
on the stage the condition has reached before therapy of gravel, thorns or metallic debris, and stones and
is commenced. In the early stages parenteral antibio- dried mud becoming trapped between the claws.
sis may be effective. As the condition becomes more
visible, and particularly if the abscess has burst, then Foot and mouth disease
poulticing and lesion irrigation may be attempted. In Foot and mouth disease should always be consid-
severe cases, digit amputation should be considered ered as a differential diagnosis if a number of goats
(Fig. 9.27) and can be highly effective in reducing become lame simultaneously. (See Chapter 17 for
pain and prolonging the productive life of the goat. detailed discussion.)
CHAPTER 10
URINARY TRACT DISEASE

237
NORMAL STRUCTURE AND FUNCTION CLINICAL EXAMINATION OF

THE URINARY TRACT
The kidneys in the goat are non-lobulated with
a smooth surface, and are about 6–7 cm long by Clinical assessment
3.5–5 cm wide. The individual sections of either Direct clinical examination of the urinary tract is
cortex or medulla are largely fused, resulting in limited in the goat. Abdominal palpation may reveal
an internal structure similar to the dog. The right pain on palpation in the kidney area, and some-
kidney lies between the last rib and second lumbar times an enlarged bladder. Behaviour during urina-
vertebra. The left kidney is pushed over to the right tion, such as straining or remaining in a crouched
by the rumen and lies more caudal under the 4th position, and urine flow are important observations.
to 6th lumbar vertebrae. Similarly, the left ureter Differential diagnoses for two common presenta-
initially travels to the right of the midline. The ure- tions, haematuria and haemoglobinuria, are shown
ters enter the bladder near its neck. The urethra is in Table 10.1. Haemoglobinuria is secondary to hae-
about 5–6 cm long in the doe, with a 1–1.5 cm long molytic anaemia, therefore the plasma is discoloured,
suburethral diverticulum near its caudal end. The as well, and the goat may show signs of anaemia.
buck also has a urethral diverticulum, at the level
of the pubic bone. In the male, the urethra ends in Ancillary diagnostics
the urethral process or filiform appendage, which Urinalysis
extends beyond the glans penis (see Fig. 2.31, Obtaining urine is not straightforward in the goat,
p. 45). An adult goat produces on average 2 litres of but worth pursuing. Some females will respond to
urine per day (20–40 ml/kg/day). gentle stroking of the perineal area, taking care not
Table 10.1 Diseases presenting with haematuria or haemoglobinuria.
HAEMATURIA HAEMOGLOBINURIA
Cystitis Bacillary (Clostridium haemolyticum)
Pyelonephritis Nutritional (brassica species; nitrite/nitrate)
Urolithiasis Babesiosis, anaplasmosis, theileriosis
Septicaemia (in particular salmonellosis) Leptospirosis (Leptospira interrogans serovar Pomona)
Enzootic haematuria (bracken fern toxicity) Chronic copper poisoning
Renal infarction Photosensitisation (some cases)
Embolism of renal artery Post-parturient (phosphorus deficiency, possibly also copper deficiency)
Water intoxication
238 Chapter 10
appendage, sigmoid flexure and urethral diverticu-

lum make catheterisation impossible.
Urine dipsticks are useful for initial goat-side
assessment (Fig. 10.1). Their indication of specific
gravity is not accurate and, in the alkaline urine of
goats, there may be false-positive results for protein-
uria. Both these parameters should be established
with a refractometer.
Normal urine parameters are: alkaline with a pH
of 7.0–8.0; specific gravity of 1.020–1.040 and osmo-
larity of 800–1,200 mOsm/kg. The urine typically
contains low concentrations of sodium, chloride,
phosphorus ions, calcium and magnesium, but high
Fig. 10.1 Human urine dipsticks provide for concentrations of potassium. A trace of protein is
convenient goat-side urinalysis. However, they are not common, as is a small amount of ketones in lactat-
reliable for specific gravity or protein. ing goats.
Sediment is examined for presence of blood cells,
bacteria, cell casts and crystals. The latter are not
to hold the tail and touching or holding the goat as significant unless present in large numbers; for
little as possible. A good proportion will urinate on example, calcium carbonate and triple phosphate
standing up. Catheterisation, using a bitch catheter, crystals are common in normal urine.
is reasonably easy in the doe, but care must be taken Culture is useful to aid choice of antimicrobials
to avoid the urethral diverticulum. The urethral and monitor response to treatment.
opening lies ventrally at the junction between the Changes detectable by urinalysis and their inter-
vagina and the vestibulum. In the buck, the filiform pretation are shown in Table 10.2.
Table 10.2 Abnormalities detected by urinalysis and their interpretation.
CHANGE SEEN COMMON CAUSE

pH abnormal Usually falls with urinary tract disease, but can rise with some bacterial infections. Despite
metabolic alkalosis, the urine may be acidic (paradoxic acidosis)
Low specific gravity (<1.015) If no change despite water deprivation or administering a large quantity of water, indicates renal
or osmolarity (<500 mOsm/kg) insufficiency
Proteinuria Physiological: stress (e.g. transport), pyrexia, heavy lactation. False-positive result with human
dipsticks. Otherwise indicates renal involvement
Bacteria – direct counts <10,000 bacteria/ml = contamination
10,000–100,000 bacteria/ml = questionable relevance
>100,000 bacteria/ml = infection
Glycosuria Diabetes (a rare condition)
Haematuria Presents as blood clots or discolouration or brown sediment. Sediment examination confirms
presence of red blood cells. Usually also positive for haemoglobinuria. Contamination from the
reproductive tract must be ruled out in does. See Table 10.1
Haemoglobinuria False-positive results from haemolysed red blood cells, therefore sediment examination is
important. See Table 10.1
Myoglobinuria Due to myopathies. Usually concurrent rise in blood muscle enzymes (CK, AST)
Ur i n a ry Tr ac t D is e a s e 239
Radiography
Radiography is most usefully employed in the form
of an intravenous urogram, especially to detect con-
genital malformations of the urinary tract.
Cystoscopy
A paediatric endoscope is required and, because of
the males’s anatomical features (described earlier),
cystoscopy is restricted to the female.
Renal biopsy
Renal biopsy is performed under local anaesthesia
through a stab incision, and ideally ultrasound guided.
Complications such as haematuria appear to be rare.
Fig. 10.2 Transabdominal ultrasonogram of a
normal urinary bladder in a 10-year-old Pygmy doe. Renal function tests
Of note are the thin wall, clear urine (appearing •• Serum urea:creatinine ratio. This ratio is
black) and lack of sediment. Ventral to the bladder is a increased in renal insufficiency, but because
thicker-walled, slightly fluid-filled uterine horn. ruminants recycle urea, results are not very clear
cut and do not allow differentiation of a prerenal
Ultrasonography versus renal cause.
Ultrasonography is invaluable to assess the uri- •• Phenolsulphonphthalein (PSP) excretion.
nary tract and is easy to perform transabdomi- A simplified version entails: inject 0.4 mg/kg of
nally in the conscious goat. The bladder is assessed PSP i/v; collect blood into EDTA 30 minutes
for size, wall thickness or neoplasia, and debris or later and measure concentration. Normal
foreign bodies in its lumen (Fig. 10.2). The kid- concentration is <50 µg/dl serum. Elevated
neys are both visualised through the right flank serum levels indicate decreased tubular action.
and assessed for size, changes in the appearance •• Fractional excretion of electrolytes. There
of the cortex and medulla, hydronephrosis, cal- appear to be no validated normal values in
culi in the renal pelvis and neoplasia (Fig. 10.3). the goat, in particular for different feeds or diets.
(a) (b)

Fig. 10.3 Transabdominal ultrasonogram of a normal kidney in a 10-year-old Pygmy doe. (a) Longitudinal
scan; (b) cross-sectional scan. The medulla may appear more echodense than in this case.
240 Chapter 10
Common sites for the calculus to lodge are the sig-
moid flexure or the urethral process. The goat shows
abdominal discomfort (e.g. arched back, colic, short-
ened stride; Fig. 10.4). There is dysuria or strangu-
ria, with no or only a few drops of urine produced.
Sometimes crystals are present on the preputial hair
or the inner thigh. Digital rectal examination reveals
pulsation or spasms of the urethra. A distended blad-
der may be palpable through the abdominal wall in
young, thin goats.
Rupture of the urinary bladder or urethra may
Fig. 10.4 A buck with obstructive urolithiasis, with occur after about 48 hours. This results in sud-
an arched back indicating abdominal discomfort and a den relief of discomfort and, in the case of ure-
raised tail indicating stranguria. thral rupture, ventral subcutaneous fluid swelling,
cellulitis and possibly toxaemia. Bladder rupture
NON-INFECTIOUS DISEASES results in uroperitoneum, uraemia, anorexia and
depression.
Urethral obstruction
caused by urolithiasis Diagnosis
Definition/overview Signs of colic or dysuria in the male should always
Obstruction of the urethra is of particular impor- prompt investigation for urethral obstruction.
tance in meat and pet goats. Uraemia is present on bloods. A serum phosphate
level >2.9 mmol/l is associated with a poor progno-
Aetiology sis in cattle. A creatinine concentration in peritoneal
Castrated males are most at risk of urethral obstruc- fluid 1.5–2 times higher than serum levels indicates
tion because of a narrower urethra due to lack of tes- uroperitoneum.
tosterone. Uroliths may form in the female goat, but Calcium-containing stones (e.g. calcium-oxalate,
rarely lead to obstruction in their short and relatively calcium-carbonate, silicate) can be detected on radi-
wide urethra. Predisposing factors include rations ography, but ultrasonography is often easier to per-
rich in concentrates (≥2.5% of body weight dry mat- form. The various abnormalities that can be detected
ter intake for 2 months or more), alfalfa (high calcium on ultrasound, depending on the stage of disease, are
content) or pasture with high levels of silica, oxalate or a distended bladder or urethra (Fig. 10.5), the calcu-
oestrogens. Urethral obstruction may also be caused lus if lodged in the externally accessible part of the
by high levels of magnesium in milk replacers, and urethra, free peritoneal fluid or subcutaneous fluid
retinol (vitamin A) deficiency may play a role. A con- accumulation.
tributing factor is ‘nidus formation’ – organic material
as the core of the calculus; for example, epithelial cells Differential diagnosis
or necrotic tissue after local infection. Diets with low Other abdominal problems for colic. For dysuria:
salt content and restricted access to water favour pre- prostatitis, cystitis or pyelonephritis. For subcu-
cipitation of solutes. taneous swelling: ruptured penis, snake bites or
The types of calculi in ruminants are: haematoma.
•• Clover pasture – calcium carbonate. Treatment/management/control

•• Extensive pasture– silica. Pain, considerable electrolyte disturbances and onset
•• Meat/fattening ration – phosphates (calcium, of hydronephrosis by 48 hours (Fig. 10.6) mean that
magnesium, ammonium). prompt treatment is required. In small ruminants,
X X
Fig. 10.5 Ultrasonogram showing enlarged diameter Fig. 10.6 Cross-sectional ultrasonogram showing
of the perineal urethra (arrow) resulting from hydronephrosis in a 12-year-old Pygmy goat.
obstructive urolithiasis. (The image is of an alpaca,
hence the small testicles [X].)
17–55% long-term recovery after urethrostomy and •• Ultrasound-guided cystocentesis and lavage with
88% after cystotomy are reported. Walpole’s solution (effective against struvites)
has been described, but carries the risk of
Supportive treatment inducing peritonitis.
The goat should receive intravenous fluids at main-
tenance rate once urinary output is established, Removal of urethral process
and maximum water intake should be encouraged This is worthwhile, regardless of any further approach,
(including adding salt to the diet – see below). either to cure or to prevent other calculi becoming
NSAIDs are best avoided for pain relief until nor- lodged at this point. With the goat on its haunches,
mal kidney function is restored. Opioids can be used the penis is exteriorised and the process cut with sharp
for analgesia in the meantime (e.g. butorphanol is scissors as close to the glans penis as possible. In entire
available under the cascade in the UK). Antibiosis bucks, breeding capacity is not majorly affected.
is indicated.
Surgical treatment
Medical treatment (not indicated if bladder rupture Urethrotomy or tube cystotomy are the two most
has occurred) commonly used procedures (see below). Both can
•• Passing a urinary catheter in the male goat also be tried if bladder rupture has occurred: they
is impossible because of the urethral process, will ensure that pressure within the bladder is kept
sigmoid flexure and urethral diverticulum. low while the defect is healing. Urethroscopy and
•• A smooth muscle relaxant (e.g. xylazine, laser lithotripsy, and bladder marsupialisation are
clenbuterol, Buscopan®, acepromazine; note: all other options.
constitute off-licence use) may be tried. The
animal is placed onto concrete or shavings to Salvage slaughter
monitor urine output. Xylazine increases urine Uraemia is likely present at the time clinical signs
output, so if not successful, prompt surgical are detected, making the animal unfit for human
treatment is required. consumption. Euthanasia is, of course, an option.
242 Chapter 10
Prevention and control Technical description

•• Ensure calcium:phosphorus ratio is at least 1.2:1 A 5–8 cm long skin incision is made midline in
in ration. the perineum. The centre point of the incision
•• Adequate water intake can be helped by should coincide with the most caudal point of the
adding 4% salt to the ration. Salt also perineum (i.e. where it begins to slope cranio
prevents silica calculus formation. Plus basic ventrally). After incision of the fascia, blunt
husbandry of providing readily accessible, clean d issection is used to part the retractor penis mus-
water. cles. If the penis cannot be visualised, it can be
•• Ammonium chloride at 100–200 mg/kg identified on palpation as a firm tubular structure
q12h or 0.5–1% of ration dry matter prevents of about small finger thickness. A curved pair of
phosphate calculi. Note: This salt is bitter and artery forceps is pushed underneath the penis and,
must be mixed with feed or molasses. using blunt and sharp dissection staying close to
• In fattening kids, 0.5% ammonium chloride the penis, it is freed around its entirety to gain
may be routinely added to concentrates, plus some movability. The penis is cut at a right-angle
<1% sodium chloride. to its axis near the ventral margin of the skin
• In dogs and cats, prolonged use of acidifying wound. The aim is to have the stump just ventral
agents causes skeletal decalcification. to the most caudal point of the perineum to avoid
Therefore, continuous use of ammonium urine scalding, but not too ventral to avoid irrita-
chloride may not be appropriate for breeding tion from hind leg movements.
or pet animals. Using 3–4 metric suture material on a cutting
needle, the penile stump is fixed to the skin by a
Urethrotomy and urethrostomy figure-of-eight suture (through skin on one side,

Indication then through corpus cavernosum and skin on the
Urethrotomy is a salvage procedure to allow other side, then tied off underneath the stump).
u rination while the animal recovers from the
Great care must be taken not to include the ure-
effects of urolithiasis, such as uraemia, prior to thra (which lies dorsally in the reflected stump) in
slaughter. this suture. If pressure application is not sufficient
to arrest haemorrhage, the dorsal penile artery
Preparation and equipment is ligated. The skin incision is closed in a routine
The tail is tied away and the perineal area clipped manner. It is not necessary to remove the distal por-
and surgically prepared. A small procedure instru- tion of the dissected penis. The urethra may be spat-
ment kit is sufficient. A small gauge tomcat urinary ulated over a length of a centimetre or so, suturing
catheter is useful if patency is not obvious at the the mucosa to the skin. This should be considered if
end of surgery. Suture materials: polyglactin 910 there is marked oedema around the urethra.
(Vicryl®), polyglycolic acid (Dexon™) or polydioxa- An alternative to the above technique, which
none (PDS®). may provide longer survival, is urethrostomy. The
approach is the same, but instead of cutting through
Restraint the penis, the surgeon dissects onto the urethra and,
Light sedation and either caudal epidural or local following its incision lengthwise, sutures it to the
infiltration anaesthesia. The patient is placed into skin to create a stoma (Fig. 10.7).
sternal recumbency with flexed hind legs and the
backend slightly overhanging the edge of the oper- Aftercare
ating table. Alternatively, the patient may be placed Fly-repellent, ointments such as Vaseline® to reduce
into either left or right lateral recumbency, with the urinary scalding and the supportive treatment
uppermost hind leg elevated. described above.
Fig. 10.7 Stoma created by an urethrostomy in a pet Fig. 10.8 Tube cystotomy. The bladder is
wether. The swelling ventral to the stoma resulted exteriorised through a paramedian abdominal
from subcutaneous urine pooling after pre-operative incision. After placing a purse-string suture, a Foley
urethral rupture. catheter is inserted into the bladder.
Potential complications Technical description

Stricture, scalding, fly strike, ascending infection. An incision long enough to allow passage of the sur-
Adhesions from sterile peritonitis if bladder rupture geon’s hand is made in the caudoventral left flank,
has occurred. just above and roughly following the knee-fold. If
the urinary bladder can be exteriorised, an absorb-
Tube cystotomy able purse-string suture is placed, a stab incision
Indication made in the centre of this suture into the bladder,
Tube cystotomy is indicated in patients where repro- and a Foley catheter passed into the ventral bladder,
ductive function or long-term survival are desirable, close to the apex (Fig. 10.8). If the bladder cannot be
such as a breeding buck or pet animal. exteriorised, a Steinman pin is placed into the Foley
catheter, the bladder grasped intra-abdominally
Preparation and equipment with one hand, and the catheter pushed blindly into
The left flank is clipped and surgically prepared. the ventral bladder.
Required are: a standard instrument kit, Steinman The cuff of the Foley catheter is inflated with
pin, Foley catheter of suitable size (e.g. 14 Fr), zinc saline and pulled against the bladder wall (Fig. 10.9).
oxide tape, tomcat urinary catheter, sterile saline, The catheter end is passed out through a stab inci-
suture material (polyglactin 910 [Vicryl®], polygly- sion 2–3 centimetres away from the surgical incision,
colic acid [Dexon™] or polydioxanone [PDS®]). and secured with a butterfly-tape anchored with skin
sutures. The abdominal wound is closed in a rou-
Restraint tine manner. Using the Foley catheter, the bladder is
GA or lumbosacral epidural anaesthesia, or sedation lavaged several times with sterile saline. Retrograde
and local infiltration, with the animal in right lateral lavage via a tomcat catheter placed into the distal ure-
recumbency. thra (after urethral process removal) can also be tried.
244 Chapter 10
Fig. 10.9 Foley catheter secured in the bladder by Fig. 10.10 Two infarcts (white nodules) in a kidney
inflating the balloon, but catheter not yet passed out after septicaemia.
through a stab incision a few centimetres away from the
abdominal incision and secured with butterfly tapes.
An alternative is to place a human percutaneous Aetiology

transabdominal catheter, under ultrasound guid- Pre-renal causes include: reduced cardiac output
ance, via a cutaneous stab incision in either the left (e.g. in rumen tympany or congestive heart failure),
or right flank. acute circulatory compromise caused by shock,
marked haemorrhage or dehydration, or septicaemia
Aftercare (Fig. 10.10); nephrosis. Renal causes include pyelone-
Continuous urine passage is allowed through the phritis, interstitial or glomerulonephritis, or amyloi-
Foley catheter for the first few days. Supportive ther- dosis. Post-renal causes include obstruction of ureters
apy is given during this time (see earlier). The bladder or the urethra and bladder rupture. Dehydration, or
may be flushed with Walpole’s solution (50–200 ml an increased susceptibility to it, is present.
of a 1:10 Walpole:water dilution, retained in the
bladder for 30–60 minutes by blocking the catheter). Clinical presentation
After a few days, the catheter is blocked for trial peri- In the acute phase, signs include depression and
ods of several hours, and the animal observed for inappetence, reduced rumen activity, tachycardia,
normal urination. Once normal urination has been colic or abdominal pain, and watery or haemorrhagic
established for 24–48 hours, the Foley catheter is diarrhoea. The goat is often recumbent and shows
removed (but not before 7 days post operation). muscle tremors. Polyuria or oliguria is present, and
bleeding diathesis may occur (e.g. epistaxis, melena,
Potential complications or bleeding of mucous membranes or at a venepunc-
Peritonitis: either septic from the surgical procedure ture site). Chronic cases show marked weight loss,
or sterile from bladder rupture. Non-resolution of anorexia, dependent oedema and, in addition to poly-
urethral obstruction. uria or oliguria, polydipsia. Marked hypocalcaemia
and sodium–potassium imbalance may result in cir-
Renal insufficiency and failure culatory failure, muscle weakness and nervous signs.
Overview
Because causes of renal insufficiency and failure are Diagnosis
not restricted to the urinary system, renal function Metabolic alkalosis and blood electrolyte imbal-
should be considered in a range of clinical conditions. ances are common: increased levels of phosphate,
magnesium and sulphate; decreased levels of cal- (risk of crystalluria if long-acting forms are used,
cium, sodium, chloride and often potassium (in con- urine is acidified, or animal is dehydrated).
trast to non-ruminants). Atypical hypocalcaemia
(i.e. in a doe outside the periparturient period) often Clinical presentation
indicates renal insufficiency. Progressive depression, inappetence, poor milk yield
Goats in terminal failure show hypoproteinaemia and further signs specific to the causative agent.
and metabolic acidosis.
Diagnosis
Differential diagnosis Blood analysis shows high urea and creatinine levels.
Other causes of abdominal discomfort, diarrhoea
or marked weight loss. For goats in peak lactation, Differential diagnosis
hypocalcaemia. A wide range of other conditions may cause similar
signs, but in particular abdominal catastrophe and
Treatment/management/control septicaemia or toxaemia.
Specific treatment is given for the underlying cause.
Intravenous saline, potentially spiked with potassium Treatment/management/control
(10 mEq/litre of fluids) and calcium. Once urination Fluid therapy and diuresis. Prognosis is guarded to
has been established, furosemide (1–2 mg/kg every poor.
2 hours) or mannitol (0.25–2.0 g/kg as a 20% solu-
tion) can be considered. Slaughter is not an option Neoplasia
because of the uraemia. Lymphosarcoma (Fig. 10.11) may affect the k idney
The following serum values have been suggested as a primary tumour or as metastases of other
as a guideline for poor prognosis in cattle: magne- neoplasia. Kidney tissue-specific tumours include
sium >3.5 mmol/l, phosphate >2.9 mmol/l, creatinine nephroblastoma.
>130 mmol/l and urea >16.5 mmol/l. Some animals
with much higher urea levels (<40 mmol/l) may sur- INFECTIOUS DISEASES
vive; of particular concern is urea levels remaining
elevated despite fluid therapy. Cystitis and pyelonephritis
Overview
Toxic nephrosis Compared with companion animals, cystitis and
Overview pyelonephritis are far less often detected clinically in
A variety of plants or chemicals can cause degenera-
tive changes to the renal tubules.
Aetiology
Some of the poisons that may lead to nephrosis
include arsenic, some wood preservatives, mercury,
ethylene glycol (antifreeze) and mycotoxins such as
ochratoxin A or citrinin. In other species oak (young
leaves or buds in spring, acorns in autumn) may be a
cause, but goats appear to have some resistance to oak
poisoning. Some antibiotics can also induce nephro-
sis, including: aminoglycosides (e.g. neomycin if
given at 10 mg/kg for more than 10 days, or at lower
doses in dehydrated animals), oxytetracycline (if
long-acting formula accidentally given daily, or one- Fig. 10.11 Lymphosarcoma affecting the kidney of a
off high dose rates ≥40 mg/kg) and sulphonamides 7-year-old Anglo-Nubian goat.
246 Chapter 10
livestock, but are regularly found at slaughter, with a gastrointestinal problem are common complaints in
prevalence of about 10%. cases of pyelonephritis.
Cystitis presents as frequent urination with only
Aetiology small amounts of urine passed, and the animal remain-
Almost always bacterial, involving both gram- ing in the urinating position for some time. There may
negative (e.g. Escherichia coli, Klebsiella spp., also be bruxism or other signs of pain when urinating.
Pseudomonas spp., Proteus spp.) and gram-positive In very acute cases, there are temporary colic signs,
(e.g. Corynebacterium spp., Streptococcus spp.) patho- such a kicking at the belly, tail swishing and shifting
gens. Route of infection is more likely ascending weight on the back legs. Digital rectal examination
than haematogenous. may trigger a pain response in acute cases.
Cystitis (Figs. 10.12, 10.13) occurs after contam- The first sign of pyelonephritis often is haematu-
ination or trauma of the urinary bladder caused, for ria in an otherwise healthy animal. There may be a
example, by dystocia, retained fetal membranes or history of episodes of acute pain. Rectal temperature
prolapsed uterus. Urine stasis often facilitates infec- often fluctuates, and milk yield and body condition
tion, such as pressure in late stage pregnancy, mal- are reduced.
formation of vagina after dystocia, or inflammation
or obstruction of the urethra or ureters. Urolithiasis Diagnosis
will also cause cystitis. Pyelonephritis occurs mainly Blood and pus are often present macroscopically in
via ascending infection from the lower urinary tract. the urine, and urine sediment contains erythrocytes
Because of their shorter urethra, females are more and leukocytes. If the kidneys are involved, protein-
often affected than males. Both conditions are rela- uria, a urine pH above 8.5 and reduced specific grav-
tively rare in young animals. ity results. Neutrophilia is commonly present on
haematology, and raised blood creatinine and urea
Clinical presentation levels suggest kidney involvement.
Goats present because of frequent urination or mal- Interpretation of culture results must take into
odour being noticed in the milking parlour. Weight account the normal bacterial flora of the vulva
loss, acutely reduced milk yield or a suspected (e.g. some Corynebacterium spp.).
Fig. 10.12 Acute cystitis with purulent urine and Fig. 10.13 Chronic cystitis with purulent urine
mucosal plaques. and marked mucosal inflammation and bladder wall
thickening.
Ultrasonography may show debris within the ampicillin are useful against E. coli and procaine
bladder or renal pelvis and, in chronic cystitis, a penicillin against Corynebacterium spp. While cur-
thickening of the bladder wall. Kidney enlargement rently not licensed in many countries against urinary
may be detected. tract disease, ceftiofur, enrofloxacin and florfenicol
may also be considered. Aminoglycosides, although
Differential diagnosis effective against gram-negative pathogens and
Where colic is caused by a gastrointestinal catastro- mainly excreted renally, should be avoided because
phe, pain typically persists, faeces may be abnormal of their nephrotoxic potential. Antibiosis must be
in quantity or consistency, and the goat develops continued for at least 7 days for cystitis and at least
shock and toxaemia. Auscultation, abdominal palpa- 3 weeks for pyelonephritis. Ideally, cessation of
tion and ultrasonography will aid differentiation. treatment is based on negative urine culture. Repeat
Urine sediment examination is used to rule out culture is advisable, as recurrence is common.
cystitis secondary to urolithiasis. Acidifying the urine will enhance the efficacy of
Enzootic haematuria will also present with a procaine penicillin: monobasic sodium phosphate
thickened bladder wall, but no pus or bacteria are at 10 g daily or ammonium chloride at 100–200 mg/kg
present in the urine. There is often evidence of q12h, each orally for 5–7 days.
anaemia. Prognosis of between 35% and 85% is reported in
cattle after prolonged antibiosis. Nephrectomy may
Treatment/management/control be considered in unilateral cases, carrying a progno-
Because of the quite varying antimicrobial sensi- sis of about 75%.
tivities of likely pathogens involved, urine culture Control includes good hygiene around kidding
is important. Trimethoprim and sulphonamide or and prompt treatment of post-partum disease.
CHAPTER 11
SKIN DISEASES
249
CLINICAL EXAMINATION OF THE only one goat in a group is affected, particularly with
SKIN AND INTEGUMENT a typically contagious disease.
Clinical assessment Ancillary diagnostics

Skin disease should be suspected when presented First-line diagnostics
with any of alopecia, erythema, coat staining, skin Lice and ticks are usually visible with the naked eye,
thickening, crusting, hyperkeratosis, swellings, dis- and detection can be made easier in coat brushings.
charge and excessive grooming or other signs of pru- For other ectoparasites, hair plucks can be used to
ritus. Lesion distribution, depth and characteristics detect lice nits (Fig. 11.1) and follicular pathogens
are determined. This may require putting the ani- such as Demodex spp. or dermatophytes. Skin scrapes,
mal into lateral recumbency to inspect ventral body using a scalpel blade along the edge of the lesion
areas. Hair is parted or clipped where necessary to (or in the interdigital space) until blood is drawn,
allow examination. are particularly useful in mange cases (Fig. 11.2).
Historical factors that are of particular interest are For these methods, the samples are mixed with 20%
number and age affected, current or recent environ- KOH or paraffin, and examined under a cover slip.
ment, and type of animal (e.g. recently introduced). Tape strips are useful to detect ectoparasitic or
Because the skin can reflect general health status, a microbial agents and for cytology: a piece of clear
general clinical examination is important, potentially adhesive tape, such as Sellotape®, is pressed onto
combined with blood analysis and serology. Causes the lesion, then transferred onto a microscope
of immune suppression should be considered where slide. Impression smears are obtained by pressing
Fig. 11.1 Hair plugs are useful to confirm some Fig. 11.2 For a skin scrape (here in the interdigital
ectoparasites. Here, lice nits are present on calf hair. space) a scalpel blade is used, going deep enough to
(Image courtesy Aiden Foster.) draw blood.
250 Chapter 11
NON-INFECTIOUS SKIN DISEASES
Pemphigus foliaceus
Definition/overview
Cases of pemphigus foliaceus (a condition more fully
understood in dogs, cats and horses) are occasionally
reported in goats.
Aetiology
The condition is considered to be an immune-
mediated skin disorder, although the triggers for the
autoantibody production are poorly characterised in
animals.
Fig. 11.3 A punch biopsy taken at the edge of a
muzzle lesion in an alpaca. Note that no clipping or Clinical presentation
disinfection was carried out. The main presenting signs include a generalised
severe pustular eruption involving most of the body.
a microscope slide directly onto the lesion, and are Pustules are very transient and associated with
useful for microbial agents and cytology. marked crusting and multifocal alopecia.
Bacterial and fungal culture Diagnosis

Samples obtained by direct swab, fine needle aspirate Definitive diagnosis is by histological examination
or skin biopsy can all be used to isolate infectious of skin biopsy samples.
agents. Normal commensals need to be taken into
consideration when interpreting results. Treatment/management/control
Treatment or control of clinical signs is based pre-
Biopsy dominantly on the use of corticosteroid therapy;
Biopsy is performed under local anaesthesia, ide- for example, 1.0 mg/kg prednisolone i/m q12h for
ally by infiltrating some distance from the biopsy 7 days, followed by 1.0 mg/kg q48h for maintenance,
site (e.g. in a square pattern). The biopsy site itself tapering the dose further if possible. Regular bath-
is not clipped; however, surrounding hair may need ing is useful for removing crust material and may be
to be removed to allow accurate positioning of the combined with systemic antibacterial agents where
biopsy. To avoid distortion of histological features, there is evidence of secondary bacterial infection.
no disinfection is carried out unless the area is
particularly dirty. (Note: Disinfection will render Zinc deficiency (zinc-
the sample unsuitable for culture.) A punch biopsy responsive dermatosis)
(6–8 mm diameter) is preferable over a wedge biopsy Definition/overview
(Fig. 11.3). The sample is taken at the leading edge of Zinc deficiency is probably more common than gener-
the lesion, without including normal skin. Multiple ally recognised, particularly in pygmy goats. Disease
samples are useful where the lesion shows variable can be associated with skin and/or foot disorders.
characteristics or to submit for culture in addition to
histopathology. Aetiology
Deficiency can occur if there is an absolute dietary
Ultrasonography shortfall or uptake is inhibited by excessive copper
Ultrasonography is useful to investigate swellings, or calcium in the diet (e.g. animals on lucerne/alfalfa
allowing identification of content and the extent of diets), or in goats fed excessive dietary levels of oxa-
the lesion. Also useful to guide a fine needle aspirate. lates, cadmium, iron or molybdenum. There may be
Sk i n D is e a s e s 251
individual goat variation in the ability to absorb and supplementation, despite normal plasma and dietary
also to metabolise any zinc ingested. Zinc deficiency levels.
is not regarded as a clinical problem of grazing ani-
mals in the UK. Differential diagnosis
There are a number of potential contagious and
Pathophysiology non-contagious causes of such skin lesions, and these
Zinc is required for the proper function of a wide need to be eliminated by a structured skin examina-
variety of enzymes. Deficiency signs include loss tion, particularly the pygmy goat syndrome in which
of appetite and anorexia, reproductive disorders, there are clinical similarities. Zinc deficiency may
impairment of the immune system and abnormali- also be an exacerbating factor in other causes of skin
ties of the skin and coat. disease.

The skin is the most common site for signs of defi- Zinc is a trace element, and daily requirements
ciency to be identified. These include alopecia, pruri- are low but should be consistent, as there are no
tus, hyperkeratosis and crust formation on the back, readily available body stores. Presenting drinking
legs, udder or scrotum, face (particularly around the water in galvanised containers may be sufficient, as
eyes, nose and mouth), neck and ears (Fig. 11.4). Dry zinc (a component part of the galvanising process)
scaly skin linked to poor keratin production can also will leach into the water. Supplementation can be
be widespread over the animal’s body. Coat quality achieved by administration of a daily dose of 1 g zinc
can be affected in fibre goats. sulphate either in crushed tablet form or as a drench
for 3–4 weeks. Slow release boluses containing zinc
Diagnosis and other trace elements marketed for sheep are also
The clinical signs are relatively non-specific, and available.
other causes should be eliminated. Blood zinc levels
can be estimated using a sample taken into a sodium Pygmy goat syndrome
citrate vacutainer, but correlation between serum (syn. seborrhoeic dermatitis)
and dietary zinc levels may be poor. Skin biopsy Overview
may confirm keratin production disorders. A clinical Pygmy goat syndrome is a condition confined to
response trial to daily supplementation may also be the Pygmy goat breed, and is relatively common in
of benefit, although some goats may respond to zinc the UK.
Aetiology
Appears to have an underlying hereditary basis,
which can be an issue because the genetic pool of the
breed is relatively limited.
Hair loss, and skin flaking and/or crusting seen
around the eyes, lips, ears, chin, ventral skin surface
and perineal area (Figs. 11.5, 11.6).
Diagnosis
Diagnosis is based on elimination of other causes and
the breed of goat affected. Skin biopsy may indicate
Fig. 11.4 Skin hyperkeratosis. Zinc deficiency was abnormalities of keratin production, a recognised
confirmed, with no other aetiology identified. feature of the disease.
252 Chapter 11
Fig. 11.5 Pygmy goat syndrome – hyperkeratosis. Fig. 11.6 Pygmy goat syndrome – skin flaking, poor
keratin production (shoulder region).
Differential diagnosis Clinical presentation

Zinc deficiency presents similarly; mange lesions are Clinical signs are seen most commonly in the thin-
typically drier. ner coated areas of the body, particularly those
covered with white non-pigmented hair. Erythema
Treatment/management/control (Fig. 11.7) is followed by superficial skin necrosis
Treatment may be disappointing as the condition will and sloughing. In the secondary form there may be
often recur. Some relief can be given via the topical use additional signs of liver disease such as icterus.
of corticosteroid and antibiotic creams, parenteral cor-
ticosteroids and antiseptic skin washes. Anecdotally, a Diagnosis
selenium sulphide wash has proved beneficial. There Diagnosis is based on a history of access to photody-
are occasional reports of the condition gradually namic plants for the primary form and raised liver
resolving as affected immature goats grow. enzymes (gGT, GLDH, SDH) for the secondary
form.
Photosensitisation
Overview
Photosensitisation has been occasionally reported in
goats.
Aetiology
Primary photosensitisation occurs as a result of the
ingestion of photodynamic toxins found in many
different plants worldwide, for example St John’s
Wort (Hypericum perforatum). Other potentially pho-
todynamic agents include tetracyclines and sulphon-
amides. Secondary photosensitisation is linked to
liver disease, resulting in a failure to excrete the pho-
todynamic agent phylloerythrin itself, a degradation
product of chlorophyll. Any severe liver disease can Fig. 11.7 Erythema is seen in the early stage of
lead to secondary photosensitisation, including those photosensitisation, particularly on areas with little hair
caused by hepatotoxic plants (e.g. ragwort [ Jacobaea coverage, such as the ear in this sheep. Hypersensitivity
vulgaris, syn. Senecio jacobaea]). to biting midges may present similarly.
Differential diagnosis the pregnant dam may lead to improved fibre yield
Acute bacterial or ectoparasite infection. Skin and quality in her progeny.
scrapes and culture to rule out.
Hypotrichosis
Treatment/management/control Hypotrichosis is occasionally seen as a congenital
Treatment consists of moving affected goats indoors condition, and may affect one kid only in a litter
away from sunlight and any potentially toxic plants (Fig. 11.8). It is caused by partial or complete absence
they may be consuming. Anti-inflammatory and of hair follicles, resulting in either a very fine coat
antimicrobial therapy is indicated, plus liver support or no hair at all. Partial anodontia is often present.
therapy (like B vitamins, glucose or glucose precur- Prognosis is guarded because of increased suscepti-
sors). Fly repellents are important, and skin emol- bility to infectious disease such as pneumonia.
lients may aid local skin recovery. Severely affected
cases, particularly those with marked liver damage, INFECTIOUS SKIN DISEASES (PARASITIC)
carry a poor prognosis.
Chorioptic mange
Physical and toxic causes Definition/overview
Skin lesions can result from a variety of physical or Chorioptic mange is a common form of mange
toxic insults. Repeated contact with solid material reported in goats worldwide. Lesions tend to be
in the goat’s environment (e.g. poorly bedded con- restricted to the lower limbs and are colloquially
crete lying areas or metal bars such as feed rails) referred to as foot mange. The condition can cause
can result in hair and skin abrasion and callus for- widespread problems once established.
mation. Poll lesions may result from head-butting,
in particular in bucks. Diarrhoea or prolonged Aetiology
contact with urine may result in scalding along the Caused by the surface dwelling mite Chorioptes
hind legs. Skin burns result from stable fires, close spp., which resembles morphologically those seen
proximity to heat lamps, clippers overheating dur- on cattle. It is likely that all livestock carry C. bovis,
ing shearing of fibre goats, and contact with strong although C. texanus has also been reported in goats.
chemicals. Venom typically also results in skin
lesions. Frost bite and toxaemia (especially caused
by salmonellosis) may result in necrosis of the ear
tips and the coronary band.
The location of the lesions often hints at the
cause; for example, foot or nose in chemical burns,
head in snake bites or heat lamp burns, neck in metal
barrier contact, hocks in poor bedding surface.
Fibre break or loss

Fibre problems range from fibres breaking, either on
the animal or during processing, to complete shed-
ding of the fleece. This is of economic importance in
fibre breeds, but also as an indicator of suboptimal
husbandry or health in other breeds.
Severe stress or acute severe disease (e.g. diar-
rhoea) are common causes. Goats fed a diet that is
limited in energy and/or non-degradable protein
often produce finer fibre (less in diameter), but it Fig. 11.8 Hypotrichosis in a neonate. This kid’s twin
tends to be more brittle. A good level of nutrition in was normal in size and coat coverage.
254 Chapter 11
Fig. 11.9 Goat with mange showing self-mutilation, Fig. 11.10 Typical foot lesions associated with
leading to skin damage on her leg and spread of the chorioptic mange.
mange to the head.
Pathophysiology performing a skin scrape at the leading edge of the

Lesions are mainly the result of self-inflicted trauma lesion.
due to the physical presence of the mites (Fig. 11.9).
This will vary from goat to goat, with some infested Differential diagnosis
individuals showing no or only minimal signs, The location of lesions confined to the lower limbs
whereas others may be particularly susceptible to is highly suggestive of chorioptic mange, although
infestation and develop a marked hypersensitivity there may be a spectrum of severity within an
response, leading to more significant self-trauma. affected group. A full skin work-up will eliminate
other ectoparasitic causes.
Clinical signs can include intense pruritus, foot Treatment/management/control
stamping, rubbing, scratching and biting and the Management of chorioptic mange can be extremely
production of a scaly scab, often fissured and haem- difficult because these mites can survive off the host
orrhaging, ranging in colour between grey and for up to 3 weeks in the environment, therefore
yellow–brown. Lesions are most commonly found disposal of potentially infested bedding should be
on the feet (interdigital space, coronet, accessory part of any control strategy. It is also important to
digit) and occasionally on the udder, scrotum and remember that many infested goats are not severely
tail or around the mouth from nibbling at affected affected and may even be asymptomatic carriers. As
areas (Figs. 11.10, 11.11). most of the mites will be on the goats, however, it
is advisable to treat the whole group with a suitable
Diagnosis ectoparasiticide.
Diagnosis is by identification of the mites on micros- A variety of topical agents are applied on an
copy of skin scrapes, looking for the characteristic empirical basis, such as topical macrocyclic lactones
short wine glass-shaped pedicels (Fig. 11.12). This (MLs), fipronil-based sprays and selenium sulphide
can sometimes be problematic in severely affected shampoos. The absence of a drug licence in many
cases in which mites may no longer be present at the countries and of pharmacokinetic data in goats
lesion site. In such cases, it is worth clipping away makes the use of topical MLs (e.g. eprinomectin)
normal hair from the margin of the lesion, and then problematic. Topical treatments should be pursued
Fig. 11.11 Mouth lesions associated with chorioptic Fig. 11.12 A chorioptic mite under the microscope.
mange self-inflicted trauma. Note the pedicle shaped like a wine glass/suction cup.
(© Crown Copyright 2017. Used with kind permission
of the Animal and Plant Health Agency)
for up to two mite life cycles (i.e. up to 6 weeks, given migrate to the skin surface, from where they can
every 7–14 days). Systemic treatment with MLs has spread from host to host. Adults die burrowed into
shown limited efficacy for the control of Chorioptes the skin, resulting in a significant allergen source
mites because of its surface dwelling habit. and hypersensitivity.
Consideration should be given to the use of prod-
ucts in milking goats because of either the long milk Clinical presentation
withholding periods or restrictions on their use in Clinical signs include itching and rubbing, redness
lactating goats in many countries, and the potential and papules at the site of infestation, leading to exco-
impact on nematode anthelmintic resistance. In a riation, scabs and crusts (Figs. 11.13, 11.14).
commercial herd, culling severely affected individu-
als may be part of the control strategy. Diagnosis
Although other ectoparasitic causes need to be elim-
Sarcoptic mange inated, the more widespread distribution of lesions
Definition/overview and intense pruritus are characteristic features.
Sarcoptic mange is a common form of mange A skin scrape may be examined for mites.
reported in goats worldwide. Lesions can be found
over most of the body surface, often with intense pru- Differential diagnosis
ritus. This type of mange, once established, can have A full skin work-up will eliminate other ectopara-
a serious impact on goat welfare and productivity. sitic causes. Scrapie should also be considered (see
Chapter 8).
Aetiology
Sarcoptes scabiei var caprae, a burrowing mite and zoo- Treatment/management/control
notic pathogen. Some control can be achieved by removing and
treating individual goats, but when many goats
Pathophysiology are affected, whole herd treatment may be a better
Once infested, the mites burrow into the horny option. Systemic products based on MLs have been
layer of the skin, where eggs are laid. Hatched larvae the mainstay of treatment for this condition, with
256 Chapter 11
Fig. 11.13 Generalised sarcoptic mange. Fig. 11.14 Sarcoptic mange affecting the udder.
(Image courtesy Kathy Anzuino.)
at least two treatments 7–14 days apart (see above become distended with mites, their faeces and
under chorioptic mange treatment). Many goats will sloughed skin together with epithelial cells forming
continue to show pruritus after treatment due to the the characteristic nodules.
presence of parasite antigen on the skin surface –
washing with keratolytic or keratoplastic shampoos Clinical presentation
2–3 times a week is often beneficial. Where self- Small lesions (often only detectable by careful palpa-
trauma has led to secondary bacterial infection, tion) develop principally over the head and neck but
a 3–5 day course of systemic antibiotic (e.g. a poten- also along the neck and over the shoulders. These
tiated penicillin) is indicated. Quarantine of incom- may enlarge to 1–2 cm diameter, often with a case-
ing goats is important, treating any visibly affected ous necrotic core in which large numbers of mites
goats before they enter the herd. The condition is can be seen.
extremely contagious and will spread rapidly if it gets
into a herd. Diagnosis
Diagnosis is by demonstration of the typical cigar-
Demodectic mange shaped mites found when the nodule content is
Definition/overview squeezed onto a microscope slide.
Demodectic mange is a sporadic (rather than herd)
problem, mainly affecting growing kids, and not of Differential diagnosis
great economic significance. The age of goat and appearance of the lesions is
fairly characteristic.
Aetiology
Demodex caprae, a small cigar-shaped mite. Treatment/management/control
There is rarely a need to treat this condition, which
Pathophysiology is mainly unsightly and therefore a particular prob-
Infection appears to be contracted from the dam as lem in show goats. Individual nodules can be excised,
kids are suckling, but lesions are not usually seen or incised with expression of the content. Multiple
until they are around 10–15 months of age. Many nodules may respond to systemic ML therapy, but
infestations are asymptomatic and inapparent. even then nodules may not regress for some time.
Demodex spp. infect the hair follicles, which can Most will regress spontaneously in time.
Psoroptic mange
Definition/overview
Psoroptic mange infestation is usually limited to
the ear canal and referred to colloquially as ear
mange.
Aetiology
Psoroptes cuniculi (syn. P. caprae).
Pathophysiology
Mites feed off the exudate and debris in the ear
canal, and many infestations are asymptomatic.
Susceptible goats, or those carrying heavy infesta- Fig. 11.15 Biting louse Bovicola limbata.
tions, may develop a build-up of scale and wax in the
ear canal, and this may extend outwards onto the ear Aetiology
pinna in severe cases. Goats can be infested with the blood sucking louse
Linognathus africanus and Linognathus stenopsis and the
Clinical presentation chewing species Bovicola (Damalinia) caprae. Of more
Head shaking and scratching of the ear with the significance in fibre producing goats are two spe-
hind feet. Aural haematoma formation is a potential cies of chewing louse: the red louse, Bovicola limbata
complication. (Fig. 11.15), and the less common Bovicola crassipes.
Diagnosis Pathophysiology
Diagnosis is based on clinical signs and the demon- It is the feeding behaviour of these two classes of lice
stration of typical mites in ear canal wax or scale. that dictates the clinical signs seen.
Differential diagnosis Clinical presentation

The clinical signs and presence of scale and debris in Heavy burdens of sucking lice, particularly in young
the ear canal are fairly typical. kids, can cause anaemia, increased susceptibility to
other infectious diseases and, in severe cases, may
Treatment/management/control even cause death. Biting lice cause general irrita-
If treatment is deemed necessary, then the use of bility in goats due to their movement and feeding
dog/cat ear mite preparations can be useful in indi- behaviour resulting in alopecia through self-inflicted
vidual goats (if drug licensing rules permit). Such trauma. This is a potentially serious issue in Angora
preparations are more effective if the ear is cleaned goats. The irritation may also result in reduced feed
first. If a larger number of goats are to be treated, intake, leading to weight loss and reduced milk yield.
then systemic MLs have been shown to be effective
(see above under chorioptic mange treatment). Any Diagnosis
treatment should be repeated 14 days later. The clinical signs, particularly if many goats are
affected, should raise a suspicion of lice. They
Lice (or their eggs or ‘nits’ sticking to hair shafts;
Definition/overview Fig. 11.1) can often be seen, either with the naked
Lice are found on goats worldwide, and once estab- eye or a hand lens, after parting the hair. At least
lished can have both a serious welfare and economic ten areas of the body should be inspected, chang-
impact, particularly in goats that are kept indoors in ing the angle of view onto each area. If just one or
large numbers where spread can be rapid. two individuals are affected, the louse problem may
258 Chapter 11
be secondary to a debilitating disease (e.g. a heavy example, the most common species is Ixodes ricinus
endoparasite burden). (Fig. 11.16), transmitting the following infections
between goats and other hosts on which ticks feed
Differential diagnosis such as sheep, cattle and deer:
A full skin work-up will eliminate other ectoparasitic
causes and confirm lice as the cause of the anaemia. •• Tick-borne fever (see Chapter 2).
•• Tick pyaemia – as ticks penetrate the skin,
Treatment/management/control they can under certain circumstances inoculate
Disease is rarely limited to one or two goats, and surface Staphylococcus aureus, causing local abscess
any treatment regime should include the remainder formation and bacteraemia or pyaemia. This in
of the cohort in which disease may be subclinical or turn leads to abscess formation in a variety of
developing. sites including the vertebral column, joints and
As a general rule, injectable MLs are highly effec- internal viscera such as liver.
tive against sucking lice, but ineffective against •• Louping ill (see Chapter 8).
chewing lice. A number of preparations have been
used to treat chewing lice including pour-on prod- Individual ticks can be removed by simple plas-
ucts, such as cypermethrin or deltamethrin, and tic tick removers. Heavy infestations can be treated
sprays or washes with 12.5% amitraz solutions (care and controlled by the strategic use of suitable sprays,
in pregnant does). Shearing thick coated goats such dips and pour-on products such as amitraz, cyper-
as Angoras before treatment is beneficial. The avail- methrin or deltamethrin.
ability of licensed ectoparasiticide products and
their potential use in goats will vary from country to Flies
country. Blood transfusion should be considered in Overview
severely anaemic animals (PCV <0.12 l/l). Fly worry, caused by nuisance flies, and blow fly
Lice infestations are often an indication of other strike (myiasis) are the two main fly-induced disease
underlying management problems such as over- entities in the UK. Warble fly (Przhevalskiana silenus)
crowding, concurrent disease or poor nutrition, and problems occur outside the UK, including southern
any investigation into a louse problem should con- Europe.
sider the overall management.
Aetiology
Ticks Biting (stable and horn flies) and non-biting (house,
Ticks are important ectoparasites of goats, causing face and head flies) species lead to fly worry. Fly
disease directly by actively sucking blood in very strike may be caused by fly species able to pene-
heavy infestations, and indirectly by spreading dis- trate intact skin (Lucilia spp., Phormia terranovae),
ease. Tick species and the diseases they transmit but any fly species can act as opportunist when
will vary from country to country. In Europe, for skin is damaged. Risk factors for fly strike include
soiled skin, damp coat, wounds (including surgi-
cal) and grazing on pastures containing thistles or
other rough vegetation. Grazing animals are more
exposed, but marked problems may also be seen in
housed goats.
Nuisance flies cause three main problems: (1) irri-
tation, leading to reduced feed intake, stress and
possibly self-trauma; (2) blood loss causing anaemia
Fig. 11.16 Ixodes ricinus tick. (e.g. horn flies may take up to 200 ml blood/day);
Fig. 11.17 Fly bite dermatitis on the leg. Fig. 11.18 Myiasis (fly strike) on the neck of a ram,
that was in toxaemic shock as a result.
and (3) acting as vector (e.g. for mastitis or ocular Treatment/management/control

pathogens). Clinical signs include epiphora and tear Treatment of struck goats includes physical removal
scalding. Biting flies are capable of causing superfi- of larvae, application of a pyrethroid or ivermectin
cial skin damage to outright wounds, especially on to kill remaining larvae, wound lavage and applica-
areas with less coat covering such as the bridge of tion of a restorative ointment, and administration
nose, ears, caudoventral abdomen, udder and teats of an antibiotic and a NSAID. Goats suffering from
(Fig. 11.17). toxaemic shock are treated accordingly (including
Affected goats often show restlessness, stamping i/v fluids).
of feet and rubbing on housing structures. Staining Environmental steps in the control of nuisance
of the fleece commonly occurs. Fly strike may be flies include reducing proximity of goats to fly-
anywhere on the body if associated with a wound; favouring features such as trees, water and dung
otherwise it is commonly found in the perineal area (Fig. 11.19). Fly numbers in stables can be reduced
or over the goat’s dorsum. It can lead to severe tox- by installing fly curtains (to sweep off the majority
aemia, with recumbency, dehydration and shock of flies as goats enter the building), predatory wasps
(Fig. 11.18). and fly traps. On pasture, pheromone-based traps
mounted on fence posts can also be useful.
Diagnosis Control options on the animal include pyre-
Biting flies are typically found on the legs of affected throids (e.g. permethrin, deltamethrin, pyrethrin
goats. More than ten biting flies or more than 50 non- and, for organic farms, chrysanthemum extract),
biting flies on an animal should prompt intervention. either as pour-on or sprays. Impregnated ear tags
Areas of stained fleece should be examined closely for or tail tapes must be manufactured specifically for
fly strike, with larvae visible by the naked eye. goats, as their fleece and skin characteristics are dif-
ferent to cattle (i.e. a cattle product may not disperse
Differential diagnosis as expected). Care must be taken regarding milk
Mange will cause crusting lesions and pruritus. withholding periods, and several products are highly
Photosensitisation may manifest predominantly in toxic to aquatic life (i.e. goats must be kept away
areas with thinner coat. from natural watercourses).
260 Chapter 11
Other ectoparasites, hormonal skin conditions,
dermatitis.
Housing at dawn and dusk is labour intensive, but
often reduces the effects. If primarily the head is
involved, fly masks designed for miniature ponies
can be useful. Repellents (e.g. deltamethrin) have
variable persistence.
Besnoitiosis
Besnoitia caprae is a coccidian parasite causing oedema
and gross thickening of the skin in goats. It has been
reported in Africa and the Middle East. The defini-
tive hosts are believed to be domestic cats and wild
felids, with transmission to ruminants via faeces.
Fig. 11.19 Having the dung heap close to goats’
B. caprae may be transmitted between ruminants by
stabling will increase fly worry unnecessarily.
biting flies. Besnoitiosis is a threat when importing
Blowfly strike prevention relies on prompt atten- goats from affected countries. After initial pyrexia
tion to wounds and diarrhoea, avoiding routine and painful ventral oedema, the skin hardens and
procedures like castration during the fly season and thickens and develops wrinkles and cracks (with
applying fly-repellent ointment to surgical wounds, the risk of fly strike or secondary bacterial infec-
plus strategic use of topical insect growth regulators tion). The presence of parasitic cysts in the scleral
(e.g. dicyclanil). conjunctiva is suggestive, supported by skin biopsy
samples. Treatment is symptomatic, with response
Insect bite reactions to antibiosis limited.
Overview
Insect bite reactions typically affect individual ani- INFECTIOUS SKIN DISEASES
mals, where it can cause marked irritation. (VIRAL/BACTERIAL/FUNGAL)
Aetiology Contagious pustular dermatitis

Biting midges (Culicoides spp.) are the most common (syns. orf, contagious ecthyma)
cause. Definition/overview
Contagious pustular dermatitis (CPD) occurs in
Clinical presentation goats and sheep worldwide, and is a significant zoo-
Hair loss, erythema and mild to moderate crusting. notic pathogen.
Often found on the head, but can be anywhere on
the body and is always symmetrical between left and Aetiology
right body sections. Lesions are seasonal, occurring The cause is an epitheliotropic parapox virus.
in spring and summer.
Pathophysiology
Diagnosis The virus gains access via superficial skin abrasions
Seasonality and symmetry of lesions are strong indi- whereupon it replicates in proliferating epidermal
cators. Trial housing may be useful to confirm the keratinocytes, resulting in the development of typi-
diagnosis. cal lesions. Transmission is by direct contact with an
infected sheep or goat or indirectly from infected Treatment/management/control

scab material in the environment. There may also Lesions will regress spontaneously over 4–6 weeks,
be asymptomatic carrier animals acting as a source and this will result in natural immunity lasting
of infection. up to 3 years. There is no specific treatment for
this condition, although a number of proprietary
Clinical presentation preparations are marketed as having a beneficial
After a short incubation period, papules appear effect. Antiseptic and antibacterial ointments or
first, progressing rapidly to form pustules. These in sprays applied to the lesions will control secondary
turn become crusted, proliferative and coalescing infection. If an outbreak develops, it is important
lesions, which can be extremely painful. They are to identify any possible underlying risk factors and
typically found on the lips, muzzle and in the mouth remove or control them, particularly those caus-
(Fig. 11.20). Lesions may also be found on the udder ing superficial skin abrasions such as feeding on
and teats, a particular problem when does are nurs- thistles or brambles. A number of vaccines are
ing infected kids. The pain can prevent kids from available, and these are usually administered via
suckling and these may require bottle or tube feed- scarification of the superficial epidermis in thin-
ing. Nursing does with lesions on their udders may skinned areas of the body such as the axilla or per-
abandon their kids. ineal area (although this latter site is best avoided
in does with kids at foot). The vaccine is usually
Diagnosis non-attenuated and as such should only be used
The lesions are quite characteristic. Laboratory in herds in which infection is present and control
diagnosis is based on electron microscopy examina- is needed. Its use in a clean, uninfected herd may
tion of typical scab material. inadvertently introduce infection. Care should be
taken at all times to avoid this zoonotic infection
Differential diagnosis being acquired by those handling infected goats –
The most important differential diagnoses are foot and the skin of the hands and arms is most commonly
mouth disease (FMD) (see Chapter 17) and goat pox. affected (Fig. 11.21).
Fig. 11.20 Contagious pustular dermatitis (orf) at Fig. 11.21 Confirmed CPD (orf) lesions on the
the lip commissure. fingers of a farm worker.
262 Chapter 11
Goat pox implements, vehicles or material such as litter or

Definition/overview fodder can occur. After a short incubation period,
Capripox viruses are among the most serious of all a viraemia develops and the virus is redistributed to
animal poxviruses. They cause economic loss by the skin, regional lymph nodes, lungs, kidneys and
damaging hides and fibre and by forcing the estab- spleen. Virus is then excreted through skin lesions,
lishment of trade restrictions in response to an out- nasal exudate and milk, with spread being facilitated
break. At the time of writing, goat pox is endemic by close housing.
in Africa north of the Equator, the Middle East,
Turkey, Iran, Iraq, Afghanistan, Pakistan, India, Clinical presentation
Nepal, parts of the People’s Republic of China and Clinical signs vary from mild to severe, depending
Bangladesh. It is a scheduled OIE listed disease and on host factors such as age, breed, immune status,
as such is subject to strict statutory control measures and viral strain virulence. In the acute phase, an ini-
in each country. The morbidity rate in endemic tial pyrexia is quickly followed by the appearance
areas is between 70 and 90% with a mortality rate of skin papules, rhinitis, conjunctivitis and enlarge-
of 5–10%, approaching 100% in recently imported ment of all superficial lymph nodes, especially pres-
goats into infected herds. capular lymph nodes (Figs. 11.22, 11.23). Papules
on the eyelids cause blepharitis of varying severity
Aetiology and papules on the mucous membranes of the eyes
The goat pox virus is a member of the genus and nose ulcerate, creating a mucopurulent dis-
Capripox, which also contains the sheep pox virus. charge. Breathing may become laboured and noisy
Capripox virus strains are often recognised by how due to pressure on the upper respiratory tract from
the main target host responds; they cannot be distin- the swollen retropharyngeal lymph nodes draining
guished using routine laboratory tests. The virus is developing lung lesions. The mucosae of the mouth,
very resistant to desiccation and is capable of surviv- anus and prepuce or vagina become necrotic. If
ing in scab material for up to 3 months. the goat survives this acute phase, papules become
necrotic from vascular thrombosis and ischaemic
Pathophysiology necrosis, forming scabs that may persist for up to
Transmission is usually by aerosol after close contact 6 weeks.
with severely affected animals with ulcerated papules
on the mucous membranes of the nose and mouth. Diagnosis
Infection may also develop following virus trans- Diagnosis is based initially on the clinical signs
fer directly through mucous membranes or dam- and the presence of the disease in the locality.
aged skin. Indirect transmission via contaminated Samples for laboratory confirmation include
Fig. 11.22 Goat pox. Conjunctivitis and developing Fig. 11.23 Cutaneous lesions of goat pox. (Image
facial lesions. (Image courtesy Paul Kitching.) courtesy Paul Kitching.)
vesicular fluid if available, scabs, lymph node aspi- Staphylococcal dermatitis/folliculitis

rates, EDTA or heparin blood samples and paired Definition/overview
sera. Post-mortem examination findings include skin Staphylococcal skin infections are relatively com-
lesions often extending full thickness into the under- mon in goats, and may be either primary or second-
lying musculature. In addition, massively enlarged ary to some other skin insult.
lymph nodes and typical pox lesions are evident on
the mucous membranes of the eyes, mouth, nose, Aetiology
pharynx, trachea, vulva and prepuce. Lung pathol- Staphylococcus aureus is most commonly associated
ogy is often severe and includes well established and with the condition, although Staphylococcus inter-
extensive pox lesions, focally and uniformly distrib- medius and Staphylococcus hyicus are also seen. The
uted throughout the lungs. Fresh skin, lymph node recently recognised pathogen S. aureus subsp. anaero-
or lung lesions can be taken for virus isolation. bius has been associated with the condition referred
to as Morel’s disease, which is described later in this
Differential diagnosis chapter.
Includes CPD (orf), insect bites, bluetongue and
peste des petits ruminants (PPR). Pathophysiology
The resulting dermatitis is referred to as a folliculi-
Treatment/management/control tis, where infection involves hair follicles, or impe-
There is no treatment. As goat pox is an OIE listed tigo (or non-follicular), which is a more superficial
disease, it is controlled globally by the implementa- condition. The primary lesion is a papule, develop-
tion of statutory measures designed to keep the virus ing into a pustule, which in turn may burst, liberat-
out of those countries in which it is not found, and ing pus and leading to superficial scab formation, or
eradicating or controlling infection in countries in coalesce to form larger lesions.
which it is currently a problem. Confirmation of dis-
ease must be reported to the World Organisation for Clinical presentation
Animal Health (as per the OIE Terrestrial Animal Multiple small impetigo lesions may develop on
Health Code). the thin skin of the udder and teats (colloquially
Vaccines are available and are used in infected areas. referred to as udder impetigo (Fig. 11.24). These
can be easily spread during milking and, if con-
Bluetongue centrated around the teat end, may predispose
See Chapter 17. Classic signs of bluetongue are a
swollen face (oedema of the face, muzzle and ears),
with buccal and nasal mucous membrane ulceration.
Peste des petitis ruminants

Goats with PPR can develop lesions and scabs on the
lips in the early stages (see Chapter 5).
Foot and mouth disease

FMD vesicles, which rupture and produce scabs, can
develop on the visible mucous membranes of the lips
and nose and the coronary band (see Chapter 17).
Aujeszky’s disease (syn.

pseudorabies) Fig. 11.24 ‘Udder impetigo’. Multiple small ‘acne’-
Goats with Aujeszky’s disease can develop a severe like lesions associated with Staphyloccocus aureus.
pruritus (see Chapter 8). Bacteria around the teat end pose a mastitis risk.
264 Chapter 11
to staphylococcal mastitis. Some goats appear to Mycotic dermatitis (syns.

be more susceptible to infection and may develop dermatophilosis, streptothricosis)
multiple lesions, which may be superficial and only Definition/overview
identified by palpation (important in show goats), or Mycotic dermatitis is a common skin condition in
be more severe, leading to focal areas of hair loss. goats in many countries, and it can also affect both
Lesions can be found initially on the skin of the sheep and cattle.
ventral abdomen, inguinal and axillary areas, but
may become more widespread. Secondary staphylo- Aetiology
coccal infection can develop as a result of other skin Dermatophilus congolensis, an environmental actino-
disorders, such as mange. mycete-forming motile zoospore that can invade the
skin.
Diagnosis
Diagnosis is based on bacterial culture of swabs, Pathophysiology
which will confirm staphylococcal infection, but The organism gains access to the skin via superficial
this must be interpreted in the context of the lesions abrasions or bites, and is most common following
identified, as staphylococci are common skin com- excessive wetting of the coat or when goats are kept
mensals in healthy goats. in a warm humid environment. Secondary bacterial
infection can develop.
Includes fly bites (Fig. 11.17), Dermatophilus congo- Clinical presentation
lensis infection, demodectic mange and ringworm. There are raised ‘paint brush’ tufts of hair or scabs
that appear over the body surface, including ears,
Treatment/management/control face, limbs, scrotum and perineal area. In severe
Many cases are self-limiting. If treatment is deemed cases lesions may coalesce and cover a large area of
necessary, shampooing with antibacterial washes the dorsum of the back. They are generally non-
can be beneficial, with parenteral antibiosis in more pruritic. The crusty lesions are easily knocked or
severe cases. Care should be taken to prevent mas- peeled off, and leave raised, circular granulating
titis during the milking process, particularly avoid- lesions beneath. Focal alopecia is a further sequela to
ing any action (such as udder washing) that may long-standing infection.
spread infection from the udder surface to the teat
end if lactating goats are affected on the udder or Diagnosis
teat skin. Diagnosis is based on clinical signs and laboratory
examination of hair and scab material.
Malassezia
Malassezia organisms, including Malassezia pachy- Differential diagnosis
dermatis and Malassezia slooffiae, are opportunistic Although the lesions are fairly characteristic, they
pathogens producing scaling, dry or less commonly can be confused with ringworm, CPD (orf: if con-
greasy seborrhoea, alopecia and crusting lesions, fined to the face) or staphylococcal dermatitis.
often involving most of the body. Diagnosis of
Malassezia dermatitis in goats can be made by Treatment/management/control
cytological examination of skin impression smears. Treatment of individual goats with broad-spectrum
Topical antifungal therapy using chlorhexidine and antibiotics, combined with housing away from envi-
miconazole shampoo or selenium sulphide is sug- ronmental moisture, is usually successful. Brushing
gested, soaking animals for 10 minutes, twice weekly and combing out scab material, combined with con-
for 3 weeks. Any predisposing or underlying disease trolling other exacerbating factors such as concurrent
will also need treating. ectoparasitism, will improve the goat’s appearance.
Ringworm (syn. dermatophytosis) which may be useful for epidemiological investiga-

Definition/overview tion into zoonotic links.
Ringworm is a fungal skin condition affecting most
animal species worldwide, with cross species infec- Differential diagnosis
tions occurring. It is also an important zoonotic risk Dermatophilus sp. and staphylococcal infection are
to anyone handling infected goats. the primary differential diagnoses.
A number of dermatophyte species have been iso- Most cases will regress spontaneously, particularly
lated from cases of ringworm in goats, including if any underlying problems related to manage-
both Trichophyton and Microsporum spp. ment, nutrition or concurrent disease are addressed.
Treatment includes topical administration of
Pathophysiology enilconazole or natamycin, repeated depending on
Infection can be acquired from an infected goat response. Oral use of griseofulvin is effective, but
or, in theory, from direct or indirect contact with has been banned for use in food producing animals
another infected animal species, both livestock and in many countries. All in-contact goats should be
companion. Lesions tend to develop more in goats treated and a thorough cleaning and disinfection
that are ill-thrifty or debilitated through concurrent programme applied to the housing environment to
disease. inactivate resistant spores on fixtures and fittings.
Clinical presentation CUTANEOUS SWELLINGS

Lesions in goats may present as the typical annular
lesions seen in other species, but they can also be Caseous lymphadenitis
more diffuse, consisting of areas of alopecia, skin CLA produces swellings associated with superficial
scaling and crust formation. Moist eczematous lymph nodes (see Chapter 7).
lesions can also develop (Fig. 11.25). Lesions can be
found mainly over the head, neck and limbs. Morel’s disease
Morel’s disease is caused by Staphylococcus aureus
Diagnosis subsp. anaerobius. It is a disease identified in both
Laboratory examination of scab, scale and hair plucks goats and sheep and is a differential diagnosis for
will confirm a diagnosis of ringworm, and culture CLA in those countries in which infection has been
techniques can also identify the species involved, confirmed. Superficial abscesses are located near
major lymph nodes, most commonly the cranial
cervical, subiliac, parotid and mandibular nodes.
Abscesses can be very large and debilitating.
Lymphoma
Lymphoma causes lymph node enlargement and is
discussed in Chapter 7.
Neoplasia
The most common cutaneous tumours in the
goat are:
•• Papilloma (warts) – usually small and self-

Fig. 11.25 Crusty moist dermatitis lesions – limiting, found on the head, neck and
confirmed as ringworm (T. mentagrophytes). occasionally on the skin of the udder and teats.
266 Chapter 11
Fig. 11.26 Perineal mass in an entire 2-year-old Fig. 11.27 Injection site abscess in front of the
Saanen buck. shoulder.
•• Carcinoma – can occur over the head and resulting in rupture of subcutaneous blood vessels
neck, perineal area (Fig. 11.26) and skin and haemorrhage into the subcutaneous tissue. If
covering the udder, but also at other sites. several goats develop these lesions, then the investi-
White goats (or goats with areas of white hair) gation should focus either on the goat’s environment,
kept in sunny climates may be particularly identifying sites of potential injury, particularly in
susceptible. their daily movement routes (e.g. a projecting gate
•• Melanoma – has been reported to develop most hinge), or alternatively at identifying an underlying
commonly involving the perineal area and clotting disorder.
earlobes.
Injection site abscesses
These tumours can be identified initially by their Goats appear to be susceptible to developing injec-
appearance and confirmed by examination of biopsy tion site reactions (ISRs) or abscesses (Fig. 11.27).
samples. Management will depend on location, size If the swelling is close to a superficial lymph node,
and tumour type, with metastasising tumours carry- CLA must be ruled out prior to lancing and lavage
ing a poor prognosis. of the abscess.
Prevention relies on carrying out injections in
Thymus enlargement goats with dry fleece and away from obvious skin
Swelling of the skin over the lower part of the neck contamination, using the correct dose, ensuring the
in kids may be an indication of thymus enlargement needle is in the target tissue (subcutaneous not intra-
(see Chapter 7). The condition should not be con- dermal; deep intramuscular) and using a clean, sharp
fused with goitre involving the thyroid gland. needle (i.e. frequently discarding for a new one when
treating a larger group). In show or sale animals, it
Haematoma may be possible to place the injection at a less obvi-
Sporadic haematoma formation can occur (mainly ous site (e.g. the axilla) where a product is known to
in housed goats) as a result of a traumatic insult have an ISR risk.
SURGERY OF SKIN ADNEXA
Disbudding
Indication
Disbudding is currently routinely performed in
many herds in the UK in order to avoid horn-induced
injuries to handlers and during hierarchical fighting,
and to allow higher stocking densities. In the UK
the procedure can only be undertaken by a veteri-
nary surgeon. Several countries have banned routine
disbudding, and sentiment towards its routine use is
starting to change in the UK.

Ideally performed in 2–4 day-old kids, and no
older than 7 days. A disbudding iron with a large
Fig. 11.28 A wide-diameter disbudding iron is
enough diameter to encompass the entire horn bud
applied for a few seconds at a time until an obvious
is required. (Note: Disbudding heads designed for
rim forms and the surrounding skin has become
young calves are usually too narrow in diameter.)
detached from the horn bud.
Restraint Potential complications

Options for anaesthesia are (see Chapter 18 for fur- Common complications include horn-growing tis-
ther details): (1) cornual block, taking care not to sue not removed, resulting in re-growth; death
exceed the toxic dose of local anaesthetic (maximum under anaesthesia (especially if xylazine is used); and
total dose across both sides is 3 ml of 1% lidocaine meningoencephalitis as a result of prolonged iron
for a 5 kg kid); (2) injectable general anaesthe- application. Clinical signs typical of encephalitis
sia (GA); and (3) inhalation GA using a face mask. develop after 2–3 days, usually followed by death.
GA is recommended by the UK’s Royal College of
Veterinary Surgeons. Dehorning
(Note: Oxygen supports combustion: the disbud- Indication
ding iron must be ignited outside and only brought Dehorning of an adult goat is a very invasive pro-
close to the kid after shutting off the anaesthetic cedure, resulting in opening of the sinuses, with a
machine). relatively long wound healing period. It should,
therefore, not be undertaken lightly. However,
Technical description undue aggression in a horned goat against other
Apply iron for 3–4 seconds at a time with even pres- goats or humans, or fracture of the horn, may require
sure until the horn-growing tissue is destroyed dehorning (Fig. 11.29).
(Fig. 11.28). It is not necessary to ‘scoop out’ the For an in-growing horn, it is usually sufficient to
bud, and no attempt should be made to do this. Kids regularly (every 6–12 months) cut a few centimetres
have a much thinner skull than calves and care must off the horn tip with fetotomy wire (Fig. 11.30),
be taken not to overheat the meninges and brain rather than fully dehorn the animal.
(see Fig. 8.9).
Aftercare The goat is starved and preoperative antibiosis and
Administration of NSAIDs is recommended. Fly NSAIDs given. The site is clipped and surgically
repellent should be used depending on the time of prepared. A standard surgical kit, plus either a sterile
year and country. hacksaw or sterile fetotomy wire, is required.
268 Chapter 11
Fig. 11.29 Trauma may warrant removal of the Fig. 11.30 An in-growing horn is addressed by
injured horn. removing the distal section with a fetotomy wire.
(Image courtesy Nichol Fisher.)
Restraint
GA is recommended, because the procedure will
lead to bleeding into the sinuses, potentially caus-
ing stress to a sedated only animal through smell and
obstruction of nasal passages. In addition, a cornual
block is applied (see Chapter 18).
For bilateral dehorning, a figure-of-eight incision
is made at a distance of 8–10 mm around both horn
bases (i.e. a circular incision around each horn
base with an incision connecting the two circles
at the poll; Fig. 11.31). The skin is undermined
for 1–2 cm along the entire incision. The horns
are sawed off flush with the skull. A hacksaw gives
better control of the cutting angle compared with
using a fetotomy wire. To facilitate placement
of the saw, the bulk of the horn may have to be
removed first a few centimetres above the skull Fig. 11.31 For bilateral dehorning, a figure-of-eight
(Figs. 11.32, 11.33). incision is made about 1 cm away from the horn base
The incision is closed with interrupted horizon- (photo taken after removal of left horn).
tal mattress sutures, using a 3.5 to 4 metric non-
absorbable suture material (e.g. Prolene®). Closure Aftercare
can be facilitated by making a relief incision caudal A tight figure-of-eight bandage is placed around
to each horn base, but full apposition may not be the head either side of the ears, starting with a non-
achievable (Fig. 11.34). adherent wound dressing (e.g. Melolin) and taking
Fig. 11.32 The horn is cut close to the skull. To Fig. 11.33 View into the opened sinuses after
facilitate a good angle for this, the bulk of the horn dehorning.
was removed first in this goat (lateral view, with the
goat’s nose to the left-hand side).
Fig. 11.34 The wound edges are apposed as closely

as possible, using relieve incisions where necessary Fig. 11.35 A tight figure-of-eight bandage applied
(arrow). after unilateral dehorning to aid haemostasis and
provide wound protection. The bandage was cut out
care not to encroach onto the eyes (Fig. 11.35). around the eye.
The bandage is first replaced after 3 days, and then
again after 7 days. Occasionally, a fourth bandage Potential complications
is required. Sutures are removed after 12–14 days. Sinusitis and wound breakdown or prolonged wound
Postoperative analgesia is provided. healing.
CHAPTER 12
MAMMARY GLAND DISORDERS

271
NORMAL STRUCTURE AND FUNCTION teats are visually examined and palpated, particu-
larly the teat end for trauma or other lesions. Milk
In goats, the udder consists of two glands (or halves), is drawn from the udder and examined grossly for
with each half culminating in a teat with a single and clots, pus, blood or abnormal colour and consistency
very narrow streak canal. Milk production in the (Fig. 12.3).
mammary gland is by the physiological process of
apocrine secretion, unlike the cow in which the pro-
cess is merocrine secretion. One major implication
of this difference is its effect on the milk somatic cell
count (SCC), typically being higher in goats and less
correlated with udder infection.
CLINICAL EXAMINATION OF THE UDDER
The most common disorder of the udder is mastitis,

which, if acute, can result in systemic signs of toxae-
mia such as pyrexia. Visual examination of the udder
may reveal disparity in size between the two halves
(Fig. 12.1), and skin discolouration (Fig. 12.2). This
is followed by palpation of the udder for pain, swell- Fig. 12.2 Early gangrenous mastitis, with marked
ing, oedema, firmness or nodular abnormalities. The discolouration of the overlying udder skin.
Fig. 12.1 Udder induration and asymmetry (left Fig. 12.3 Mastitic milk with clots (on left) compared
half affected) associated with caprine arthritis with normal milk secretion (on right).
encephalitis.
272 Chapter 12
Sampling for culture Teat biting

Any sample for laboratory examination must be Teat end damage can also occur as a result of the
taken aseptically to avoid contamination. Loose recognised vice of teat biting (Fig. 12.4). This is a
dirt, bedding or hair is manually brushed off the behavioural abnormality, seen particularly in adult
udder and teats. Dirty teats are washed and dried. dairy goats, in which one or more goats in a group
Several streams of milk are discarded from each teat start biting the teats of other goats. Careful observa-
that is to be sampled. Ideally, pre-milking teat dis- tion is required to identify the culprits, which should
infectant is applied for 30 seconds, followed by dry- be culled or removed. Injuries can be severe and pre-
ing off using individual paper towels. Using a gloved dispose to mastitis.
hand, the teat end is thoroughly scrubbed with
70% alcohol, using several pieces of cotton wool or Neoplasia
gauze until no dirt is visible on the swab. A stream Neoplasia affecting the udder lactiferous tissue has
of milk is directed into a sterile container held at a been occasionally recorded. An adenocarcinoma
45 degree angle, taking care not to contaminate the of the udder of a lactating Saanen doe is shown
inside of the lid. When sampling from both teats, (Fig. 12.5). The tissue was firm and nodular on pal-
the order of cleaning is furthest away teat to near- pation, had ulcerated through the lower skin surface
est, followed by sampling in a nearest to furthest and metastasised to the local lymphatic system, but
away order, thereby avoiding touching cleaned teats without evidence of further metastatic spread.
prior to sampling. Post-milking teat disinfectant is
applied to sampled teats. The sample is kept cool Enlarged pendulous udder
until submission. An enlarged pendulous udder can be a problem par-
ticularly in elderly goats, in which slackening of the
Ultrasonography suspensory ligaments are often the underlying prob-
Ultrasonography can be useful in examining lem (Fig. 12.6). A hormonal aetiology, such as ovar-
the udder, particularly for deep seated chronic ian abnormalities or pyometra, should be ruled out.
pathology such as abscesses or fibrous scar t issue. In pet goats, a mastectomy may be considered.
The normal udder will display a relatively uni-
form mix of hyperechogenic parenchyma and Maiden milkers
anechogenic alveoli and milk. Lesions will show It is not uncommon for non-bred females to come
up as hyperechogenic delineated areas. Teat ultra- into milk, and this precocious milking may well be
sonography is best carried out using a stand-off a hereditary trait, since the condition is more com-
(e.g. a p
lastic cup filled with water or contact gel) mon in those breeds and lines known for their heavy
to avoid distortion of any features. Four distinct milk production. The exact cause remains unknown,
layers can usually be identified: (1) anechoic milk
in the lumen of the teat; (2) a moderately ech-
odense, thin mucosal layer; (3) a mid-echodense
thick layer of connective tissue and muscle; and
(4) hyperechoic outer skin.
NON-INFECTIOUS DISEASES
Trauma
Traumatic damage to the udder
The inquisitive nature of goats makes them vul-
nerable to traumatic injury, and the udder and teats
can be damaged by horns, barbed wire or crush Fig. 12.4 Trauma caused by teat biting –
injuries. a recognised vice.
M a m m a ry G l a n d D isor de r s 273
Fig. 12.5 Udder adenocarcinoma. Note the Fig. 12.6 Enlarged pendulous udder. Mastectomy
ulcerative change on the surface (blue oxytetracycline may be an option.
spray applied to skin).
and as such, there is no specific treatment that can •• Disruption of the milk let-down stimulus (can
guarantee success. It is important where possible not be stress- or pain-related), in which case an
to start milking these goats, as more milk will be injection with oxytocin may help (2–5 IU).
produced once the pressure has been relieved, and •• Nutritional problems (i.e. energy balance not
the teat seal will have been broken, predisposing to sufficient to support milk production).
mastitis. Milk should only be removed if the goat •• Acute mastitis or other causes of pain, in which case
is in pain or discomfort, when the udder should be NSAIDs may help; udder fibrosis from infection
completely stripped out under strict hygienic con- during previous lactation or the dry period.
ditions and teat disinfectant used afterwards. If •• Premature kidding, in which case continued
desired, a normal lactation will ensue with regular stimulation may help; and hormone imbalances.
milking, and the milk will be suitable for human •• The teat may not be patent because of stenosis or
consumption. obstruction, in which case surgery may help.
Various hormonal treatments have been tried
with limited success. Reducing any concentrate or Effects on milk stimulation of products such as
cereal in the diet and feeding only good quality hay domperidone or herbal products are ambiguous.
may help, but water must never be withheld on wel- The kids of affected goats must receive colostrum
fare grounds. In older goats with a heavy pendu- from an alternative source to ensure passive transfer.
lous lactating udder, mastectomy is a final option to
consider. Induction of lactation
Inducing lactation has been investigated to reduce
Post-partum agalactia the risk to the dam associated with kidding and the
There are several potential reasons for a dam to not number of surplus kids. It can be achieved using a
have any milk: combination of hormones and mammary gland
stimulation. An example protocol is: (a) 17-beta
•• Severe oedema, in which case an anti- oestradiol (0.25–0.5 mg/kg i/m) plus progesterone
inflammatory drug may help. (0.75–1.25 mg/kg i/m) either daily for 7 days or every
274 Chapter 12
other day over 14 days; (b) combined with predniso- Clinical presentation

lone (0.4 mg/kg i/m) or dexamethasone (10 mg/day) Early signs include inappetence and depression,
for 3 consecutive days anytime between days 14 followed by the development of agalactia and a
and 20; (c) reserpine (1 mg/day i/m) may be added change in milk secretion, which is initially watery
every other day between days 12 and 20; (d) the then becomes progressively thicker and more puru-
mammary gland is massaged from days 5–7 or the lent. Other clinical features that may accompany
goat is machine milked from day 20. the udder changes include keratoconjunctivitis and
Peak yield tends to be much lower compared with arthritis. However, young goats, males and some
naturally induced lactation (around 55%), and subse- females may only show non-specific signs, such as
quent pregnancy rates are often poor, as well. depression, pyrexia, keratoconjunctivitis and arthri-
tis, with no evidence of mastitis. Udder atrophy
INFECTIOUS DISEASES and agalactia is a significant feature, which can be
permanent. Mortality rates of up to 20% have been
Contagious agalactia recorded, and morbidity in infected herds can be
Definition/overview very high, with repetitive waves of apparent resolu-
Contagious agalactia affects both goats and sheep, tion and subsequent breakdown due to chronically
and is one of the most serious mycoplasma diseases infected individuals.
of small ruminants worldwide after contagious cap-
rine pleuropneumonia. It occurs in many countries Diagnosis
including parts of southern Europe, Asia and Africa, The clinical signs are fairly characteristic, in par-
in which its economic importance can be consider- ticular the combination of mastitis and other signs.
able due to dramatic falls in milk yield. It is an OIE Diagnosis is confirmed by laboratory examination of
listed disease, and as such is notifiable or reportable milk samples. Specialist culture techniques are being
to the relevant authorities and is subject to statutory replaced by molecular testing such as the denatur-
controls. ing gradient gel electrophoresis test, which can be
undertaken on milk, body fluid, tissue samples or
Aetiology cultures to identify the Mycoplasma spp. involved. In
Although Mycoplasma agalactiae is often considered cases of contagious agalactia presenting with non-
the classic agent, Mycoplasma mycoides subsp. mycoides mastitis signs, paired serology in individuals may be
(large colony type) and Mycoplasma capricolum subsp. of benefit, and serology is a useful screening tool.
capricolum can produce similar clinical pictures.
Pathophysiology Other causes of mastitis need to be eliminated by
Despite its descriptive term, it is essentially a dis- laboratory examination of milk samples.
ease syndrome involving multiple organs including
the udder and articular and ocular tissues. The main Treatment/management/control
sources of infection include ocular and nasal secre- Treatment of infected goats, using antimicrobials
tions, faeces and milk. Contaminated milking equip- such as tetracyclines, tiamulin, erythromycin, flor-
ment, milking utensils and the milker’s hands can all fenicol or fluoroquinolones (where permitted), will
transmit new infection. After infection is acquired, alleviate the clinical signs, but recovered goats will
a bacteraemia develops, followed by progressive often become carriers and pose a particular problem
localisation in lungs, lymph nodes, eyes, mammary if the disease is to be eradicated. Live attenuated and
glands, joints and tendons. Udder infection leads to inactivated vaccines are available and are used as a
atrophy and agalactia. Goats suffering from masti- control measure in endemically infected areas. Unless
tis can spread disease to kids through colostrum or the goat is from a herd in a heavily infected area, how-
milk. If goats and sheep are kept together, cross spe- ever, statutory control measures including slaughter
cies transmission can also occur. of all known infected goats is the usual route taken.
Most cases and outbreaks of contagious agalac- Coagulase-negative staphylococci

tia result from the purchase of infected goats or Coagulase-negative staphylococci are the most com-
sheep. A ban on imports from known infected areas monly isolated udder organism in many goat milk
is applied by many disease-free countries, or, alter- bacteriology surveys. Opinions vary as to their path-
natively, laboratory testing of purchased goats is a ological significance. Some reports state that they
pre-import requirement. In those countries in which are non-pathogenic even commensal in the udder,
the disease is a local problem, a sound biosecurity whereas others believe that they are potentially
protocol should be in place to test goats and sheep pathogenic if no other causative agent is identified.
on the premises of origin (where possible), and test A high herd prevalence may be linked to reduced
again on arrival after being placed in suitable quar- milk production, and a possible indication of a sub-
antine facilities. optimal milking regime.
Mastitis Corynebacterium pseudotuberculosis and

Definition/overview Trueperella pyogenes
Mastitis is a broad, overarching term for any inflam- These two organisms are both opportunistic
mation of the udder tissue in association with pathogens, potentially colonising teat and teat
changes in the appearance of the milk secretion. end lesions, and gaining access to udder tissue if
there is heavy infection around the teat end and/or
Aetiology damage to the sphincter. C. pseudotuberculosis is the
There are many species of bacteria, mycoplasma, causative organism of caseous lymphadenitis (see
fungi, algae and yeasts that have been isolated from Chapter 7).
clinical cases of mastitis. Some may be involved in
outbreaks of mastitis, such as Staphylococcus aureus Escherichia coli and Pseudomonas aeruginosa
(the most common cause of mastitis in dairy herds These are environmental organisms potentially
spreading from goat to goat), whereas others may gaining access to the udder as a result of heavy con-
be sporadic and environmental in origin such as tamination of the udder and teat end from goats
Escherichia coli. Mastitis may also be a clinical pre- lying in wet dirty conditions, or being milked
sentation in systemic diseases such as caprine arthri- when the udder itself is dirty. E. coli can produce a
tis encephalitis (CAE). Any mastitis investigation potent toxin, resulting in severe tissue damage and
should include identification of the causative organ- gangrenous change.
ism or underlying syndrome.
Tuberculosis
Pathophysiology Mastitis associated mainly with Mycobacterium
This will vary from pathogen to pathogen. bovis (and only rarely with other mycobacterial
Staphylococcus aureus organisms such as Mycobacterium avium) has been
Staphylococcus aureus is a contagious mastitis patho- recorded in goats. In new M. bovis cases, there is
gen and can be found in the udder tissue as a chronic most often spread either directly from infected
infection, or residing on the skin of the udder or cattle or goats, or indirectly via infected wildlife,
teats, spreading between goats predominantly dur- particularly in areas with a high bovine tubercu-
ing the milking process. The organism can colonise losis incidence. Udder disease occurs as a sequela
teat lesions such as cuts, abrasions or skin lesions to dissemination of either respiratory or alimentary
resulting from, for example, sarcoptic mange. infection to a number of systemic sites, including
Mastitis will develop mainly as a result of transfer of also the lungs and associated lymph nodes, and the
infection between goats during mechanical or hand liver and spleen.
milking. S. aureus can produce a potent necrotoxin,
causing severe udder tissue damage and gangrenous Mycoplasma spp.
change. See contagious agalactia earlier in this chapter.
276 Chapter 12
Caprine arthritis encephalitis becomes watery and dark in colour due to secretory
One of the manifestations of CAE seen in infected tissue cell necrosis, and gas may be stripped from
herds is an interstitial mastitis resulting in atrophy the teat end.
and induration of the affected udder half (Fig. 12.1). In acute bacterial mastitis, signs can range from
Even in the absence of clinical disease, milk from severe with systemic involvement (grade 3), to udder
CAE-positive does will contain high levels of cell- and milk changes (grade 2), to milk changes only
associated CAE virus, making milk and colos- (grade 1). Affected goats are often inappetent and
trum one of the main routes of dissemination (see pyrexic. The udder may be firm, oedematous and
Chapter 9 for more details). painful, and milk drawn from the affected half will
be of an abnormal appearance, such as watery, thick
Clinical presentation or discoloured, and may contain clots.
The clinical signs of mastitis will vary (depending In chronic mastitis, the udder will be firm and
mainly on the organism involved) from peracute often nodular when palpated. The nodules represent
gangrenous mastitis, to mild mastitis with little chronic suppurative areas associated with S. aureus
change or subclinical mastitis with no change to the or T. pyogenes infection, effectively walled off by tis-
gross appearance of the milk secretion. sue fibrosis (Fig. 12.8). The associated milk secre-
In gangrenous mastitis caused predominantly tion may be abnormal or unremarkable.
by S. aureus and E. coli, affected goats show a rapid Other clinical signs may be apparent in indi-
onset of severe dullness, depression and inappe- vidual goats or within the goat cohort if udder
tence. Initial pyrexia gives way to subnormal tem- infection is a manifestation of a more complex
peratures due to systemic shock. The affected part disease. In CAE, for example, lameness and joint
of the udder becomes cold to the touch and pro- enlargement are most commonly reported in addi-
gressively purple to black in colour, usually with tion to udder changes (see above). In contagious
a clear line of demarcation, and serum may ooze agalactia, arthritis and severe keratoconjunctivitis
from the skin surface (Fig. 12.2). This gangrenous are other associated clinical signs in both adults
tissue may eventually slough (Fig. 12.7). The milk and kids (see above).
Fig. 12.7 Advanced gangrenous mastitis with Fig. 12.8 Marked udder fibrosis associated with
sloughing. (Image courtesy Kathy Anzuino.) chronic mastitis.
Diagnosis commercial dairy goat units, the average individual

Clinical mastitis somatic cell count was 1,258,000 cells/ml. In samples
In clinical cases of mastitis, changes in milk and/ that yielded no significant bacterial growth it was
or the udder will be present. Aseptically taken 1,080,000 cells/ml and in those samples in which
milk samples should be submitted for laboratory there was significant bacterial growth suggesting
examination. The majority of the bacterial pathogens udder infection it was 2,053,000 cells/ml, with some
will grow on blood agar and MacConkey agar, and individual samples considerably higher. Applying
can be differentiated by colony morphology, Gram cattle interpretation values to the California mastitis
staining and other confirmatory tests. Laboratory test (CMT; Fig. 12.9) will undoubtedly lead to false-
isolation of Mycoplasma spp. is more problematic (see positive results, although a modified CMT has been
Contagious agalactia). developed with goat-specific figures for individual
In tuberculosis infection, culture is difficult but CMT scores. The conventional CMT can also be of
acid-fast organisms may be identified in a spun milk benefit in excluding a diagnosis of mastitis if nega-
sediment, and a holistic approach is required based on tive. To further complicate the picture, there is a
the herd profile supported by the single intradermal breed difference in SCC values and also a seasonal
comparative cervical skin test. If CAE is suspected, variation linked to stage of lactation, daily yield and
milk examination is of limited value. The CAE sta- onset of oestrus.
tus can be confirmed by an ELISA test on blood, The following guidelines may be useful to assess
but emphasis must be placed on herd status as not all udder health in goats:
CAE-positive goats produce a hard udder or serocon-
vert. Histopathology of udder tissue may aid a diagno- •• Classifying a CMT score of 0 or 1 = uninfected
sis, either by biopsy or at post-mortem examination. gland (versus score of 2 or 3 = infected gland);
has a specificity of around 80% and negative
Subclinical mastitis predictive value of about 85%.
There are several ancillary tests available for con-
firming subclinical mastitis or monitoring milk
quality, both in individual goats and for use on bulk
milk samples from goat herds.
In dairy cows, the SCC is widely used as an indi-
cator of udder infection. In the healthy bovine udder
the SCC is made up predominantly of epithelial
cells. In response to inflammation, white blood cells
enter the udder tissue and milk to combat infection
and the SCC rises, giving good correlation with
the infection status of the udder. In the goat, how-
ever, during the process of apocrine milk secretion,
small portions of the cytoplasm of the epithelial cells
lining the glandular structure are pinched off and
appear in the milk, before degenerating and releas-
ing the milk secretion. These cytoplasmic portions
are similar in size to leucocytes and are the main
reason why SCC values for both individual and bulk Fig. 12.9 Different reactions in cow quarter samples
milk samples are considerably higher in goats, and to the California mastitis test: strong positive top left,
thus of more limited value for mastitis monitoring, moderately positive top right, and normal milk (no
and can easily lead to a false-positive result that a reaction) bottom row. Interpretation of such reactions
goat’s udder is infected. As an example, in a UK gov- is more difficult in goats because of their different
ernment study of 2,800 milk samples taken on four milk secretion process.
278 Chapter 12
•• Classifying a SCC <500,000/ml = uninfected; category comprises the thermoduric organisms that
identifies about 60% of glands correctly, with a survive the normal machine, pipework and tank
negative predictive value of 90%. cleaning process. Checks should also be made on the
•• Using a SCC >1,500,000/ml at peak lactation as bulk tank cooling to ensure refrigeration tempera-
an indicator of S. aureus infection has a reasonable tures are being met.
sensitivity and specificity percentage (80–90%).
•• The bulk milk SCC should gradually decrease in Differential diagnosis
the first 6 months of the herd’s milking period Udder trauma or neoplasia may present with pain
(if block-kidding). and swelling, but milk culture will be negative. In
those more complex conditions, such as CAE, con-
Current studies have not found a consensus on what tagious agalactia and tuberculosis, the combination
parameters and cut-offs constitute an intramammary of the clinical presentation, post-mortem findings,
infection in goats. However, when investigating a laboratory test results and morbidity and mortality
potential subclinical mastitis problem, the guidelines figures will aid the diagnosis.
above may be of help. Bulk milk somatic cell counts
can also used as an indication of milk quality as it Treatment
leaves the farm, and thresholds/targets applied will The choice of antibiotics, both parenteral and intra-
vary from country to country (see Milk quality, later). mammary, should be based on culture results, ide-
Milk conductivity testing is increasingly being ally from the particular case, but as a minimum from
carried out in many commercial dairy goat herds, previous herd samples. Availability of licensed prod-
with sensors placed at each milking unit in the par- ucts will vary greatly from country to country, and
lour. Care should be taken in interpreting results, country-specific bans on particular agents (such as
taking other factors into consideration. fluoroquinolones) must be taken into account. In the
Culturing a bulk milk sample is a useful first indi- UK, a minimum withholding period of 7 days must
cator of potential pathogens involved. The milk is be observed for milk under the ‘prescribing cascade
agitated for several minutes before a sample is taken regulations’ for any product used off-licence (e.g. any
with a sterile ladle or pipette and transferred into intramammary preparation).
a sterile container. Because bacterial counts are as
important as type of pathogen, the sample must be Acute mastitis
kept cool during transport to the laboratory. Treatment of clinical mastitis depends on the severity
and chronicity. For acute grade 1 or 2 mastitis, intra-
Milk quality mammary antibiosis is usually sufficient. Product
Investigations into milk quality may be requested groups to consider are cloxacillin, clavulanic acid
based either on SCC or total bacterial count (TBC) preparations, cephalosporins, macrolides and tetracy-
figures. Individual countries will apply upper SCC clines. The distribution within the udder or, for sys-
limits for milk sold for human consumption, and this temic administration, into the udder must be taken
will vary from country to country with <1,000,000 into account.
cells/ml a typical figure. Less is known about the For grade 3 mastitis (i.e. causing systemic illness),
overall significance of TBC figures in goats, but the treatment consists of NSAIDs, intramammary and
starting point must always be to identify potential systemic antibiosis, fluid therapy and nursing care.
sources of the bacteria counted. Levels of environ- Frequent stripping of the affected gland is advisable,
mental organisms, such as E. coli, may rise if goats if necessary facilitated by administration of 2–5 IU
are kept in dirty conditions with faecal contamina- oxytocin.
tion of the udder and teats during milking. The sec-
ond source comprises the udder pathogens such as Gangrenous mastitis
S. aureus and non-pathogenic/commensal organisms These cases carry a poor prognosis, and if tis-
such as coagulase-negative staphylococci. The third sue necrosis is advanced, immediate euthanasia on
humane grounds should be considered. In valuable or The benefits of using teat sealants, either alone or
pet goats treatment may be attempted with i/v anti- in combination with intramammary antibiotics, are
biotics such as: oxytetracycline 10 mg/kg q12–24h; as yet not fully established in goats.
where available, ampicillin 3 mg/kg q8–12h; where
culture and sensitivity indicates ceftiofur 1–2 mg/kg Management/control
q12h or cefquinome 1–2 mg/kg q12h. NSAIDs pro- The major factors in the prevention and control
vide important supportive therapy (e.g. flunixin of ordinary bacterial mastitis are a sound milking
meglumine 2 mg/kg i/v q12–24h; carprofen 1.4 mg/ regime, a well maintained machine and a clean stress
kg i/v or meloxicam 0.5 mg/kg i/v q48h). Affected free environment:
goats should be kept warm and hydrated. Teat ampu-
tation may be indicated in the acute stage of gan- •• Milking goats should be kept in a clean,
grenous mastitis, followed by partial or complete well-ventilated, dry environment, free from
mastectomy depending on the residual udder dam- condensation, on bedding that is regularly
age present if the goat survives. topped up (Fig. 12.10). Bedding material should
be stored under cover to ensure it is dry when
Chronic or recurrent cases being used.
Prolonged antibiosis may be required for chronic •• They should be fed a good wholesome diet that
or recurrent cases (observing prolonged milk with- eliminates any change away from the normal dry
holding periods as necessary), but carries the risk pelleted faeces they normally produce.
of inducing fungal or yeast mastitis. Other options
include selective drying-off of the affected gland In the parlour:
or early drying off (with or without systemic anti-
biosis in addition to use of intramammary dry cow •• Gloves should be worn, and regularly
therapy). Culling should be considered if a doe has disinfected, to eliminate spread of infection
multiple episodes of either clinical mastitis or raised between goats.
SCC, especially if caused by contagious pathogens,
such as Staphylococcus spp.
Dry goat therapy

Dry goat therapy is not as widely adopted in goats as
in the dairy cow sector, not least because there are
few, if any, intramammary products licensed for use
in goats. Indications include an intractable or per-
sistent mastitis in individual goats or a herd prob-
lem. A positive effect on the SCC in the subsequent
lactation has been shown. The general recommen-
dation is to use half the contents of a dry cow tube.
However, great care must be taken when inserting an
intramammary tube into the teat of a goat because of
the much reduced diameter of the sphincter, which
can easily become damaged. The procedure must be
carried out using strict asepsis. The routine use of
dry goat therapy is particularly problematic if goats
kid early. Enquiries should be made with the manu-
facturer about suitable milk withholding times, and
antibiotic residue testing carried out prior to the Fig. 12.10 Poor bedding hygiene in this high-
milk entering the bulk tank. yielding goat’s pen.
280 Chapter 12
•• Teats should only be washed if they are visibly •• Ideally, after milking goats are encouraged to
dirty. If they are washed, they should be dried stand for 30 minutes to allow teat sphincter
with individual disposable paper towels. closure, for example by having fresh feed available.
•• Pre-milking teat disinfection should be
considered to control environmental mastitis The milking machine can impact on the inci-
where this is a problem. dence of mastitis in a number of ways:
•• Each goat should be checked for mastitis at
every milking. This may be by udder palpation, •• Spread of infection between goats via
by drawing milk from each half into a strip contaminated liners.
cup, or by the use of in-line filters or electrical •• Defective pulsation rates or excessive vacuum
conductivity meters. This procedure is, levels at the teat end can cause damage to
inadvisably, often omitted in high throughput the sphincter, allowing bacteria to enter
parlours. (Fig. 12.11a).
•• Post-milking teat disinfection should be used •• Rapid fluctuations in vacuum level at the
routinely, but as a minimum in herds with a teat end can lead to ‘teat end impacts’ in
known mastitis problem. which potentially infected milk droplets can
•• Prompt recognition and treatment of new be driven back up into the udder. This is
clinical cases, and culling of chronic cases, particularly important if infected milk from a
is essential. Some mechanism for identifying previous goat remains in the cluster, and this is
affected goats, such as spray marking or leg a potential mechanism for spread of the CAE
tapes, should be in place. virus.
•• Known infected goats should be segregated where •• Over-milking can cause teat end damage
possible and milked last, using either dedicated (Fig. 12.11b) and may result from insufficient
clusters and dump buckets or thorough flushing stimulation of milk let-down at the start of milking
and disinfection of clusters and milk lines. or delayed cluster removal at the end of milking.
(a) (b)

Fig. 12.11 Teat end damage should prompt investigation into plant function, liner quality and over-milking.
(a) Acute damage, and (b) hyperkeratosis as a result of recurrent insult to the teat end (both images are cow
teats).
Milking machines must be designed and cali- teat discolouration, be less effectively cleaned and
brated specifically for milking goats as operating therefore harbour pathogens, and milk slower.
parameters are different to those employed for dairy
cows (Fig. 12.12). In the UK, the following param- Tuberculosis management/control
eters have been suggested: See Chapter 17.
•• Vacuum levels 37–38 kPa. Caprine arthritis encephalitis

•• Pulsation speed 90–120 ppm. management/control
•• Pulsation ratio of 50% (50:50). See Chapter 9.
Vacuum levels should be checked at the start of Udder impetigo (syn. staphylococcal
every milking session and pulsation rates should be folliculitis of the udder)
assessed on a weekly basis. This can be done easily See Chapter 11.
by inserting a thumb into an activated teat cup and
counting the number of times the liner collapses on SURGERY OF THE MAMMARY GLAND
the thumb every 60 seconds. The service require-
ments of a milking machine will depend greatly Supernumerary teat removal
on the number of hours the machine operates. Indication
Generally, the plant will require some service input Supernumerary teat removal is carried out either for
from a dairy engineer every 750 operating hours. For cosmetic reasons or because the surplus teat is likely
a plant milking and washing 5 hours each day, this to interfere with cluster attachment (Fig. 12.13). As
equates to a service every 150 days (5 months). If the this is an inherited abnormality and may result in
plant is operating for 8 hours each day, the service disqualification in show goats, there is often an ethi-
interval will fall to 94 days or three monthly. Rubber cal dilemma as to whether removal should be done.
liners require changing after milking 2,500 animals.
Silicone liners require changing after approximately Preparation and equipment
5,000 milkings. Liners that go beyond their normal Antiseptic, haemostats, sharp scissors or scalpel
life expectancy will result in increased liner slip and blade.
Fig. 12.12 A purpose built commercial rotary Fig. 12.13 Supernumerary teat in a 3-month-old kid
parlour for milking goats. Regular plant maintenance (in dorsal recumbency).
is important for mastitis control, including exchanging
any rubber ware and liners.
282 Chapter 12
Restraint the so-called ‘fishtail’ teats (Fig. 12.14). These can

In the UK, there are currently no guidelines for the be removed at birth, although problems can occa-
removal of such teats in goats, but in cattle this pro- sionally develop later when the doe comes into milk,
cedure must be carried out under local anaesthesia potentially resulting in mastitis. Culling may be a
and by a veterinary surgeon if the animal is 3 months better option.
of age or older.
Teat surgery
Technical description Indication
After application of an antiseptic, the teat is Teat surgery may be necessary because of obstruc-
grasped with haemostats as close to its base as tion of the teat canal or lacerations of the teat.
possible and crushed. After moving the haemostats Occasionally, amputation of the teat is indicated
slightly closer to the teat end, and using either as a salvage procedure to manage severe puru-
sharp scissors or a scalpel blade, the teat is cut lent or gangrenous mastitis or severe teat trauma.
close to its base. Haemostasis is usually achieved Teat fistulae may be congenital or secondary to
by applying pressure with a gauze swab for several trauma.
minutes. Lacerations should be viewed as any acute wound
and attended to as soon as possible (Fig. 12.15).
Aftercare Chronic lesions and fistulae are best dealt with
Topical antibiotic spray. Clean, dry environment. during the dry period if they do not interfere with
Monitoring by owner for bleeding or infection. normal teat drainage. (Note: Mastitis risk is height-
ened in such glands.)
Supernumerary teats occasionally have associated Preparation and equipment
glandular tissue, potentially leading to mastitis once A clean environment is essential. A tourniquet (e.g.
the goat starts lactating. A supernumerary teat close rubber band), teat bandage and spray, teat cannula,
to the main teat may have a connection to the teat fine gauge polydioxanone (PDS®) on a round bodied
sinus. Where it is difficult to differentiate between and cutting needle and a small procedure instrument
the proper and the supernumerary teat, the removal kit are required. For obstructions, various instru-
is best delayed or the decision on which teat to ments may be useful, including a Hudson teat probe,
remove left to the owner. teat spiral, Barrett’s papillotome and a McLeans
There are a number of other potentially inherited knife.
teat abnormalities that have been identified, includ-
ing double or fused teats, an example of which are Restraint
Sedation to facilitate lateral recumbency, with the
uppermost hind leg tied out. For procedures involv-
ing the teat wall, anaesthesia is achieved via intra-
venous regional anaesthesia or a ring block, using
local anaesthetic without adrenaline (epinephrine).
For anaesthesia of the teat canal, 2–3 ml of local
anaesthetic is infused into the canal and distributed
by massage.
Small obstructive lesions can often be removed via
the streak canal, using teat instruments. Larger
obstructive lesions may require surgical opening of
Fig. 12.14 Bilateral congenital ‘fishtail’ teats. the teat canal.
Post-milking teat dip or spray is applied after each

such ‘m ilking’. Sutures are removed after 10–14 days
if non-absorbable material was used.
Mastitis, stenosis of teat canal, breakdown of suture
line and sinus formation are the main problems.
Mastectomy
Indication
Mastectomy is indicated to address udder changes
caused by gangrenous mastitis, non-healing wounds,
inappropriate lactation syndrome (pseudolactation)
in pet goats or neoplasia.

If possible, the procedure is delayed until the udder
is undergoing involution. A large instrument kit
with good number of haemostats, suture material for
vessel ligation and skin sutures, and a Penrose drain
are required.
Fig. 12.15 Horizontal laceration, leading to Restraint

substantial detachment of the distal teat in a cow. General anaesthesia is preferred as surgery time
Such injuries should be treated like any other wound, can be unpredictable. Alternatives include sedation
aiming to preserve as much tissue as possible. combined with high epidural anaesthesia. For

total mastectomy, the goat is placed into dorsal
For surgical procedures, a rubber band is placed recumbency. For unilateral mastectomy, lateral
at the base as a tourniquet. Teat lacerations are pre- recumbency with the affected gland uppermost and
pared like any wound with pressure lavage, debride- the upper hind leg tied out may be used.
ment and, if presentation is delayed, freshening of
the wound edges using a scalpel blade. Full-thickness Technical description
wounds (i.e. breeching the teat canal) are ideally During the incision to expose the gland, as much
repaired in three layers: the mucosal lining using healthy skin as possible is preserved to main-
simple interrupted or continuous sutures (round tain a skin flap large enough to cover the defect.
bodied needle), the connective tissue and muscle Blunt dissection is used to separate the skin from
layer using vertical mattress sutures (cutting nee- the mammary tissue. The mammary gland is then
dle), and the skin using simple interrupted sutures freed en bloc from its attachments. Haemorrhage
(cutting needle). is controlled immediately by tying off any vessels,
ideally prior to cutting through them. Some of
Aftercare the main vessels include the internal and external
Intramammary and systemic antimicrobials and pudendal and superficial epigastric ones, and their
NSAIDs. The teat is bandaged with purpose course varies from goat to goat. However, multiple
made tape and spray, and the bandage possibly other vessels will be present, especially if the gland
anchored proximally with a suture. A self-retaining is still producing milk. Great care must be taken
teat cannula is inserted for several days, and the not to incise into the glandular tissue, as resulting
plug removed 3–4 times a day to allow drainage. milk leakage will greatly obscure the surgical field
284 Chapter 12
and contaminate the site. Dead space is reduced as Depending on the season, fly repellent. The Penrose
much as possible with interrupted sutures. One or drain is removed after 48–72 hours.
several Penrose drains are placed prior to routine
skin closure. Potential complications
Marked blood loss if haemorrhage control proves
Aftercare difficult and wound breakdown are the main com-
Parenteral antibiosis for a minimum of 5 days, plications. Overall, prognosis is reasonable in goats
NSAIDs and nursing care in a clean environment. not systemically ill at the time of surgery.
CHAPTER 13
SENSORY ORGAN DISEASE

285
THE EYE The eye background shows the optic disc, the
tapetum lucidum (roughly a horizontal strip just
NORMAL STRUCTURE AND FUNCTION above the optic disc), the tapetum nigrum and
loosely arranged vessels. The tapetum lucidum and
The palpebral conjunctiva lines the inside of the eye- width of the retina supports good night vision. As in
lids and the bulbar conjunctiva overlies the sclera, other prey animals, goats have a wide field of vision
together forming the conjunctival sac. A fold of con- but limited perception of depth. They can see blue,
junctiva in the medial canthus forms the nictitating purple and green well.
membrane (syn. third eyelid). It contains an anchor- The tear apparatus consists of the lacrimal gland
shaped cartilage. and a dorsal and ventral lacrimal puncta with associ-
About 90% of corneal depth is formed by the ated small ducts. These combine and drain via the
stroma, covered by the outer epithelium consisting lacrimal sac into the nasolacrimal duct, which ends
of several cell layers and the innermost Descemet’s in the ventral corner of the nostril at the mucosal–
membrane. The anterior chamber, containing aque- skin border.
ous humour, and the posterior chamber, containing Cranial nerves of interest are shown in Table 13.1.
vitreous humour, are demarcated by the pupil, which
is formed by the iris, lens and ciliary body. The CLINICAL EXAMINATION OF THE EYE
iris is mid-brown in colour in most breeds. When
constricted, the pupil adopts a rectangular shape, The examiner’s hands should be clean and ide-
becoming more rounded when dilated (Fig. 13.1). ally gloved. Equipment for a basic eye examination
includes: pen or head torch, haemostats, cotton buds,
fluorescein and an ophthalmoscope. To reduce pain
during examination or manipulation of the eye,
topical anaesthetic is applied (e.g. lidocaine hydro-
chloride, tetracaine hydrochloride, amethocaine
hydrochloride; note: none are licensed for veteri-
nary use in the UK.) An auriculopalpebral block is
useful if blepharospasm is severe (see Chapter 18).
Dilating the pupil with 2–4 drops of atropine sul-
phate aids examination of the eye background; how-
ever, the goat must be kept out of bright light for
several hours until the effect has worn off.
The conjunctival sac should always be explored
for foreign bodies (see below).
Fig. 13.1 Normal eye of a goat, with the pupil Ocular swabs can be obtained effectively with
dilated. The iris has the typical mid-brown colour of human interdental brushes. A smear is prepared with
many breeds. The downward curvature of the upper Romanowsky stain (e.g. Diff-Quik®) for cytology.
eyelid is not unusual. Swabs for culture must be harvested prior to application
286 Chapter 13
Table 13.1 Cranial nerves involved in eye sensation, movement and reflexes, and vision.
NUMBER NAME FUNCTION

II Optic Vision
III Oculomotor Pupil constriction, eye movement (ventral and ventral oblique, dorsal, medial)
IV Trochlear Eye movement (dorsal oblique)
V Trigeminal Sensory to orbit, cornea and eyelids including medial canthus
VI Abducens Eye movement (lateral, retraction), third eyelid protrusion
VII Facial Motor supply to eyelids (auriculopalpebral branch). Facial expression
Fig. 13.2 Neovascularisation in response to a Fig. 13.3 A Schirmer tear test strip placed in the
melting corneal ulcer in a bovine. conjunctival sac of an alpaca. The test is read by
measuring the advancement of the blue discolouration
on the strip after 1 minute.
of any medication or prolonged examination, and both •• A Schirmer tear test reading of ≥18 mm (adults)
bacterial and fungal culture should be carried out. or ≥14 mm (kids less than 1 month old) after
The position of the eye in the orbit may be altered 1 minute indicates good tear production
by ocular pathology, but also by hydration status and (Fig. 13.3).
body condition (with reduced retrobulbar fat in thin •• Normal intraocular pressure (IOP, in mm Hg)
animals). is reported as 19–20 in adults and 15–16 in
Damage to the corneal epithelium can be high- young kids using Schiotz tonometry, with lower
lighted using fluorescein strips or drops placed into IOP values of 9–11 reported for a TonoPen™
the conjunctival sac. Patency of the nasolacrimal (Fig. 13.4).
duct can also be established. The stain should appear •• A white aqueous flare when examining the
at the corresponding nostril within 5–10 minutes. anterior chamber with an ophthalmoscope
Neovascularisation indicates pathology and can indicates debris. For direct ophthalmoscopy,
be used to roughly age the lesion. It tends to start the fundus will typically be in focus at a setting
3–4 days after the ocular insult, and vessels advance of –1 to –2.
about 1 mm per day (Fig. 13.2).
Ultrasonography
Further diagnostics Corneal oedema is often marked in goats with ocu-
Schirmer tear test, intraocular pressure, lar disease, preventing visual assessment of deeper
ophthalmoscopy structures. Ultrasonography allows examination of
Normal parameters for more advanced examination external and internal structures and aids detection
include: of inflammation, neoplasia, abnormal structures
Se nsory O rg a n D is e a s e 287
Fig. 13.4 Measuring intraocular pressure (IOP) with Fig. 13.5 Placing an ultrasound probe directly onto
a TonoPenTM in an alpaca. IOP values of 9–11 have been the globe is well tolerated by animals with the aid of
reported in normal goats using this instrument. topical anaesthesia.
Owners should never attempt to force a swollen or

painful eye open. Disinfectants must not be used
in or around the eye. A cold towel or wrapped ice
pack can be gently applied if the ocular region
suffered blunt trauma or bruising. Owners may
attempt to flush out a foreign body that is not
embedded in tissue and is causing only minor
irritation. The lower eyelid is gently pulled down
and lukewarm, clean water poured in a steady
stream onto the eye for up to 15 minutes, peri-
odically checking whether the foreign body has
gone. Chemical contamination of the eye needs
to receive immediate flushing (note that trauma
is more severe with alkaline fluids than acidic).
Fig. 13.6 Ultrasonogram of a normal eye, Eyelid tears, just like other wounds, have the best
highlighting some of the structures that can be chance of healing and restoring normal contour
assessed such as anterior and posterior chamber, and function if they receive veterinary attention
thickness of sclera and iris, lens position and within 6 hours. An owner should never cut off any
periocular tissues. The apparent debris in the eyelid fragments.
posterior chamber in this image is an artefact.
NON-INFECTIOUS DISEASE
and material and disruption of normal features.
After applying a topical anaesthetic and coupling Entropion
gel, a linear or curved probe (7.5–12 MHz) is placed Overview
either directly onto the globe or onto the eyelid Entropion is inward rolling of the eyelid. This may
(Figs. 13.5, 13.6). The procedure is well tolerated. be uni- or bilateral and affect the lower or upper
eyelids.
FIRST AID FOR OCULAR TRAUMA
Aetiology
To prevent further injury or self-trauma, the A genetic predisposition exists, with some breeds or
goat’s head is cross-tied with the aid of two halters. individual bucks producing affected offspring.
288 Chapter 13
Fig. 13.7 Epiphora caused by entropion affecting the Fig. 13.8 A neglected conjunctival foreign body in
lower eyelid. a bovine, leading to marked conjunctival and corneal
irritation and trauma, with loss of vision.
The condition is present at birth or develops within (using the same technique as in dogs). Several days
24 hours post partum. Entropion is acutely painful, of topical antibiotic is required in addition if corneal
leading to blepharospasm and epiphora (Fig. 13.7). ulceration has occurred.
If left untreated, corneal ulceration follows within Bucks producing affected offspring should be
24–48 hours. removed from the breeding pool.
Diagnosis Foreign bodies

Kids should be inspected for entropion within Overview
24 hours of birth. The abnormal contour is obvious Conjunctival sac foreign bodies (FBs) are a common
on visual inspection. ocular problem, leading to marked irritation and
potentially corneal ulceration. Sharp FBs may also
Differential diagnosis be found lodged in the sclera or cornea. These may
An ocular foreign body will present similarly. lead to loss of vision.
Infectious keratoconjunctivitis (IKC) (see below) is
rare in neonates. Aetiology
Grass seeds are commonly involved, either caused by
Treatment/management/control animals grazing long mature pasture or feeding hay
Measures that cause temporary eversion are usually from racks above head height. Using straw blowers
sufficient. This may be achieved by: (a) placing a pair to top up bedding can also lead to ocular FBs.
of haemostats parallel to the affected eyelid as close to
its margin as possible and pinching the eyelid skin for Clinical presentation
20–30 seconds; this procedure is repeated every few Typical signs are blepharospasm and epiphora.
hours over the next 24 hours; or (b) injecting 0.5 ml Conjunctival FBs often cause localised corneal opac-
of a non-irritant drug (penicillin, lidocaine, water for ity or ulceration (Fig. 13.8). Embedded FBs may
injection) s/c into the eyelid to form a s ubconjunctival lead to stromal abscess formation.
bleb. A single treatment is often enough, but may be
repeated at 12–24 hours if required. Diagnosis
Surgical treatment is rarely required, but is an Topical anaesthetic greatly aids examination. For
option if the entropion is severe and persistent conjunctival FBs, digital pressure is used on either
Fig. 13.9 Stromal abscess in the ventral cornea Fig. 13.10 Corneal ulceration secondary
(arrow), causing epiphora and neovascularisation. to entropion in a 2-day-old lamb. Infectious
keratoconjunctivitis (‘pink eye’) would appear similar,
but with the ulcer in the centre of the cornea.
the upper or lower eyelid to gently push the eyeball Corneal ulceration and
into its socket. The opposite eyelid is everted and the stromal abscessation
corresponding conjunctival sac visually examined. Overview
A moistened cotton bud can be passed through the The pain element with ulceration, and the risk of
conjunctival sac to dislodge any FB. A cotton bud or loss of vision with both conditions, means prompt
pair of fine haemostats is used to lift the third eyelid and assertive intervention is required.
to allow examination behind it.
An ophthalmoscope or magnifying lens may be Aetiology
required to detect small embedded FBs. Ulcers may result from physical trauma or infec-
tious processes. A stromal abscess is caused either by
Differential diagnosis infection becoming trapped underneath the epithe-
In cases with IKC, the ulcer is almost always placed lium when an ulcer heals, or by pathogen or foreign
centrally, whereas the corneal changes caused by FB body deposition into the stroma secondary to a cor-
are often more peripheral. neal puncture.

The FB is removed either manually or flushed out Blepharospasm, photophobia, epiphora and localised
(using clean water). If the cornea is damaged, a course of or generalised corneal oedema are typically present
topical or systemic antibiosis and a NSAID is indicated. with ulceration, but often less marked with stromal
FBs embedded in the sclera or cornea should be abscessation. The latter present as single or multiple
treated as ocular emergencies and receive prompt yellowish deposits in the cornea (Fig. 13.9). Corneal
attention. Heavy sedation or general anaesthesia (GA) neovascularisation is common in both conditions
is advisable to allow removal without the risk of further (Fig. 13.9).
trauma if the patient moves during the procedure. If
the FB has created a large defect, this is sutured. Diagnosis
Prevention involves placing hay racks at a suitable The surface of the eye is viewed from different
height. Goats should be moved out of the housing angles, including the sky-line view, to detect any
prior to using a straw blower. defects (Figs. 13.2, 13.10). Fluorescein staining
290 Chapter 13
Fig. 13.11 Fluorescein staining highlighting a Fig. 13.12 Third eyelid flap and subpalpebral lavage
corneal defect near the lateral canthus. system to address a full-thickness corneal ulcer in
an alpaca cria. The white substance near the lateral
canthus is ointment.
highlights any epithelial damage (Fig. 13.11). Stain to provide corneal protection (Fig. 13.12). Advanced
underrunning the epithelium indicates poor healing, techniques include conjunctival grafts or flaps and
with newly formed epithelium not becoming tightly keratectomy. Healing typically takes 2–6 weeks.
attached to the underlying stroma. In non-healing ulcers (as indicated by stain under-
Bacterial and fungal cultures should be performed running the epithelium), under topical anaesthesia a
for progressive or non-healing ulcers. Culture or dry sterile cotton bud is used in a rubbing motion
cytology of a corneal swab is not useful for a stromal to remove any loose epithelium. This is followed by
abscess, as the pathology affects deeper structures. antibiosis and a corneal protection technique plus,
potentially, a grid keratotomy.
Differential diagnosis For a stromal abscess, because the epithelium tends
Acute physical trauma to the cornea may present to be intact, antimicrobials need to be administered
similarly. Hypopyon involves the ventral anterior parentally. A superficial abscess may benefit from
chamber, rather than the stroma. debridement, using a dry sterile cotton bud rubbed
vigorously over the area under topical anaesthesia.
Treatment/management/control A 4–6-week healing period should be expected, and
Treatment of ulcers up to 50% corneal depth con- healing is indicated by the abscess changing from a
sists of topical or subconjunctival antimicrobials. yellowish to a white colour and corneal vessels disap-
Collagenase inhibitors, such as autogenous serum, pearing. If severe uveitis develops, surgical interven-
0.2% calcium-EDTA or tetracycline, are a useful tion such as a keratectomy is indicated.
adjunct (apply a few drops 4–8 times per day). Topical
or subconjunctival NSAIDs should be considered Neoplasia
to provide analgesia. To prevent iris adhesions, 1% Overview
atropine sulphate drops may be applied twice a day There are few reports of ocular neoplasia in goats
(see Note, p. 293). An uncomplicated ulcer will heal and the likely incidence is unknown.
within 5–7 days.
If the ulcer is more than 50% in depth or progres- Aetiology
sive, surgical procedures such as a tarsorrhaphy (see Reported types include squamous cell carcinoma
p. 293) or a third eyelid flap are carried out additionally (SCC) and lymphoma. Usually mature animals
are affected. The role of viral agents (e.g. papilloma- Treatment/management/control

virus) and genetics in the aetiology of SCC remains Surgical excision may be possible for relatively dis-
unclear. creet lesions affecting the conjunctiva, cornea or
third eyelid. A margin of 2 mm into healthy tissue
Clinical presentation should be aimed for. Excising lesions on the upper or
Common sites for SCC are the eyelids and the junc- lower eyelid should only be undertaken if the eyelid
tion between the sclera and the cornea. From early contour and function can be maintained. Excision
white nodules, the tumour progresses to prolifera- can be performed under sedation and local anaes-
tive nodular lesions, often pink in colour. thetic blocks (see Chapter 18), but GA is preferable.
Lymphoma may affect any lymphatic tissue in Enucleation is the best option for extensive lesions
and around the orbit (Fig. 13.13). Keratitis is often or those affecting the eyelids or orbital tissues.
marked and a degree of facial asymmetry may be Adjunct treatments such as cryosurgery, radiother-
present. apy or chemotherapy are useful in valuable pedigree
Both SCC and lymphoma can affect intraorbital or pet goats.
tissues, leading to exophthalmos or changes to the The recurrence rate is unknown in the goat.
normal eye axis (Fig. 13.14). In cattle, recurrence of SCC befalls one in three
Regional lymph nodes should always be assessed patients after surgical excision.
for metastasis. If present, rejection at the abattoir is
likely and prognosis is poor. INFECTIOUS DISEASE
Diagnosis Infectious keratoconjunctivitis

Biopsy is the most reliable method. Neoplastic cells (syn. pink eye)
can sometimes be detected on impression smears. Definition/overview
IKC is a contagious disease affecting goats (and
Differential diagnosis sheep) and is common in many countries. Disease
For early SCC eyelid lesions, scar formation after can vary from mild to severe, one or both eyes can be
trauma. Other causes of severe keratitis need to be infected and morbidity, particularly in housed goats,
ruled out for lymphoma. can be very high.
Fig. 13.13 Ocular lymphoma affecting the cornea Fig. 13.14 Exophthalmos caused by ocular lymphoma
and conjunctiva. on the left-hand side in a 9-year-old Toggenburg.
292 Chapter 13
result in rupture of the eye. Even following healing

and remission, the cornea may remain ‘cloudy’ for
many weeks. Outbreaks can occur and care should be
taken to observe both eyes when examining groups of
affected goats as the vision impaired eye will invari-
ably be facing away from the observer.
Diagnosis
Diagnosis is based mainly on clinical signs and
several animals being affected. Swabs taken from
affected eyes can be submitted for denaturing gradi-
ent gel electrophoresis testing to confirm infection
with M. conjunctivae.
Includes entropion in young kids, an ocular for-
eign body or keratoconjunctivitis associated with
listeriosis. Cobalt deficiency can lead to excessive
lacrimation.
Fig. 13.15 Blepharospasm affecting the right eye. There are a number of treatment regimes that have
This typically indicates ocular pathology and the goat been tried, including:
should be examined promptly.
•• Use of dedicated antibiotic-containing
Aetiology ophthalmic ointments administered q4h to q48h
Mycoplasma conjunctivae is most commonly associated (depending on the product).
with disease in goats and sheep in those countries •• Subconjunctival antibiotic injection. The head
in which laboratory testing has been undertaken. of the animal is rotated to expose as much sclera
A number of other organisms capable of causing as possible. Using an episcleral vessel as the
clinical disease in isolation or in combination with reference point, topical anaesthetic is applied
other agents have been incriminated. These include with a cotton bud to the scleral conjunctiva.
Chlamydophila pecorum, Moraxella spp., Listeria mono- A 23–25 gauge needle is inserted under the
cytogenes and other Mycoplasma spp. such as M. agalac- conjunctiva and advanced for a few millimetres
tiae (contagious agalactia) and M. arginini. parallel to the eye ball (see Chapter 1, p. 18).
•• Parenteral antibiosis (at full BW dose) has also
Pathophysiology been shown to be effective, including long-
Infection is spread from one goat to another via a acting tetracyclines, macrolides or fluorfenicol.
number of routes including flies and direct contact,
particularly when housed and fed in close contact Severely affected goats should be isolated and
with each other or with infected sheep. kept in subdued lighting because of the marked pho-
tophobia that occurs. If there is marked ulceration,
Clinical presentation the cornea can be protected by the use of a tarsor-
Clinical signs include conjunctivitis with marked rhaphy, third eyelid flap or a conjunctival pedical
hyperaemia, excessive lacrimation and blepharospasm flap. For extensive damage, or where full-thickness
(Fig. 13.15). This is followed by corneal opacity and ulceration has resulted in prolapse of the Descemet’s
vascularisation and corneal ulceration, which may membrane, enucleation should be considered.
Uveitis and iritis

Overview
Inflammation of the iris and its surrounding tissues
is occasionally seen in goats.
Aetiology
Listeria monocytogenes uveitis is linked to silage feed-
ing, in particular big bale silage where fermentation
is often suboptimal, leading to an insufficient drop
in pH and survival of this pathogen. Trauma to the
cornea appears to be a prerequisite, and the condition
is limited to times of silage feeding. Mycoplasma spp.,
Chlamydophila psittaci and Toxoplasma gondii may also
cause uveitis, presenting either with just ocular signs or
also with signs of systemic disease (including abortion).
Blepharospasm, epiphora, photophobia and conjunc-
tivitis are seen. Closer examination of the eye shows Fig. 13.16 Synechia (adhesion of iris) secondary to
opacity of the anterior chamber in addition to cor- uveitis in a lamb.
neal oedema and typical folds in the iris.
OCULAR SURGERY
Diagnosis
The swelling and undulation of the iris are typical. Tarsorrhaphy
History of feeding silage supports the diagnosis. Tarsorrhaphy is a useful first-line option to support
corneal healing. The eyelids are sutured together
Differential diagnosis with a single horizontal mattress suture using
IKC is the main differential, but typically leads to 4–6 metric suture material on a cutting needle.
corneal ulceration without uveitis. Ideally, the suture is tied with a single knot and
shoelace bow, rather than a series of knots. This
Treatment/management/control allows periodic release of the suture to monitor
Oxytetracycline or penicillin are administered, progress and apply topical medication.
together with dexamethasone (or a NSAID in
pregnant females). These are ideally given as a Third eyelid flap
subconjunctival injection, otherwise topically or A third eyelid flap is also employed to aid corneal
systemically. Atropine sulphate 1% applied twice healing and is beneficial because of the close contact
daily is thought to reduce the risk of iris adhesions that is established between cornea and conjunctiva.
forming (Fig. 13.16) and to provide some analgesia 3–3.5 metric suture material on a cutting needle is
by reducing ciliary spasms. (Note: Not licensed in placed through the upper eyelid close to the lateral
food producing animals and may possibly negatively canthus (in direction skin to conjunctiva), then, with
affect gastrointestinal tract motility.) Healing typi- a good-sized bite, through the external conjunctiva
cally takes 2 weeks. overlying the third eyelid, and fed out through the
Prevention relies on avoiding any feed presen- upper eyelid again (direction conjunctiva to skin).
tation that leads to the goats burying their head The free ends are passed through a stent (e.g. a but-
into silage. Additionally, good silage production to ton or short piece of tubing) and tied off. A shoelace
achieve a low pH, little soil contamination and few bow is useful to allow periodic release to monitor
aerobic pockets. progress and apply medication (Fig. 13.12).
294 Chapter 13
Fig. 13.17 After incising the skin close to the eyelid Fig. 13.18 Wound closed, leaving an opening near
margin, blunt and sharp dissection are used to free the medial canthus for drainage. In this case, the orbit
the eyeball. was packed with a gauze swab.
Conjunctival pedicle flap Technical description

A conjunctival pedicle flap is performed under GA. The transconjunctival approach may be used in goats
A club-shaped piece of bulbar conjunctiva is freed under GA. More tissue is retained, resulting in a better
(leaving the ‘stalk’ attached) and secured over cosmetic appearance and the procedure is as in dogs
the corneal ulcer with multiple single interrupted or cats. The transpalpebral approach is preferable if
sutures, using absorbable fine gauge suture material. the procedure is performed under local anaesthesia,
Ophthalmic instruments and magnifying lenses are especially if any vision is left in the eye or where neo-
required to perform this procedure. plasia makes more substantial tissue removal desir-
able. For this, the eyelids are sutured together with
Enucleation 1–2 horizontal mattress sutures. Using a scalpel blade,
Indication the eyelid skin is incised all the way around, as close
Any condition where vision is unlikely to be retained to the eyelid margin as possible without leaving any
or restored or pain remains uncontrolled, includ- cilia behind. The skin is undermined to the level of
ing physical trauma (e.g. fighting injury) and non- the bony orbit. Using a combination of blunt and
healing corneal ulceration. Also ocular neoplasia, sharp dissection, the eyeball is freed from attaching
either as stand-alone treatment or to debulk prior to muscles and connective tissue (Fig. 13.17). Care must
chemotherapy or radiotherapy. be taken not to apply excessive traction on the eye-
ball, as this may traumatise the optic chiasm, leading
Preparation and equipment to blindness in the opposite eye. Equally, excessive
Preoperative antibiosis (e.g. potentiated penicil- inward pressure must be avoided, as this may lead
lin) and a NSAID. The ocular area is clipped to bradycardia. Once connections have been broken
and scrubbed. A standard surgical kit is required. down to the depth of the orbit, a haemostat is applied
A pair of haemostats with right-angle jaws is useful to the optic nerve and its adjacent blood vessels. The
for clamping the optic vessels in the depth of the eyeball is removed and the stump ligated. An alterna-
orbit. tive for haemostasis is to remove the eyeball and pack
the cavity with a large single gauze swab or a gauze
Restraint bandage. Otherwise, packing is not usually required
Lateral recumbency under light sedation combined in the goat. The wound edges are closed in a routine
with a retrobulbar block or a Petersen plus auriculo- manner, leaving a 5–7 mm opening near the medial
palpebral block (see Chapter 18), or under GA. canthus for drainage (Fig. 13.18).
Aftercare •• Listeriosis.
Antibiosis and analgesia are continued for several •• Space-occupying lesion such as a brain abscess.
days and, if necessary, fly repellent applied. If pack- •• Brainstem lesions caused by caseous
ing was used, this is removed, ideally gradually over lymphadenitis.
several days from 24 hours postoperatively, or all at •• Neurological disorders of the eye (see Chapter 8).
once after 72 hours. Skin sutures are removed after •• Toxicities (e.g. lead).
10–14 days.
If vision was lost suddenly, the goat should be
handled and guided gently until it becomes accus- THE EAR
tomed to unilateral vision.
CLINICAL EXAMINATION OF THE EAR
Excessive haemorrhage, infection of the orbit and The ear lobe is examined for any lacerations or other
surrounding tissues, fly strike, wound breakdown trauma and swellings (e.g. insect sting or haematoma).
and, in the case of neoplasia, recurrence. Blindness The skin of the external ear lobe is inspected for any
in the remaining eye if excessive traction was applied lesions (such as mange, sunburn, necrosis, infection
to the eyeball during surgery. or abscess, lacerations). Of interest on the internal ear
lobe are signs of inflammation, crusting or deposits of
SYSTEMIC DISEASES debris (e.g. wax). Notice is taken of any unusual smell
AFFECTING THE EYE or discharge emanating from the ear canal. A small
animal otoscope is used to examine the ear canal, with
Ocular lesions may be caused by systemic disease. the head of the goat well restrained.
This should be considered in particular where lesions Also of interest is the position of the ears and
are bilateral and the animal shows, or has a history their muscular tone. If abnormal, this may indicate
of, other abnormalities such as pyrexia. There may a neurological defect, such as facial paralysis, or sys-
also be a mix of clinical signs in a group of goats. temic disease such as tetanus.
Examples include:
NON-INFECTIOUS DISEASE
•• Hypopyon secondary to septicaemia, in
particular in neonates. Ear lacerations
•• Conjunctivitis in conjunction with respiratory Common causes include trauma from the goat’s
tract infection. environment (e.g. barbed wire fencing, protruding
•• Diseases affecting the ability to blink often nails) and ear tags becoming caught and torn out
lead to a dry eye keratitis (e.g. tetanus, or facial (Fig. 13.19). Typically, these are allowed to heal by
paralysis caused by trauma or listeriosis). secondary intention, after cleaning the wound and
•• Injected conjunctivae are often seen with administering a course of antimicrobials (e.g. poten-
endotoxaemia. tiated penicillin) and a NSAID. In show animals,
•• Hyphaema secondary to bleeding disorders. surgical repair to achieve optimum cosmetic results
•• Uveitis caused by Mycoplasma spp., Chlamydophila is an option. This is best carried out under GA. After
psittaci, Toxoplasma gondii. thorough cleaning, the wound edges are freshened up
and sutured together using a simple interrupted pat-
Some systemic causes of true or apparent blind- tern. The ear is bandaged to the head for 7–10 days.
ness include: These lacerations pose a considerable welfare con-
cern, and every care should be taken to reduce their
•• Pregnancy toxaemia. occurrence; for example, by choosing well-fitting ear
•• Cerebrocortical necrosis or tags and appropriate types of fencing and removing
polioencephalomalacia. any injury risks from the environment.
296 Chapter 13
Fig. 13.19 Laceration caused by an ear tag catching Fig. 13.20 Inflammation and infection around an
in the environment and tearing out. ear tag.
Tagging injuries
Incorrectly placed ear tags may lead to haemor-
rhage, infection (Fig. 13.20) with potentially sec-
ondary fly strike, and chronic inflammation with
tissue hyperplasia or distortion (‘cauliflower ear’).
These problems are entirely avoidable by adopt-
ing a good ear tagging technique. Treatment is
as for any other acute or chronic injury: pressure
or ligation to control haemorrhage, and cleaning,
lavage, tissue debridement and antibiosis to deal
with infection, combined with a NSAID to address
inflammation.
Ear tagging technique

Ears should be visibly clean and dry. Housing
the goats for 12–24 hours beforehand facilitates
this. Tags are placed into the ventral half of the Fig. 13.21 Reasonable tag placement in the goat
ear, not more than one-third of the way from lying down. The tag in the standing goat has been
the base of the ear, and through the ear cartilage placed too far away from the ear base, leading to
(Fig. 13.21). Blood vessels are easily visible and drooping of the ear.
must be avoided. The correct applicator for each
particular type of tag must be used. Good head Equally, growth should be allowed for in goatlings.
restraint is essential, and periods of fly activity Animals are checked 1 week after application for
should be avoided. inflammation or infection, which is dealt with as
The male part is always inserted from the back necessary.
of the ear, and application of an antiseptic or sterile
lubricant (e.g. K-Y® Jelly) onto the male part reduces Aural haematoma
trauma and infection risk. When placing loop tags Overview
in kids, the thickness of a pencil is left between the Aural haematoma is typically seen in individual
edge of the ear and the tag loop, to allow for growth. goats.
Aetiology commencing disinfection, and after the procedure

In most cases caused by irritation of the ear by mange the ear is tightly bandaged to the head to prevent
mites (see Otitis, below), grass seeds or other foreign movement:
bodies, leading to repeated and forceful headshaking
or rubbing. Occasionally caused by direct trauma, 1 Fluid aspiration. A scrupulously aseptic
including bite wounds. technique is essential. Under mild sedation, the
goat’s head is restrained well and anaesthetic
Clinical presentation gel applied to the point of needle entry (internal
Noticeable swelling of the ear lobe, which is soft and surface of lobe). A 16 g hypodermic, or 18–20 g
fluctuant on palpation. butterfly, needle is inserted, the fluid drained
and the cavity flushed with sterile saline. In non-
Diagnosis pregnant goats, this may be followed by injecting
Palpation findings are usually sufficient. Ultra dexamethasone into the cavity (0.2–0.4 mg
sonography may be used to confirm a haematoma diluted to about 1 ml total volume, q24h for up
(accumulation of echolucent fluid), as well as a fine to 5 days).
needle aspirate (observing strict asepsis; Fig. 13.22). 2 Surgical drainage under GA. The serum and any
blood clots are removed through either a single
Differential diagnosis incision or multiple smaller incisions. Several
Severe inflammation causing oedema, or ear abscess; mattress sutures (possibly with suture buttons) are
the swelling will feel firm and a pain response is placed through the ear lobe, parallel to the lobe
likely. Ultrasonography shows echodense tissue edge and any vessels, to reduce any dead space.
swelling or purulent material. 3 Cannula drainage. The owner needs to be able
to provide good nursing care and a very clean
Treatment/management/control environment for this technique. After drainage
Small haematomas that do not induce further head- and lavage as above, a bovine disposable
shaking typically do not require any treatment. teat cannula is placed through the incision.
Marked haematomas should be treated to avoid The plug-end is positioned to lie distally once
ear lobe distortion caused by fibrosis, and this can the goat is standing. The plug is removed
be addressed in three ways. For all three ways, 2–3 times each day to allow drainage. Because
a sterile swab is placed into the ear canal prior to of the risk of ascending infection, a course of
antibiosis is advisable.
The underlying cause (e.g. ear mites) must be

addressed to avoid recurrence.
INFECTIOUS DISEASE
Otitis
Overview
Otitis is possibly less often recognised than in com-
panion animals because the prevailing husbandry of
goats limits owner’s observations.
Aetiology
In the UK, Psoroptes ovis is the main pathogen involved
in otitis externa. In other countries, Raillietia caprae
Fig. 13.22 Fine needle aspiration of an ear swelling. is commonly found in the ear canal of goats, and
298 Chapter 13
Psoroptes cuniculi has been reported. All age groups manifest as lesions affecting the ears. These include
may be affected. Malassezia spp. are normal com- dermatophilosis, psoroptic mange, sarcoptic mange
mensals, but occasionally cause otitis externa. and ringworm (see Chapter 11).
Corynebacterium pseudotuberculosis and Mycoplasma For otitis media/interna: fascial paralysis and brain-
spp. have been isolated from goats with otitis media. stem lesions, and other causes of vestibular syndrome.

Otitis externa: a large proportion of goats in a group For mites, ivermectin is effective (0.2 mg/kg s/c
may have subclinical infection. The presence of wax, every 7–10 days for 2–3 treatments). Using an acidi-
purulent material, crusts and malodour indicates fying ear flush (e.g. MalAcetic) may be sufficient
clinical disease. Headshaking, rubbing against fenc- for Malassezia. Otherwise, topical antifungal drugs
ing and scratching the ear with the hind leg are com- (e.g. miconazole or clotrimazole), combined with
monly seen. antibiotics and steroids, are indicated, but are not
Otitis media or interna: a head tilt towards the licensed in goats in the UK.
affected side and other neurological signs are com- Aggressive systemic antibiosis can be tried for
mon, in particular vestibular syndrome or, if infec- acute otitis media. In non-responsive or chronic
tion has spread, signs associated with brainstem cases, the treatment options described for dogs
lesions or meningoencephalitis. may be considered (myringotomy, bulla osteotomy
or total ear canal ablation). If C. pseudotuberculosis
Diagnosis is involved, deeper CNS structures are often also
Microscopic identification of mites, either from infected, therefore prognosis is poor.
direct ear swabs or ear flushings. Identification
of vast numbers of yeasts on tape strips suggests Ear tip necrosis
Malassezia spp. Conditions causing severe vasoconstriction or dam-
Advanced diagnostic imaging is required to con- age to the capillary epithelium may lead to necro-
firm otitis media or interna. sis of the ear tips. Examples include salmonellosis,
ergot poisoning, snake venom and frost bite. Once
Differential diagnosis the damage has occurred, it cannot be reversed.
For otitis externa: secondary infection after ear However, any secondary bacterial infection should
trauma. A number of infectious skin diseases can be addressed.
CHAPTER 14
METABOLIC DISORDERS
299
Hypocalcaemia (syns. milk fever, the pulse is weak and fast. Mental depression follows,
eclampsia, parturient paresis) with death within 6–12 hours if not treated.
Definition/overview Secondary hypocalcaemia may also be a feature
Unlike dairy cows, in which clinical hypocalcae- of some toxaemic conditions such as toxic mastitis or
mia is a relatively common occurrence, true clini- enterotoxaemia.
cal disease is more unusual in periparturient goats,
although subclinical manifestation may be more Diagnosis
common and can be easily overlooked. Diagnosis is based on the clinical signs, stage of
pregnancy, response to treatment and the demon-
Aetiology stration of hypocalcaemia (normal reference range
Hypocalcaemia is associated with a decrease in blood 2.3–2.9 mmol/l) in ante- or post-mortem blood.
calcium levels in the periparturient period (includ- Calcium levels in cerebrospinal fluid (CSF) or vitre-
ing late pregnancy). ous humour can be used in does found dead. Vitreous
humour levels reflect plasma iodised calcium, which
Pathophysiology is about two-thirds of total plasma calcium, and a
Blood calcium levels are kept under tight homeo- level <1 mmol/l is suggestive of disease.
static control via parathyroid hormone, 1,25-
dihydrocholecalciferol and calcitonin. As kidding
becomes imminent, and lactogenesis commences, Includes pregnancy toxaemia, toxic mastitis, entero-
there is a sudden demand for both calcium and phos- toxaemia, uterine rupture and internal haemorrhage
phorus. Fetal growth in late pregnancy also increases associated with dystocia, metritis and rumen acidosis.
calcium demands. This is normally offset by an
increased absorption of calcium from the intestinal
tract or mobilisation from skeletal reserves. If there
is any delay in maintaining this homeostasis, hypo-
calcaemia will develop, with clinical signs being
dependent on the degree of hypocalcaemia present.
Clinical signs are confined to the periparturient
period and initially include a decrease in appetite,
lethargy, unsteady gait, muscle tremors (especially of
the shoulder muscles), mild bloat and constipation.
Uterine inertia may be a feature during parturition.
As clinical signs progress, affected goats may become Fig. 14.1 Recumbency and unresponsiveness is
recumbent and unable to rise within a few hours seen with hypocalcaemia, but also with pregnancy
(Fig. 14.1). Respiration is often shallow and fast, and toxaemia (if the doe is in late pregnancy).
300 Chapter 14
Atypical hypocalcaemia (i.e. outside the periparturient and their normal browsing behaviour is impeded.
period) may be associated with renal disease. Reduced feed intake during harsh weather or man-
agement procedures can also trigger disease.
The condition will usually respond quickly to ther- Aetiology
apy by slow i/v injection of 50–80 ml 20% calcium Clinical disease is associated with a decrease in blood
borogluconate. Injection must be stopped if cardiac magnesium levels. It is associated with improved
dysrhythmia develops. An additional 100 ml of 20% pastures, typically in spring, but also in mild, wet
calcium borogluconate with magnesium mixture is autumns. It may also be seen in goats grazing winter
given s/c. cereals. High dietary levels of potassium and pro-
The condition is often clinically indistinguish- tein, or low levels of calcium, may predispose to the
able from pregnancy toxaemia, and appropriate condition.
treatment for this should also be given, if presented
with a pregnant doe. Pathophysiology
Supplementary milk should be given to any kids Magnesium is essential for normal neuromuscular
until the doe has recovered. function. There is no physiologically relevant storage
Hypocalcaemia is usually sporadic and unpredict- of magnesium in adult animals, so daily access to mag-
able and as such is still poorly understood. If cases nesium is required. Young animals can store and mobil-
escalate, initial investigation involves identifying any ise magnesium to a degree and are less susceptible.
recent underlying stress factors or dietary changes
that may be relevant, and noting the diet fed dur- Clinical presentation
ing the dry period. Dietary calcium levels should be In its classical acute form, the disease will present
kept low (suggested target of 6.6 g/head/day) in the as hyperexcitability, muscle tremors, incoordination,
dry period to stimulate bone mobilisation, combined twitching of facial muscles and rapid ear movement,
with adequate magnesium and phosphorus levels. progressing to recumbency, convulsions and death
To facilitate this, forages with low potassium levels within 1–4 hours if not treated.
should be considered, such as straw and whole crop
or maize silage. Grass (fresh or as hay or silage) from Diagnosis
mature older pastures with little manure or potash Diagnosis is based on clinical signs, grazing history
fertiliser application may also be suitable. During and demonstration of low serum magnesium levels in
lactation, calcium requirements are in the region of acute cases (normal reference range 0.8–1.3 mmol/l).
21 g/head/day for dairy goats. By extrapolation from In a goat found dead, magnesium levels stay stable for
the dietary management of hypocalcaemia in dairy 24 hours in aqueous humour, with levels <0.33 mmol/l
cows, aiming for a negative cation–anion balance suggestive of disease in sheep. Levels in vitreous
[= (Na + K) - (Cl + S)] by acidifying the dry period humour stay stable for 48 hours, and <0.65 mmol/l
diet may be worth considering. Strategic sampling of is suggestive of disease. Care must be taken not to
the herd for calcium levels gives an indication of the aspirate the iris during humour harvest.
risk and presence of subclinical disease.
Hypomagnesaemia (syns. grass Includes lead poisoning and nervous acetonaemia.
tetany, grass staggers) Also hypocalcaemia, but this progresses less rapidly
Definition/overview and hyperaesthesia is rare.
Hypomagnesaemia is another relatively rare con-
dition in goats compared with cattle due predomi- Treatment/management/control
nantly to the differences in feeding behaviour Fifty ml of a 20% calcium borogluconate and mag-
(browsing versus grazing). The condition can occur nesium solution is given slowly i/v, plus 100 ml of
when goats are confined to an area of lush grazing 25% magnesium sulphate s/c. In advanced cases,
M e ta bol ic D isor de r s 301
i/v magnesium may be required to prevent death. by body fat laid down in the abdominal cavity – a
However, this may cause cardiac dysrhythmia and specific trait in goats. A ration of suitable energy
medullary depression leading to respiratory failure, density is therefore required. The acute lack of food
therefore it is a last measure and the client must be intake can be caused by cold inclement weather,
warned accordingly. The animal should be in a quiet, inadequate trough space, increased demand due to
dark environment with minimal stimuli. Sedation lack of shelter, gathering for management proce-
with xylazine HCl (0.01 mg/kg), butorphanol or bar- dures without provision of feed, sudden change of
biturates may be beneficial. feed and stress.
In general terms, if goats are allowed to follow
their normal browsing behaviour when outdoors, Pathophysiology
or are confined on a ration of conserved forage, the In late gestation, the liver increases gluconeogenesis
condition is unlikely to occur. There are limited to facilitate glucose availability to the fetuses. Where
data available on dietary magnesium requirements of the ration does not provide enough energy, mobilisa-
goats. Supplementation options include: magnesium tion of fat stores is increased. If this is excessive, the
oxide (7 g daily or 14 g every other day by mouth); a Kreb’s cycle becomes overwhelmed and ketone bod-
magnesium bolus (lasts about 1 month); foliar spray- ies are formed.
ing, adding to drinking water, or enriched fertiliser. This increased fat mobilisation can progressively
The provision of a simple salt lick may be useful in overwhelm the liver’s capacity and result in hepatic
reducing serum potassium levels, thus stabilising lipidosis (see Fig. 14.3) with subsequent impair-
magnesium absorption from the gut. For outdoor ment of function. The brain is affected by the hypo-
animals, turn-out or stress in inclement weather glycaemia and hyperketonaemia, resulting in an
should be avoided, and shelter and supplemen- encephalopathy.
tary feed considered during harsh weather periods.
Strategic sampling of the herd for magnesium levels Clinical presentation
gives an indication of risk. Clinical signs typically appear from 48 hours after
the triggering factor. Inappetence, initially refusing
Pregnancy toxaemia concentrate, rapidly leads to anorexia. The affected
Definition/overview goat is lethargic and spends increasing amounts of
Goats are potentially susceptible to the generic con- time lying down. Often finding it difficult to rise in
dition referred to as ketosis, either in the last 6 weeks late pregnancy, some does will adopt a dog-sitting
of pregnancy, in which it is referred to as ‘pregnancy posture (Fig. 14.2). There is marked weight loss.
toxaemia’, or during early lactation when it is referred
to as ‘lactational ketosis’ (see later). The condition
is most commonly seen in goats carrying multiple
fetuses in the last trimester. It tends to be a problem
only in goats being managed intensively or overfed
as pets, and is rarely encountered in extensive man-
agement systems with does carrying a single fetus.
Aetiology
Typically the result of longer-term undernourish-
ment, combined with an acute lack of energy. The
pregnant doe roughly requires an additional 80%
of her own glucose requirements for every fetus
she carries. In late pregnancy, appetite is reduced
because of uterine enlargement and reduced Fig. 14.2 Dog-sitting posture that goats in late
rumen capacity. In overfat does, this is exacerbated pregnancy complicated by pregnancy toxaemia may adopt.
302 Chapter 14
In the advanced stages, nervous signs may develop More severe cases that refuse to feed or have
including apparent blindness, twitching of muz- become recumbent benefit from i/v glucose
zle and lips, head pressing, coma and death within (100 ml of 40% glucose or 50% dextrose), plus B
2–3 days if untreated. Deterioration may be more vitamins, oral propylene glycol and good quality
rapid if fetal death and putrefaction develops. feed. Administration of oral electrolyte solutions
Affected goats may have an increased susceptibility (alkaline and containing bicarbonate or bicarbon-
to prolapses and dystocia, a higher kid mortality and ate precursors) has been found beneficial in ewes.
a subsequent poorer lactation. In valuable goats, i/v fluids should be considered.
Hypocalcaemia is often clinically indistinguish-
Diagnosis able and may be present concurrently, therefore
The condition should be suspected in late- calcium borogluconate should be given. Insulin has
pregnancy does carrying multiple fetuses showing been used (20–40 units of zinc protamine insulin
the clinical signs described. Elevated blood ketone i/m twice 48 hours apart). Bovine somatotropin
levels, particularly beta-hydroxybutyrate (BHB; has been used successfully, but is not commercially
normal reference range <1.2 mmol/l), and ketonu- available in the UK. Anabolic steroids are banned
ria support the diagnosis. Plasma glucose levels are in the UK.
low in early disease, but become more variable in Induction of parturition, with or without sub-
advanced cases. Evidence of renal failure and meta- sequent caesarean section, should be considered to
bolic acidosis may be seen in advanced or terminal stop the glucose drain by the fetuses, but must be
stages. At post-mortem examination, the liver is done early in the course of the disease to have any
enlarged with a rounded margin and a yellow– value. If the fetuses are still alive, dexamethasone
orange discolouration, and the adrenal glands may is the drug of choice: it stimulates lung surfactant
be enlarged. Due to fat infiltration, small portions and gluconeogenesis. Otherwise, prostaglandin-F 2
of liver may float in water. A BHB level >2.5 mmol/l alpha is given. Kids more than 1 week preterm have
in aqueous humour or >0.5 mmol/l in CSF supports a low chance of survival, but the dam’s life may be
the diagnosis. saved.
Prognosis is guarded. Inability to stand, contin-
Differential diagnosis ued disinterest in food and rising blood urea levels
Includes hypocalcaemia, enterotoxaemia and septi- indicate poor prognosis.
caemia or toxaemia secondary to fetal death. If ner- Prevention is based on the following:
vous signs have developed, listeriosis, cerebrocortical
necrosis and louping ill. •• Develop a planned breeding programme,
such that individual kidding dates are
Treatment/management/control known and dry goat feeding can be planned
Intervention must be early and aggressive. In the accordingly.
early stages (inappetence only), propylene glycol •• Use regular body condition scoring (see
and other glucose precursor products, given orally Chapter 1). (Note: Weight loss in overfat
and dosing at the manufacturer’s recommended animals must never be attempted in the last
dose, can be beneficial. Some commercial prod- trimester of pregnancy.)
ucts also contain B vitamin complex constitu- •• Scan for number of fetuses and feed accordingly.
ents such as choline, which supports the liver to Manage doelings and adult goats separately and
metabolise and clear mobilised fat. It is i mportant allow for continued growths in doelings when
to entice the goat to eat by offering good qual- calculating rations.
ity hay, green forages, herbal and non-toxic leaves, •• During the early dry period, feed a
palatable concentrates (e.g. sugar beet pulp, ration of low energy density ad libitum to
maize flakes) and potentially sprinkling molasses maintain maximum rumen capacity without
onto feeds. overfeeding.
M e ta bol ic D isor de r s 303
•• Increase energy density of the ration in the particularly at risk. This scenario is referred to as
last 6–8 weeks of pregnancy to allow for fetal primary ketosis. Secondary ketosis occurs when
demands and reduced dry matter intake. some underlying condition, such as lameness or
•• Provide adequate trough space and always mastitis, suppresses appetite, resulting in a NEB and
have feed available and easily accessible. For triggering fat mobilisation.
outdoor goats, provide shelter to decrease energy
demands for thermoregulation. Clinical presentation
•• Periodically monitor energy status in the Inappetence, leading to complete anorexia as the
dry doe group with a metabolic profile condition develops. Affected goats may be ataxic,
(BHB, non-esterified fatty acids, triglyceride, develop gastrointestinal atony and constipation,
glucose levels). and the milk yield will be reduced. The nervous
form presents with neurological signs such as
Lactational ketosis (syn. acetonaemia) blindness, head pressing, sham-chewing and con-
and fatty liver complex vulsions. Concurrent hypocalcaemia or hypomag-
Definition/overview nesaemia may also be a feature.
Lactational ketosis can be a problem in does bred
for high milk production, developing in the first few Diagnosis
weeks post kidding. In severe cases, fatty liver infil- Diagnosis is based on the clinical signs and stage
tration (Fig. 14.3) can be substantial, resulting in of lactation. Ketones may be detected on the goat’s
profound liver damage. breath. Blood samples will demonstrate high levels
of ketones and BHB, and low glucose with evidence
Aetiology/ pathophysiology of liver damage (raised GLDH, AST, gGT and bile
Most does, particularly those bred for high milk acids). Ketonuria is present.
yields, suffer a mild acetonaemia in early lacta-
tion. The increase in dry matter intake lags behind Differential diagnosis
increase in milk yield (and with it energy demand) Other causes of weight loss and reduced milk yield
until about 6–8 weeks post kidding, resulting in a should be eliminated, such as parasitic gastroen-
negative energy balance (NEB) in early lactation. teritis, fluke, haemonchosis and Johne’s disease. For
This inevitably results in fat mobilisation which, if reduced appetite, also mastitis and urogenital tract
excessive, can lead to fatty infiltration and degenera- infection.
tive liver change. Overfat does may show a marked
drop in appetite post kidding, and are therefore Treatment/management/control
Treatment follows the principles outlined under
pregnancy toxaemia earlier in this chapter.
Prevention is based on ensuring goats do not kid
down in overfat condition and paying attention
to feeding in the dry, transitional and early lacta-
tion period. The aim during the dry period is to
keep rumen capacity and dry matter intake at its
maximum (adjusting energy density in the early dry
period to avoid excessive weight gain). Three weeks
prior to kidding, the components of the lactational
diet should be introduced to allow rumen microbes
to adjust. After kidding, steps to increase dry mat-
ter intake include: feeding best quality forage
Fig. 14.3 Fatty infiltration of the liver as seen in available (e.g. first cut silage), providing sufficient
advanced pregnancy toxaemia/hepatic lipidosis. trough space, reducing competition and bullying,
304 Chapter 14
removing stale feed at least every 24 hours, ensur- Floppy kid syndrome
ing easy access to feed including regularly pushing Floppy kid syndrome is a metabolic acidosis with-
feed up, preventing rumen acidosis (e.g. by feeding out diarrhoea or dehydration, affecting kids typi-
a total mixed ration) and monitoring actual feed cally between 7 and 14 days of life (range 3 days to
intake (Figs. 14.4, 14.5). 4 weeks). Herd morbidity of between 30 and 50%
is most commonly reported, although in outbreaks
Metabolic acidosis described in North America morbidity did approach
Resulting from a primary rumen acidosis, systemic 100%. Mortality in unrecognised and untreated out-
metabolic acidosis can result in lethargy, anorexia, breaks can be high. (See Chapter 4.)
abdominal pain and teeth grinding, subnormal tem-
perature, a fast weak pulse and death if untreated. Swelling disease in Angora goats
(See Chapter 5.) (See Chapter 7.)
Fig. 14.4 Feed management to maximise dry Fig. 14.5 A poorly positioned hayrack. Being at the
matter intake could be improved in this herd. The back of the pen makes access difficult for staff. In this
ration is not provided truly ad libitum, with obvious case, this had led to stale and partially mouldy hay
competition. Sorting of the total mixed ration has being present.
taken place (although this cannot always be avoided
with goats); the goats cannot easily reach because
of the high feed barrier and feed not being pushed
up regularly. A positive aspect is the use of a feed
platform (versus troughs), making removal of stale or
leftover feed easy for farm staff.
CHAPTER 15
TRACE ELEMENT AND VITAMIN DISORDERS

305
TRACE ELEMENTS of inadequate mineral intake. There are four stages

that occur in the progression from inadequate intake
In goats, copper, selenium, cobalt, iodine and zinc to the development of clinical disease:
have all been associated with deficiency disorders
affecting health and productivity. Deficiencies are 1 Depletion. There is loss of mineral from storage
more likely to be encountered in grazing goats, goats sites such as the liver, but levels in the circulating
fed forage only diets or goats fed home grown feed blood are within the reference interval.
products – all in the absence of any mineral or trace 2 Deficiency. During this phase, the circulating
element supplementation (Fig. 15.1). Deficiencies blood levels fall.
are far less likely in goats fed a balanced ration, 3 Dysfunction. As levels continue to fall, trace
including commercial feeds such as concentrates. element-dependent enzyme systems involved
The browsing behaviour of goats, leading to con- in metabolism begin to fail and body functions
sumption of not only herbage but also mature plants, become impaired. At this stage the goat will be
shrubs and trees, may make them less susceptible to showing no clinical signs.
deficiency than grazing cattle and sheep. 4 Disease. The metabolic dysfunction gradually
The potential for deficiency-related clinical signs leads to detectable clinical abnormalities.
to develop will depend on the duration and degree
Mineral deficiencies can either be primary and
associated simply with an insufficient supply in the
diet, or secondary, when the dietary level is adequate
but other factors limit availability and uptake. There
are marked geographical differences within each
country in soil and herbage trace element availabil-
ity. In some areas outright deficiencies may be the
significant feature, in others it is an excess of antago-
nistic inhibitors (such as other trace elements) that
causes the problem. The animals’ drinking water
as a source of such antagonists must be considered
(e.g. water sulphate levels above 500 ppm are thought
to cause meaningful interference).
For supplementation, the following general
aspects are of interest. The organic form of miner-
als (complexed chelates) generally has the highest
bioavailability. Free access minerals (mineral licks,
mineral buckets; Fig. 15.2) are convenient, but have
Fig. 15.1 Rock salt and salt licks are useful dietary the disadvantage that intake is voluntary, such that
additions, but are no substitute for a balanced mineral some individual goats may consume an excessive
and vitamin supplement. (and potentially toxic) amount, whereas others may
306 Chapter 15
Fig. 15.2 Self-help mineral licks are convenient for Fig. 15.3 Mineral powder should not just be
the stockperson, but intake can be highly variable sprinkled onto feed; because of the bitter taste,
from goat to goat. animals will sort and avoid.
take nothing. Minerals typically have a bitter taste Pathophysiology

and animals will avoid eating them if they can. To Once absorbed, the liver is the main storage site of
overcome this and make the mineral powder stick body copper reserves. The majority of circulating
and prevent sorting, top-dressing of pasture should copper is bound to the acute phase protein cerulo-
be done while it is still wet with dew. If a mineral mix plasmin. Other circulating copper is bound to eryth-
is to be added directly to a feed, the feed itself must rocytes, and the remainder is free albumin-bound
be moist or be molassed (Fig. 15.3). copper. Clinical signs of copper deficiency will only
When supplementing via the drinking water, occur after liver stores have been exhausted. Blood
there must be no alternative source of water and ani- copper levels begin to fall, followed by a gradual
mals must be monitored for sufficient intake. reduction of available copper in body tissues. Copper
plays an essential role in a number of metabolic and
Copper deficiency developmental functions, but is specifically involved
Definition/overview in myelination, osteogenesis, haematopoiesis, hair
Both primary and secondary copper deficiency can pigmentation and daily growth, thus defining the
occur. A number of differing clinical presentations main clinical presentations.
have been attributed wholly or in part to copper defi-
ciency in older goats, but many remain unproven. Clinical presentation
Angoras and other fibre breeds appear to be more Deficiency during fetal development can lead to
susceptible than dairy breeds. congenital swayback in newborn kids or delayed
swayback developing between 1 week and several
Aetiology months after birth (Fig. 15.4). In the congenital
Simple copper deficiency due to lack in the goat’s form, kids are abnormal at birth, with weakness
diet can occur, but the majority of cases are second- and in most an inability to rise. Fine muscle trem-
ary and linked to copper uptake antagonists. The ors, abnormal head movements and vocalisation are
predominant ones are molybdenum, sulphur and features. Signs secondary to the inability to nurse
iron. Molybdenum, for example, reacts with sulphur properly may develop. In the delayed form, some-
in the rumen to form thiomolybdate, which irrevers- times referred to as enzootic ataxia, kids are born
ibly binds copper and prevents its absorption. normally, but develop a progressive paresis that
Tr ac e E l e m e n t a n d Vi ta m i n D isor de r s 307
central nervous system, will confirm the diagnosis.

Herd copper status is best determined by liver assay,
either from cull or dead goats, or by liver biopsy (see
Chapter 5). Blood sampling a minimum of six goats
is an alternative, but results must be interpreted with
caution. Subnormal levels indicate deficiency, but
normal levels may represent anything from depleted
to adequate to toxic status (as the body will aim to
keep blood levels stable). Diagnostic laboratories
may employ a variety of test procedures for blood
copper assay, each with the aim of identifying total
blood copper and the percentage of available copper.
Interpretation of results should always be based on
each laboratory’s own reference interval.
Fig. 15.4 Delayed swayback in a 4-week-old Differential diagnosis

Boer kid. For congenital swayback includes hydrocephalus,
border disease, hypoglycaemia and hypothermia. For
may vary in onset from 1 week to several months delayed swayback consider spinal abscess, vertebral
after birth, and from days to weeks in progression. trauma, muscular dystrophy, caprine arthritis
Paresis and ataxia are usually noticed in the hind encephalitis (CAE), floppy kid syndrome and
legs first, and are always bilateral. Affected kids can listeriosis.
initially support their weight, but slowly become
paralysed. Some may adopt a dog-sitting position Treatment/management/control
or drag themselves along with their front legs. Although goats are susceptible to copper defi-
Other clinical signs in an affected herd are less ciency, it is important to emphasise that they are
well defined, but may involve various age groups and also susceptible to a dietary excess leading to cop-
include ill thrift, anaemia, loss of hair pigmenta- per toxicity (see Chapter 16). Therefore, the decision
tion (often visible around the eyes), poor fibre qual- to supplement should always be based on liver assay
ity, diarrhoea, osteoporosis and spontaneous bone results. If deemed necessary, there are a variety of
fractures (although these skeletal abnormalities are commercially available copper supplements, includ-
complex and often involve many other co-existing ing injectable preparations, such as calcium copper
mineral or metabolic abnormalities). The extent of edetate, and oral products such as copper oxide in
copper deficiency-induced progressive ataxia and gelatine capsules or soluble glass boluses containing
subfertility, as reported in other species, is unclear copper, for slow release. Products should indicate
in goats. that they are ‘suitable for sheep or goats’.
Management of both congenital and delayed
Diagnosis swayback cases is focussed on nursing; however,
The time of onset and clinical signs exhibited are prognosis is very guarded as demyelination occurred
fairly characteristic of swayback. A blood copper in utero and response to copper administration is
assay may be useful, although this can be within often poor. Newborn kids may need artificial feed-
the reference interval, even in confirmed cases, if ing if they are unable to suckle. In the delayed form,
supplementation has been given after the myelin ensuring easy or assisted access at all times to feed
damage has occurred. Liver copper assay at post- and water is paramount. Prevention relies on suf-
mortem examination (PME), coupled with the char- ficient copper levels in the pregnant doe. A dietary
acteristic gross pathology of cerebral cavitation and copper level of 8 mg/kg dry matter total ration has
histological evidence of myelin abnormalities of the been suggested for goats. Copper supplemented
308 Chapter 15
compound feeds are available, some of which may highest rate of oxidative metabolism are most sus-
need veterinary prescribing. ceptible to damage, particularly in skeletal, cardiac
and respiratory musculature.
Selenium/tocopherol (vitamin E) Selenium deficiency has also been shown to have
deficiency (syns. nutritional muscular an adverse effect on caprine neutrophil function,
dystrophy, white muscle disease) which may impact on an immune response to con-
Aetiology current disease.
Selenium deficiency can occur where goats are
on selenium deficient pasture or fed a diet grown Clinical presentation
on selenium deficient soil, without supplementation. The predominant clinical presentation of sele-
Tocopherol (vitamin E) is synthesised by plants and nium/tocopherol deficiency is white muscle disease
levels are typically more than adequate in green pas- (syn. nutritional muscular dystrophy). It is most
ture and conserved forages (Fig. 15.5). As a result, commonly seen in growing kids, from a few days
tocopherol deficiency tends to occur in goats that are to 6 months of age. Clinical signs can present in a
housed and fed poor quality forage such as straw or number of ways, depending on the muscle group(s)
poorly conserved grass products, with inadequate affected and the severity of the insult, and in a clini-
supplementation. There is considerable overlap cal outbreak, many differing manifestations may
between selenium and tocopherol deficiency; clinical be seen. Some kids may simply be found dead due
signs are largely similar and a dietary excess of one to damage to cardiac muscle. Others may be found
can compensate for a dietary deficiency of the other. recumbent and unable to rise or displaying a stiff
legged gait. They are usually alert and aware of
Pathophysiology their surroundings and will often vocalise. If there
During selenium and/or tocopherol deficiency, a is severe muscle damage, myoglobinuria may be
failure to protect against cell damage leads to cell present. The immediate history may identify a sud-
membrane damage and cell necrosis. Cells with the den period of activity as an initiating factor, such as
turnout, being driven or transported. Other clini-
cal signs may include dyspnoea, coughing and signs
of pulmonary oedema if the cardiac muscle or dia-
phragm is involved. Stillborn kids may be born to
deficient dams. The role of selenium deficiency in
retained fetal membrane or cystic ovarian disease in
ruminants remains debatable.
Diagnosis
The clinical signs and recent history of increased
exercise are highly suspicious. For selenium defi-
ciency, the standard confirmatory laboratory test
is measurement of blood glutathione peroxidase
(GSH-Px; a selenium containing enzyme). As eryth-
rocyte GSH-Px levels depend on selenium concen-
trations during erythropoiesis, any GSH-Px result
indicates the selenium status 2–4 months ago. In
clinical outbreaks, the GSH-Px and tocopherol
Fig. 15.5 Selenium content of fresh and conserved levels are usually both low. Blood levels of the muscle
grass depends on soil levels. Tocopherol content specific enzyme creatinine kinase are often mark-
depends on good harvesting and conservation edly elevated (>20,000 IU/ml) and can be used to
technique. establish the degree of muscle damage.
At PME, in the cardiac form there will be e vidence the parenteral administration of a proprietary sele-
of white to grey discolouration of the myocardial nium and tocopherol combi-preparation can result
tissue extending into deeper tissue (Fig. 15.6). This in an improvement over a 24-hour period. Nursing
is often accompanied by evidence of congestive heart is essential for more severely affected kids, ensur-
failure such as ascites, hydrothorax, pericardial effu- ing that they have access to adequate feed and water,
sion, pulmonary oedema and a swollen liver. The and that they are on a surface (e.g. a straw bedded
main muscle masses affected are those of the legs, but area) that will reduce the risk of pressure necrosis
a detailed examination of diaphragm and intercostal if recumbent. Goats that fail to respond after 48
muscles should be undertaken. In affected muscles, hours carry a guarded prognosis. Control is based on
changes are usually bilateral and normally present as adequate selenium and tocopherol supplementation,
pale or chalky changes within the muscle belly and particularly in those units on which the condition
areas of haemorrhage alongside unchanged muscle has been encountered previously and in pregnant
tissue (Fig. 15.7). Confirmation can be undertaken does during the later stages of pregnancy. This
by histological examination of affected muscle tis- can be either via in-feed trace element and vitamin
sue (showing a hyaline degenerative change), coupled supplementation or by the strategic administration
with assay of liver selenium and tocopherol levels, or of proprietary oral or injectable supplements. Long
by blood sampling live cohort goats. term, incorporating selenium into fertiliser prills is
the most economical way, and for tocopherol ensur-
Differential diagnosis ing good grass harvesting and conservation methods.
Other causes of recumbency include trauma, delayed
swayback, the neurological presentation of CAE and Cobalt deficiency
floppy kid syndrome. Sudden death in young kids Definition/overview
can occur as a result of colisepticaemia, enterotox- Cobalt deficiency is reported in ruminants world-
aemia, congenital cardiac abnormalities, trauma or wide, being a particular problem in sheep and, to
misadventure. a lesser extent, in goats. Cobalt is a component of
cyanocobalamin (vitamin B12), which is synthesised
Treatment/management/control by the rumen microflora. This production cycle is
Treatment success depends on the severity of any reduced if the supply of cobalt is deficient, resulting
muscle damage that has occurred. In the early stages, in cyanocobalamin deficiency.
Fig. 15.6 White muscle disease (muscular Fig. 15.7 White muscle disease (muscular dystrophy)
dystrophy) changes in myocardial tissue (specimen: changes in upper hind leg musculature (specimen:
calf). (© Crown Copyright 2017. Used with kind calf). (© Crown Copyright 2017. Used with kind
permission of the Animal and Plant Health Agency.) permission of the Animal and Plant Health Agency.)
310 Chapter 15
Aetiology (often containing other trace elements, therefore

Cyanocobalamin itself is required as a co-enzyme to take care to avoid oversupplementation) or pro-
methylmalonyl-CoA mutase in the metabolic path- viding additional cobalt in the ration. Daily cobalt
ways associated with the Krebs cycle, resulting in requirements of 0.25–0.4 mg per adult goat have
the non-specific clinical signs described below. One been suggested.
further specific manifestation of cobalt deficiency is
‘ovine white liver disease’ (OWLD), which is occa- Iodine deficiency
sionally reported in goats. (See also Chapter 4.)
Pathophysiology Definition/overview
OWLD is an indirect sequela to cobalt/cyanoco- Iodine deficiency is a worldwide problem that leads
balamin deficiency, as the dependent co-enzyme to the development of an enlarged thyroid gland at
deficiency reduces the goat’s ability to convert pro- birth: congenital goitre. This must be distinguished
pionic acid to glucose via succinate in the liver. This from thymic enlargement (see Chapter 7), which can
leads to a build-up of methylmalonyl-CoA, which in also cause throat swelling in young kids. A deficiency
turn is converted to branched-chain fatty acids that of circulating iodine in pregnant does may result in
accumulate in hepatocytes, causing the characteris- abortion, stillbirth or the birth of weak kids. There
tic pale, swollen and friable fatty liver. may be a breed susceptibility to the condition in, for
example, Boer and Angora goats.
The clinical signs with both uncomplicated cobalt Aetiology
deficiency and OWLD are non-specific and include Primary deficiency can be caused by a straightfor-
chronic ill thrift or poor growth rates, anaemia, sub- ward shortage of iodine in the diet or feedstuff grown
mandibular oedema, reduced milk production, and in iodine deficient geographical regions. Secondary
poor coat quality in fibre goats. iodine deficiency is linked to the feeding of plants
that contain goitrogens, or compounds that interfere
Diagnosis with the uptake of iodine from the diet or with its
In live goats, cobalt deficiency is confirmed by metabolism in the formation of thyroxine. Plants of
serum cyanocobalamin (vitamin B12) assay. Other the Brassica family, including rape and kale, contain
clinical pathology features include hypoalbumi- the goitrogen thiocyanate, and thiouracil is found
naemia and a macrocytic, normochromic anaemia. in certain brassica seeds such as oilseed rape. High
At PME, carcases are pale and in poor or emaciated levels of calcium in drinking water may also reduce
condition. In OWLD, the liver shows widespread iodine uptake.
fatty change confirmed by histopathological exami-
nation and liver cyanocobalamin assay. Pathophysiology
Iodine is essential as a constituent of the thyroid
Differential diagnosis hormones T3 (triiodothyronine) and T4 (thyroxine).
There are many causes of ill thrift and anaemia to Approximately 80% of the body’s iodine is found in
consider including parasitic gastroenteritis, haemon- the thyroid gland.
chosis, liver fluke, Johne’s disease, insufficient dietary
protein or energy and poor weaning management. Clinical presentation
In severe congenital goitre, the thyroid gland may be
Treatment/management/control palpable in the upper part of the neck overlying the
Treatment is by oral or injectable preparations larynx. Affected kids are typically stillborn or born
containing cyanocobalamin or cobalt. Long-term weak and premature, resulting in unwillingness to
prevention in known deficient areas is based on stand and suckle. Blindness has occasionally been
the use of slow release, sheep-sized rumen boluses reported, as well as coat thinning. Some affected kids,
however, may show very few clinical signs. In adults VITAMINS

reproductive performance may be decreased, includ-
ing abortion. The four stages leading to clinical signs of defi-
ciency outlined at the start of this chapter can also
Diagnosis be applied to vitamin deficiency.
In live goats, T4 levels reflect the thyroid and
overall iodine status, and can be very high in kids Retinol (vitamin A) deficiency
affected with congenital goitre. Plasma inorganic Definition/overview
iodine measures short-term daily iodine intake, True retinol deficiency is not commonly reported in
and is thus susceptible to sudden changes in dietary goats, but has been linked experimentally to a range
intake. The two tests used in tandem can be useful of non-specific clinical signs.
in herd investigations. At PME, the thyroid gland
may be visibly enlarged and should be dissected free Aetiology
from any fat and connective tissue and weighed. The dietary precursor to retinol is beta-carotene,
The normal goat kid thyroid weight is around which is usually abundant in green leaved plants
2 grams (in cattle, the figure quoted is 0.03% of and grasses and well preserved and stored forages.
total calf weight). Thyroid total iodine concentra- Deficiencies are most likely to occur in arid or semi-
tion (<1,200 mg/kg dry matter of tissue indicates arid locations where green grazing is limited, or
a deficiency) and histological evidence of thyroid when goats are supplemented with poor old forage
hyperplasia confirms the diagnosis. or with mostly cereal grains (which are low in caro-
tene). Colostrum is a rich source of retinol, so defi-
Differential diagnosis ciencies are unlikely to occur until animals are older
Other causes of stillbirth (such as dystocia) and weak (unless colostrum deprived).
or premature neonates (including abortive agents).
Treatment/management/control Inappetence, weight loss and a general unthrifty
Treatment of clinically affected kids is typically appearance have been linked experimentally to defi-
unrewarding. However, prompt supplementation of ciency. The retinal degeneration-associated blind-
does still pregnant should be started. ness recognised in calves is not considered to be a
Management is based at ensuring a regular problem in goats.
daily intake of iodine in those areas or on those
units in which there is a known deficiency. This Diagnosis
can be achieved by a number of methods, includ- Feeding evaluation and history, and by serum or
ing intraruminal sheep-sized boluses, iodised salt liver retinol assay.
licks (care: intakes can be more haphazard) and top
dressing feed or pasture with iodised salts (potas- Differential diagnosis
sium or sodium iodide). For individual pregnant Signs are non-specific, and other causes should be
goats, potassium iodide can be given 2 months considered before retinol deficiency is incriminated.
and 2 weeks prior to kidding at a dose rate of
10 ml/20 kg BW of a mixture containing 20 g in Treatment/management/control
one litre of water. There is a lack of information Deficiency should not occur in goats fed a well-
on whether painting tincture of iodine onto preg- balanced ration based on good quality forage.
nant does is as effective as it is in cattle (the animal Dietary supplementation may be employed if defi-
licking off the iodine during grooming). ciency is identified.
Zinc deficiency Thiamine (vitamin B1) deficiency

See Chapter 11. See Chapter 8 under Cerebrocortical necrosis.
312 Chapter 15
Cyanocobalamin (vitamin B12) Tocopherol (vitamin E) deficiency

deficiency See under Selenium above. Swelling disease of
See Cobalt above. Angora goats has been linked to this deficiency
(see Chapter 7).
Calciferol (vitamin D) deficiency
See Chapter 9 (Rickets and Osteodystrophy of
mature bone).
CHAPTER 16
POISONING AND TOXICITIES

313
INTRODUCTION Poisoning can also occur after ingestion of a

range of chemical agents found in their environment
Due to their browsing and naturally inquisitive or used therapeutically or prophylactically, includ-
behaviour, goats could consume a wide variety of ing excess dietary minerals and some pharmacolog-
potentially toxic plants, shrubs and trees present in ical products. Poisonous gases that are potentially
their environment. However, they can apparently present in the goat’s environment include nitrous
ingest small quantities of such material without fumes from silage clamps and carbon monoxide or
any ill effects. This may be due to their browsing dioxide. The burning of poisonous plants can pro-
activity (avoiding ingestion of large quantities by duce toxic fumes, for example oleander.
moving from one food source to another) and to
the ‘protective’ environment in the rumen. Goats GENERAL APPROACH
may also have evolved and developed a natural tol-
erance, although this is unproven. A hungry goat The difficulty when dealing with a suspected poi-
confined to an area of limited grazing with toxic soning lies in having to consider the vast number of
plant m aterial present is most at risk. Care must potential toxins while being faced with the urgency
also be taken to avoid incorporation of poisonous to start specific treatment. The four cornerstones
plants into conserved forages, which may mask any of the investigation are circumstantial evidence
disagreeable taste and/or prevent the animal from (toxin present and signs of ingestion), considering all
avoiding the material (Fig. 16.1). clinical signs both in the patient and the rest of the
group, clinical pathology, and post-mortem exami-
nation (PME) (Tables 16.1–16.4). Useful samples for
toxin isolation include feed, blood, urine, stomach
contents, hair, bone, aqueous or vitreous humour,
and liver and kidney tissue (obtained by biopsy in
the live patient).
Treatment concepts include removing the goat
from its current environment and feed source
to limit further exposure. Elimination of the
toxin may be hastened by the use of purgatives or
diuresis. Further toxin absorption may be reduced
by force-feeding fibre, energy and proteins, or by
rumenotomy. Initial treatment is symptomatic and
supportive (e.g. fluid therapy, sedation, respiratory
support) until identification of the toxin allows the
Fig. 16.1 Ragwort is a classic example of harmful use of the specific antidote where one is available.
inclusion in hay. The fresh plant is bitter and typically The Veterinary Poisons Information Service
avoided by animals. However, drying makes the plant offers worldwide 24-hour emergency advice on a
sweet tasting. subscription basis.
314 Chapter 16
Table 16.1 Abnormal urine colour.
POISON COLOUR MECHANISM COMMENTS

Chlorate, copper, kale, rape Pink (on standing) Haemoglobinuria Due to excess haemolysis;
Dark brown (freshly prehepatic or haemolytic jaundice
collected/voided urine)
Phenols, creosote Dark green Differential diagnosis: bilirubin in
standing sample
Chlorate, bracken fern, lupins Pink Haematuria Kidney/renal tract damage
Phenothiazine Red On exposure to air
Acorns Black brown
Phenacetin, aromatic nitro compounds Bright yellow Excretion of metabolites
Hepatotoxins Red–gold colour of froth Biliuria Excessive excretion due to
on shaking obstructive or hepatic jaundice
Table 16.2 Abnormal blood colour.
POISON COLOUR MECHANISM

Nitrate/nitrite, copper, sodium chlorate Chocolate brown Methaemoglobin
Nitrous fumes (e.g. silage clamp) Light brown Methaemoglobin
Cyanide Cherry red Cytochrome oxidase inhibition
Carbon monoxide Bright red Co-haemoglobin
Carbon dioxide Dark red Displaced oxygen
Table 16.3 Abnormal breath smell. Table 16.4 Abnormal stomach contents.
POISON SMELL POISON COLOUR

Hydrogen cyanide, zinc phosphate, Bitter almonds Copper sulphate Green/blue
arsenic Chromic compounds Yellow, orange or green
Phosphorus (elementary) Smokey/choking Acids or alkalis (corrosion of mucosa) Black
Tables 16.1–16.4 from Bruère AN, Cooper BS, Dillon EA (1990) Veterinary Clinical Toxicology. Veterinary Continuing Education, Palmerston North,
New Zealand.
COMMON POISONS AND TOXINS grayanotoxin (or andromedotoxin). Ingestion may

occur directly from browsing on the shrub itself or
Genus Rhododendron from inadvertent access to discarded prunings and
Definition/overview clippings. Clinical signs may occur after the inges-
The genus Rhododendron includes rhododendrons tion of as little as 0.1% of the goat’s body weight in
(Fig. 16.2), azaleas and pieris, all of which are wild fresh leaves.
or ornamental shrubs found worldwide.
Pathophysiology
Aetiology Grayanotoxin can act directly on the autonomic ner-
These plants, and others in the Ericaceae fam- vous system, and specifically the vomiting centre in
ily such as laurel, contain the toxic principle the brain via the vagus nerve.
Poison i ng a n d Tox ic i t i e s 315
Fig. 16.2 Rhododendron bushes.
Initial signs include depression, salivation and
abdominal pain, with projectile regurgitation (or
vomiting) of rumen contents. The consumption
of large quantities of plant material may result in
rapid deterioration and death. Aspiration of regur-
gitated contents may lead to pneumonia in recover- Fig. 16.3 Rhododendron leaves found in
ing goats. the rumen of a poisoned goat at post-mortem
examination.
Diagnosis
Clinical signs are characteristic. Leaves or leaf frag-
ments (Fig. 16.3) may be present in regurgitated
contents or in rumen contents at PME.
Vomiting in goats is unusual, and poisoning with plants
from this genus should always be considered first, par-
ticularly if they are present in the environment.
If ingestion of a significant amount has occurred,
a prompt rumenotomy may be considered (see
Chapter 5), removing as much of the leaf debris as
Fig. 16.4 Yew trees (Taxus baccata) in an English
possible. Supportive therapy includes oral and/or i/v
churchyard, clipped into ornamental shapes as is
fluids and an oral activated charcoal suspension, or
common practice. Clippings must be disposed of away
products such as magnesium hydroxide to reduce
from livestock.
rumen toxin absorption. Spasmolytic agents such as
butylscopolamine bromide (Buscopan®) may con-
trol vomiting. Parenteral antibiotic cover should be in the UK (Figs. 16.4, 16.5). Although it is a com-
given to counteract aspiration pneumonia. mon cause of poisoning in other ruminants, it is only
occasionally reported in goats.
Yew
Definition/overview Aetiology
Yew (Taxus spp.) is found as wild and as ornamen- Most parts of the plant are potentially toxic, contain-
tal trees worldwide, often growing in churchyards ing the cyanogenic glycoside taxine. Goats may eat
316 Chapter 16
Oxalate poisoning
Definition/overview
Goats, like other ruminants, are potentially suscepti-
ble to poisoning if they eat excessive amounts of oxalate
containing plants. Toxicity can also develop following
the inadvertent consumption of ethylene glycol.
Aetiology
Oxalate containing plants include sorrel, docks, sugar
beet and mangold tops, rhubarb leaves, pigweed, kikuya
grass, spinach and chard. Ethylene glycol is a constitu-
ent of vehicle antifreeze and degrades to oxalates in
the rumen if consumed because of its sweet taste. It
appears that goats have an innate ability to degrade and
Fig. 16.5 Close up of yew (Taxus baccata) leaves and detoxify oxalates in rumen contents compared with
berry. other ruminants, therefore typically a large amount
needs to be consumed in a short period of time.
the leaves or branches from the tree, or consume dis- Pathophysiology

carded prunings. Oxalates that bypass the rumen and enter the
bloodstream combine with calcium ions to pro-
Pathophysiology duce calcium oxalate, thus resulting in a progressive
Taxine is a recognised cardiotoxin, ingestion of a hypocalcaemia. Calcium oxalate is insoluble, lead-
lethal dose causing heart failure and death. Only ing to crystal formation mainly in the renal tubules,
a very small amount of leaves (about 100) may be causing severe renal insufficiency.
required to kill a goat.
Clinical presentation Generally acute, with the hypocalcaemia resulting
Affected goats may simply be found dead, often with in incoordination, muscular trembling and hyperex-
fragments of yew in their mouth and yew foliage in citability, followed within hours by profound depres-
the vicinity. If still alive, they are profoundly dull sion, coma and death if untreated.
with marked cardiac arrhythmia and bradycardia.
Yew fragments may be identified in rumen contents. Diagnosis
Diagnosis is based on a history of exposure to poten-
Differential diagnosis tially toxic material, the clinical signs exhibited and
Other causes of sudden death. laboratory evidence of hypocalcaemia and renal insuf-
ficiency in live goats. Crystals may be evident in urine.
Treatment/management/control At PME, plant material may be evident in rumen con-
There is no specific antidote. If found alive and poi- tents and the kidneys will be enlarged and oedematous
soning is suspected, a very prompt rumenotomy may with characteristic histopathological changes.
be of benefit (see Chapter 5), together with support-
ive fluid therapy, oral activated charcoal and atropine Differential diagnosis
sulphate for bradycardia. Includes predominantly primary hypocalcaemia,
hypomagnesaemia and other causes of a neurological
Other plants, trees and shrubs disorder with a sudden onset such as enterotoxaemia,
potentially toxic to goats listeriosis, cerebrocortical necrosis, pregnancy tox-
See Table 16.5. aemia and hepatic encephalopathy.
Table 16.5 Other plants, trees and shrubs that are potentially toxic to goats.
COMMON NAME SCIENTIFIC NAME MAIN PRESENTING SIGNS

Bog asphodel Narthecium ossifragum Photosensitisation
Castorbean Ricinus communis Salivation, colic, cardiovascular signs
Foxglove Digitalis purpurea Sudden death, diarrhoea
Giant hogweed Heracleum mantegazzianum Stomatitis
Golden chain tree Laburnum spp. Nervous signs
Hemlock Conium maculatum Nervous signs, severe dyspnoea, diarrhoea
Houseplants Dieffenbachia spp., Calla lily (Zantedeschia aethiopica), Stomatitis syndrome
Philodendron spp.
Kale Brassica oleracea Anaemia, haemoglobinuria, jaundice
Nightshade Solanum spp. Nervous signs, dyspnoea, bradycardia,
gastrointestinal tract irritation
Oleander Nerium oleander Dyspnoea, cardiac arrhythmia
Ragwort Senecio jacobaea (syn. Jacobaea vulgaris) Liver failure, jaundice
Rape Brassica napus Anaemia, haemoglobinuria, jaundice
St John’s wort Hypericum perforatum Photosensitisation
Trumpet flower (trumpet) Datura spp. Nervous signs, dyspnoea, collapse
Water dropwort Oenanthe spp. Sudden death, nervous signs
Note: Unlike other ruminants, goats appear to have a natural tolerance to oak/acorn (Quercus spp.) toxicity.
Treatment/management/control Accumulation is promoted by disruption to normal

The prognosis for acute cases is guarded. They must plant growth (e.g. because of overcast or cold weather
be removed immediately from the likely source, and or drought). Poisoning can also occur from drinking
any hypocalcaemia treated by i/v and s/c calcium water contaminated with run-off from heavily fertil-
borogluconate. Intravenous and/or oral fluid ther- ised fields or by the direct ingestion of nitrogenous
apy may help to combat the progressive renal dam- fertiliser.
age. Prevention is based on the ability to identify
toxic plants and make them inaccessible. Pathophysiology
Normally nitrates are degraded in the rumen, and
Nitrate poisoning the resulting nitrite is converted to ammonia by
Definition/overview microbes. Toxicity is associated with excessive
Nitrate poisoning occurs worldwide. Goats can intake resulting in nitrite overload. These nitrites
develop nitrate poisoning via a number of differing are absorbed through the rumen wall, converting
routes and from different sources. haemoglobin to methaemoglobin, thus decreasing
oxygen transport. Clinical signs will become evident
Aetiology when 30–40% of the haemoglobin is converted to
The most common route is ingestion of plants con- methaemoglobin. Prognosis deteriorates as conver-
taining high levels of nitrates. Some are cultivated sion continues.
crops such as sugar beet tops, turnip tops, rape,
lucerne and maize. Worldwide there are also a num- Clinical presentation
ber of weeds that can concentrate nitrates, includ- Weakness, ataxia, progressive dyspnoea, frothing at
ing pigweed, some sorghum grasses and thistles. the mouth and cyanosis, in addition to diarrhoea and
318 Chapter 16
obvious abdominal pain. In severe toxicity goats may Clinical presentation

simply be found dead. Non-specific signs of abdominal pain, mucoid diar-
rhoea and profound depression are evident in acute
Diagnosis toxicity. As haemolysis progresses, affected goats
Evidence of actual or potential exposure is impor- become anaemic, dyspnoeic and jaundiced and the
tant. In live goats, or at PME, blood will appear dark urine is dark brown due to haemoglobinuria.
brown in colour. It can be sent for laboratory nitrate/
nitrite assay, together with other body fluids such as Diagnosis
ocular humour. Sampling and submission arrange- Clinical signs should raise suspicion, taking any
ments should be discussed with the laboratory as both copper supplementation history into account.
metabolites may be unstable and degrade rapidly. Haematology will reveal very low PCV, Hb and
erythrocyte counts. Liver enzymes (GLDH, AST,
Differential diagnosis SDH and gGT) will be elevated, as will serum bili-
Other causes of dyspnoea and cyanosis including rubin levels. Haemoglobin may be demonstrated in
anaemia, cardiac abnormalities and choking. urine. At PME, there are widespread signs of jaun-
dice (Fig. 16.6), and the liver is invariably pale, soft
Treatment/management/control and yellow in colour. Kidneys are soft, swollen and
All goats in the group should be immediately black in colour (Fig. 16.7).
removed from any potential source. Rapid treat-
ment is vital to success, using an i/v 1–2% solution Differential diagnosis
of methylene blue at a dose rate of 5–15 mg/kg, Acute enteritis or abdominal catastrophe for acute
repeated after 6–8 hours if necessary. toxicity. Other causes of jaundice include brassica
(e.g. rape, kale) poisoning and primary liver dis-
Copper poisoning ease. Other common causes of haemolytic anaemia
Definition/overview include blood parasites and clostridial disease.
Both acute and chronic copper poisoning can occur
in goats, but they do appear to be inherently more Treatment/management/control
resistant to the effects of increased copper intake Any copper source should be removed immedi-
than sheep. ately. Treatment is aimed at removal and clearance
Aetiology
Almost all cases encountered will be the result of
accidental oversupplementation. These include
excessive copper inclusion in rations and ad-libitum
high copper mineral provision. Accidental drinking
of copper sulphate footbaths has been reported.
Pathophysiology
If very high levels are ingested or administered,
goats may immediately develop signs of acute toxic-
ity. Chronic daily dietary excess is accumulated in
the liver. Levels gradually rise with no clinical signs
evident until a critical point is reached. At this point,
there is a rapid release of copper from the liver, ini- Fig. 16.6 Profound jaundice evident after the
tiating an acute haemolytic crisis resulting in intra- carcase is skinned. A confirmed case of copper
vascular haemolysis. poisoning in a calf.
Signs are seen within 90 minutes after ingestion and
include abdominal discomfort, rumen atony with or
without tympany, muscle and skin tremors, saliva-
tion, incoordination, dyspnoea, convulsions and
death.
Diagnosis
Diagnosis is based on a known availability or access
to urea, often following a period when it has not
Fig. 16.7 Typical black discolouration of kidneys at
been available and then reintroduced. Blood ammo-
post-mortem examination in copper poisoning cases
nia levels can be analysed in live goats, but testing
(ovine specimen).
must be undertaken within 30 minutes of sampling
(or samples frozen immediately). Serum urea levels
of copper from the blood and body tissues via the will be raised. There are no specific PME findings,
use of chelating agents. The most widely used agent although rumen contents pH may become markedly
is ammonium tetrathiomolybdate at a dose rate of alkaline, exceeding 7.5.
1.7 mg/kg i/v or 3.4 mg/kg s/c given three times on
alternate days. (Note: This product is off-licence Treatment/management/control
in many countries.) Control is based on ensuring Prognosis is guarded. Treatment options include
that there is an actual need for copper supplemen- administration of several litres of ice-cold water
tation (by liver or blood assay) before the inclusion via stomach tube into the rumen, together with
of copper in the ration or the introduction of other 0.5–1 litres of vinegar as an acidifying agent – both
sources of copper. to slow down ammonia production. Rumenotomy
may be indicated in valuable animals. In addition,
Urea poisoning i/v isotonic saline, together with calcium boroglu-
Definition/overview conate and magnesium sulphate, should be given.
Urea is used as a feed supplement in high-production Barbiturate or other sedative agents may help against
dairy goats. Accidental overdosing may occur, caus- convulsions.
ing toxicity. Prevention is by ensuring that any ration
containing urea is thoroughly mixed, and that any
Aetiology free access urea source is introduced gradually.
Poisoning episodes most typically occur after a Maximum recommended urea inclusion rates are
free access urea-containing product is introduced 2–3% of the concentrate portion of a diet, or 1%
suddenly or following a period of unavailability, or of the total diet.
because of uneven mixing into a ration. Urea is very
soluble and can wash out of a ration or feed blocks Mycotoxins
following heavy rain, and be consumed by goats Overview
drinking surface water. Fungal infection of growing plants, or harvested
and stored feedstuffs (Fig. 16.8), occurs frequently.
Pathophysiology It can be difficult to pinpoint the specific role or
Urea is converted in the rumen to ammonia, which, impact of mycotoxins.
in excess, diffuses out from the rumen into the blood
stream. Toxic signs will develop when the liver’s Aetiology
ability to cope with these increasing ammonia levels Some specific agents, and the disease they cause, are
is compromised, resulting in hyperammonaemia. recognised and shown in Table 16.6.
320 Chapter 16
Diagnosis
Diagnosis is difficult and often circumstantial.
Indications that mycotoxins are involved include
a large number of animals affected over a short
period and no evidence of contagious disease,
improvement once feed is withdrawn, mouldy
feedstuffs and failure to isolate other pathogens.
Mycotoxicosis from pasture typically occurs in
the autumn. Fungal isolation from feed is expen-
sive and often has false-negative results because of
only localised patches of feed being affected, heat
damage having eliminated the fungus but not the
toxin, and the causative fungus becoming over-
grown by other fungal species.
Contagious or highly infective disease for large num-
ber of animals affected in a short time. Other causes
of suboptimal performance, in particular nutritional
deficiencies, stressors, painful conditions such as
lameness. For poor reproductive performance, also
Fig. 16.8 Visibly spoiled hay. Such forages or abortive and venereal agents.
feedstuffs are not suitable for any type of animal or
production group. Treatment/management/control
Remove suspected feed. Clays and other anticaking
Clinical presentation agents and yeasts have been used as mycotoxin bind-
Signs suggestive of the specific mycotoxins are ers (e.g. sodium bentonite: available from mineral
shown in Table 16.6. However, low levels of suppliers, feed about 20 g per head per day, or 1–2%
mycotoxins may result in general suboptimal inclusion in diet; cattle products include Mycosorb®,
production. MTB100®, Nutrasound® and Mycortex®). There is
Table 16.6 Recognised mycotoxins and their presentation.
MYCOTOXIN CROP DISEASE GENERAL EFFECT

Aflatoxin B1 Cereals Aflatoxicosis Hepatotoxic
Dicoumarol Sweet clover Sweet clover poisoning Coagulopathy
Ergot alkaloids Cereals, grasses Ergotism Diarrhoea, lameness with dry gangrene of extremities
Ergot alkaloids? Festuca spp. Fescue foot Necrosis/gangrene lower limb
Lolitrem Ryegrass Ryegrass staggers Incoordination, ataxia
Penitrems All feeds N/a Tremors
Trichothecenes Cereals N/a Dermonecrotic, coagulopathy
(e.g. Fusarium spp.)
Zearalenone Cereals Fusarium infertility Oestrogenic
debate as to whether they really bind the mycotoxins

or merely act as rumen buffers, and not all myco-
toxins may be bound to the same degree. It is also
not established to what degree they bind minerals
and vitamins (i.e. whether their feeding can induce
imbalances or deficiencies). A response, for exam-
ple in the form of increased appetite or milk yield,
should be seen within about 2 weeks of feeding such
binders.
Water source poisons

The quality of the animals’ drinking water is often
overlooked, and although goats tend to be fairly fas-
tidious and will generally refuse to drink water that Fig. 16.9 Stagnant pond water with obvious algal
is not clean and fresh, its potential role in suspected overgrowth. Such water sources should be fenced off
toxicity cases should be considered. to avoid toxicity.
The most important pollutants are bacteria
(especially faecal pathogens), algae (in particular
blue-green algae), heavy metals, chemicals and [sodium hypochlorite], 30 ml in 1 litre of water,
hydrogen sulphide. Excessive levels of magnesium rinsing well after application). Stagnant water
or sulphate may have laxative effects resulting in should be fenced off and animals provided with
diarrhoea. mains or well water whenever possible.
Risk factors for poor water quality include nat- Water testing services are readily available.
ural water courses, stagnant water in particular The cost of water analysis is reasonable and a good
when exposed to sunlight (Fig. 16.9), lead piping, investment to establish the type and level of any
troughs positioned too low leading to faecal con- pollutants. The results will also support a more
tamination, and poor handling of chemicals on the targeted m ineral and vitamin supplementation. In
farm. Troughs and water reservoirs should be emp- dairy herds, ensuring good water quality will sup-
tied and disinfected weekly (e.g. with dilute bleach port optimum milk production.
CHAPTER 17
EXOTIC AND EMERGING DISEASES

323
INTRODUCTION relevant to goats and classed as notifiable (i.e. a sus-

picion of their presence must be reported to the
The World Organisation for Animal Health (OIE) relevant authority) are listed in Table 17.1.
has 180 member countries and maintains a list of
animal diseases, infections and infestations that it Foot and mouth disease
considers of most global importance (currently 117 (aphthous fever)
in total). Each member country undertakes to report Definition/overview
the listed animal diseases that it detects in its ter- Foot and mouth disease (FMD) is one of the
ritory to the OIE, which in turn then disseminates most important and economically devastating
the information to other countries, who can take infectious diseases, potentially affecting live-
the necessary preventive action. The organisation stock worldwide. All domestic (and many wild)
provides technical support to member countries for cloven-hoofed species are susceptible including
animal disease control and eradication operations. It goats, cattle, sheep and pigs. FMD is endemic in
specifically offers expertise to the poorest countries parts of Asia, Africa, the Middle East and South
to assist in the control of animal diseases that cause America. It is one of the most important entries
livestock losses, present a risk to public health or on the OIE list of scheduled diseases, and there
threaten other member countries. are very strict control measures in place to pro-
Different countries will implement the OIE list tect the borders of those countries currently free
in slightly different ways. In the EU, the diseases of infection.
Table 17.1 Notifiable diseases in goats.
DISEASE SPECIES AFFECTED DESCRIPTION

Anthrax Most mammals, particularly ruminants and humans Chapter 17
Aujeszky’s disease (pseudorabies) Mainly pigs – can occasionally infect in-contact goats Chapter 8
Bovine spongioform encephalopathy Cattle – very rare confirmation of disease in goats Chapter 8
Bluetongue All ruminants Chapter 17
Bovine tuberculosis Mainly cattle, but can affect many other domesticated and wild mammal species Chapter 17
Brucellosis Goats and sheep, but many mammalian species can be infected Chapter 2
Contagious agalactia Goats and sheep Chapter 12
Contagious caprine pleuropneumonia Goats are the primary host; in-contact sheep may become infected Chapter 6
Foot and mouth disease All cloven hoofed animals Chapter 17
Goat pox Goats and sheep Chapter 11
Peste des petits ruminants Goats and sheep Chapter 5
Rabies All mammals Chapter 8
Scrapie Goats and sheep Chapter 8
324 Chapter 17
The susceptibility of goats to FMD can vary •• Contact with exposed humans, who can harbour
with the breed of animal and the strain of the FMD FMD virus in their respiratory tract for
virus. In the UK outbreak in 2001, for example 24–48 hours. This is the reason for the common
(caused by serotype O PanAsia strain), clinical practice of 3–5 days of quarantine (away from
d isease was rapid in onset and clinically severe in susceptible livestock) for personnel exposed
cattle, but lesions were more mild in sheep and in research facilities or while dealing with an
goats. FMD was only suspected in one small herd outbreak.
of milking goats after a significant rise in masti-
tis cases prompted a request for veterinary advice. Pathophysiology
A number of goats had small ‘inconsequential’ The incubation period for FMD can vary with the
lesions on the skin of the teats that had become species of animal, the dose of virus, the viral strain
secondarily infected with Staphylococcus aureus; no and the route of inoculation. In sheep, for example,
other more typical lesions were evident. FMD sero- it is reported to be 1–12 days, with most infections
conversion was widespread, however. Conversely appearing in 2–8 days. Most new infection is con-
there are strains of serotype O FMD virus circulat- tracted by the inhalation route, spreading rapidly
ing in the Middle East where goats and sheep form within a group of animals before clinical signs
the majority of the susceptible population. There become apparent because of the massive viral repli-
are many examples where movement of subclini- cation and excretion rates. As a result, many animals
cally infected sheep and goats carried FMD into may appear to be affected almost simultaneously in
countries previously disease free. a new incident.
Once infected, virus replication leads to an ini-
Aetiology tial pyrexia lasting 2–4 days, during which all secre-
A virus of the family Picornaviridae, genus tions are highly infectious. Young kids may die at
Aphthovirus. There are seven immunologically dis- this stage due to viral myocarditis. Virus then pro-
tinct serotypes: A, O, C, SAT1, SAT2, SAT3 and gressively concentrates in the epithelial tissues of
Asia1, which, significantly, do not confer cross the oral cavity and feet, and also occasionally of
immunity with each other. The virus can be pre- the teats. Further replication at these sites leads to
served by refrigeration and freezing, but is quickly hydropic degeneration and coalescence of fluid-filled
inactivated by a pH <6.0 or >9.0. This is of real sig- cells to form vesicles. These are thin walled and
nificance as preserved infected meat products have easily ruptured, leaving raw and very painful areas,
been incriminated as potential sources of disease leading to the stomatitis and lameness considered to
incursion into countries previously free of infection, be the characteristic features. These characteristic
such as in the 2001 outbreak in the UK. erosive lesions are much smaller and far less readily
Spread of the virus can occur as a result of: observed in goats and sheep compared with cattle,
where they may reach 3–4 cm in diameter.
•• Direct contact between infected and susceptible
animals. Clinical presentation
•• Direct contact of susceptible animals with FMD in goats can be mild and inapparent, and may
contaminated inanimate objects such as hands, only be recognised when other in-contact ruminants
footwear, clothing or vehicles. (particularly cattle) show more typical signs. In goats
•• Inhalation of infectious aerosols. that do develop clinical signs, there may be an initial
•• Consumption of untreated contaminated meat pyrexia (often overlooked) and it is more common
products (e.g. swill feeding in pigs). for foot lesions than mouth lesions to be identified
•• Artificial insemination with contaminated clinically, in the form of lameness or tenderness
semen. on one or more feet. In early cases, vesicles may
•• Airborne spread, especially in temperate zones be found on the coronary band, in the interdigital
(up to 60 km overland and 300 km over sea). space (Fig. 17.1) and over the soft part of the heels.
E xo t ic a n d E m e rgi ng D is e a s e s 325
Fig. 17.1 Fresh foot and mouth lesion in the Fig. 17.2 Fresh foot and mouth lesion on the gum.
interdigital cleft. (Source: European Commission for (Source: European Commission for the Control of
the Control of Foot and Mouth Disease; permission Foot and Mouth Disease; permission granted by the
granted by the Pirbright Institute.) Pirbright Institute.)
These rupture, exposing raw areas that in turn can

become secondarily infected – lameness can be very
pronounced, and goats may be reluctant to move or
spend more time lying down. Small erosive lesions
may develop in the mouth. The common sites are
the dental pad and tongue followed by gums, lips,
hard palate and cheeks (Figs. 17.2, 17.3). They tend
to be quite shallow and may heal within 2–3 days.
These will lead to saliva drooling, lip smacking and
halitosis. Small vesicles may develop on the skin of
the udder and teats. These can rupture, become sec-
ondarily infected and predispose to mastitis. Indeed,
mastitis may be the presenting complaint at the start
of an FMD outbreak. It is important that a number
of goats within the cohort are examined before FMD Fig. 17.3 Foot and mouth lesion of 3–5 days’ duration
can be eliminated clinically, paying particular atten- on the dental pad. (Source: European Commission for
tion to any in-contact more susceptible species, such the Control of Foot and Mouth Disease; permission
as cattle and pigs in which disease is usually more granted by the Pirbright Institute.)
severe and thus more easily recognised. Young kids
may be found dead due to viral myocarditis. disease must always be high when a number of goats
(or other in-contact susceptible species) show the
Diagnosis clinical signs described, particularly if it is known
Unless classical vesicles in the early stages are evi- that disease exists in the locality. Most statutory
dent, definitive diagnosis on clinical grounds alone control measures require a suspicion of disease to
can be problematic, because healing lesions and those be reported to the relevant authority, who in turn
that become secondarily infected may not be readily will instigate a full and rapid investigation including
recognisable as FMD lesions. However, suspicion of laboratory sampling.
326 Chapter 17
Laboratory testing is based on demonstrating to the tropical and subtropical regions of each conti-
antigen by rapid detection tests such as the reverse nent, with occasional incursions outside these areas;
transcriptase PCR or antigen ELISA test. Serological for example, into northern Europe in the 2006–2008
screening for surveillance purposes is undertaken incident. This resulted in an OIE reclassification of
using a blocking or competition ELISA test. the global susceptibility to between latitudes 53°N
Young kids dying during an outbreak can be to 34°S. This global distribution reflects the dis-
examined by post-mortem examination (PME). tribution of the Culicoides spp. vectors that carry
Lesions tend to be confined to the myocardium, in and transmit infection between susceptible hosts.
which there may be gross evidence of small, white Although there are almost 1,500 species of Culicoides
to grey streaks of necrotic tissue in the myocardial spp. worldwide, only a very small proportion of
wall, leading to the use of the descriptive term ‘tiger around 20 have been identified as potential vectors,
heart’. and these will vary from region to region.
In any affected country, it is possible to classify
Differential diagnosis the susceptible population into three categories:
For mouth lesions, consider orf, bluetongue, feeding enzootic (transmission occurs throughout the year),
trauma, toxic plant or chemical induced stomatitis epizootic (mainly in more temperate areas, where
and, in an individual animal, renal failure and urae- transmission is seasonal) and incursive (experience
mia. For foot lesions consider scald, foot rot, blue- outbreaks when local climatic conditions favour dis-
tongue and chemical insult. ease transmission by vectors). There is much over-
lap, however, and local BTV status is also influenced
Treatment/management/control by livestock movements, particularly movement of
Treatment is rarely attempted, with control pre- susceptible animals into infected areas during the
dominantly based on statutory identification of midge transmission period.
infected premises and slaughter of infected and in- Bluetongue is a disease listed under the OIE
contact animals – a so-called ‘stamping out policy’. Terrestrial Animal Health Code and must be
However, increasingly vaccination programmes are reported to the World Organisation for Animal
being deployed to support this traditional policy, as Health.
vaccines improve in quality and efficacy and tests
become available to distinguish between naturally Aetiology
acquired and vaccine acquired antibody. It is caused by an RNA orbivirus in the family
The overall responsibility for the management Reoviridae. Twenty-four different serotypes have
and control of any outbreak rests with the animal been identified and the ability of each strain to cause
health policy of each country, underpinned by the disease varies considerably.
global control measures that are in place at the time.
The World Reference FMD Laboratory is at the Pathophysiology
Pirbright Institute in the UK. Worldwide, the disease is most severe in sheep.
Infection in goats may be asymptomatic, with
Bluetongue goats merely acting as reservoirs of infection.
Definition/overview Even when co-located with severely affected
Bluetongue is an infectious, non-contagious arthro- sheep, clinical signs may be mild, with lower
pod-borne viral disease of ruminants. Although morbidity and mortality. Available information on
goats can develop clinical disease, it is not common the pathogenesis of BTV in goats is minimal and
and usually fairly mild compared with disease in is mainly extrapolated from known information in
sheep. The causative agent, bluetongue virus (BTV), sheep. Following skin inoculation of infection by
has a worldwide distribution, including Africa, Asia, biting midges, initial replication occurs in local
Australia, Europe, North America and several islands lymph nodes, resulting in more generalised dis-
in the tropics and subtropics, but is confined mainly tribution and viraemia. The virus then appears to
have a predilection for vascular endothelium cells, serology will confirm infection. Gross pathology is
leading to thrombosis, haemorrhage and oedema as described above under pathophysiology and clini-
in affected tissues, most notably in the mouth, cal signs.
oesophagus, rumen and skin. This in turn results
in hyperaemia, erosion and ulcer formation, with Differential diagnosis
clinical signs including stomatitis, glossitis, rhini- Includes peste des petits ruminants, FMD, conta-
tis and enteritis. gious pustular dermatitis (orf) and goat pox.

The majority of bluetongue cases in goats tend to be There is no specific treatment. The primary method
subclinical. Signs described in clinical cases include of control in endemic areas is the use of effective
pyrexia, loss of appetite and milk yield with hyperae- vaccines, administered to give protection during risk
mia and mild erosive damage to the oral mucosa. In periods, which are linked to midge activity. Vaccines
the occasional more severe case, these oral changes used have to reflect the local serotype present or be
may progress to ulcerative and necrotic changes to multivalent, as a single serotype vaccine will give
the tongue, lips and gums and nostrils (Fig. 17.4), little or no protection against another serotype.
resulting in marked salivation. Diarrhoea may Additional control methods are aimed at reducing
also develop. In an outbreak of bluetongue in the the exposure to midges, by moving stock indoors
Netherlands in 2007, small papular lesions were when midge activity is high (early evening and dusk,
described on the skin of the udder (Fig. 17.5). humid still days), providing protective curtains
around openings in the buildings, and using insect
Diagnosis repellents on the goats and in their environment if
Due to the milder signs exhibited by goats, disease approved for use in food producing animals.
may be overlooked unless more severe signs are evi- In addition, control includes keeping disease out
dent in other susceptible in-contact species such as of clean areas by sourcing from known BTV-free
sheep. If suspected, antigen detection techniques or areas, and testing and quarantining on arrival.
Fig. 17.4 Mild lesions of bluetongue on the muzzle Fig. 17.5 Mild lesions of bluetongue on the udder
of a goat (Dutch outbreak 2007; courtesy GD Animal of a goat (Dutch outbreak 2007; courtesy GD Animal
Health, Deventer, the Netherlands). Health, Deventer, the Netherlands).
328 Chapter 17
Tuberculosis zoonotic disease when goats and humans are in

Definition/overview close contact. TB organisms in milk are inactivated
Although not commonly reported in goats, they by pasteurisation.
are susceptible to infection with bovine, avian and
human tuberculosis (TB) infections. They can act as Aetiology
spillover hosts to bovine TB in those areas in which In general mammals are infected with the Mycobacterium
the infection is firmly established in the cattle and tuberculosis (MTB) complex, with Mycobacterium bovis
associated wildlife populations, such as the UK in the type species in cattle, Mycobacterium avium in birds
which the badger is the main wildlife host. Equally, and Mycobacterium tuberculosis in humans. The causative
sporadic cases of avian TB occur when goats are organisms are referred to as tubercle bacilli, and are
kept in close contact with domesticated or wild birds very slow growing in the laboratory, requiring special-
infected with and excreting the avian TB organ- ist media. They show an acid-fast staining character-
isms. There are occasional reports of human TB istic. M. bovis has been further divided into a series of
being passed from an infected owner or keeper to spoligotypes – this technique has revolutionised the
their goat (usually a pet animal). It is an important epidemiological investigations of incidents and break-
downs in the UK.
Pathophysiology
Infection is acquired either orally or by inhalation
from other infected animals, birds or contaminated
environment. Nursing kids can be infected via con-
taminated milk or colostrum. M. bovis has a predilec-
tion for the respiratory tract and M. avium for the
alimentary tract. M. bovis abscesses can develop in
the lung parenchyma (Fig. 17.6), with more typical
TB granuloma formation in lymph nodes (Fig. 17.7)
and on serosal surfaces such as the pericardial sac
and pleura. In advanced cases observed in the UK,
Fig. 17.6 Bovine tuberculosis lesion in lung lobe of other widely distributed visceral lesions were evident
a Golden Guernsey goat. Note the liquid pus (rather (Fig. 17.8). Unlike in cattle, the pus is often liquid
than caseous as in cattle).
Fig. 17.7 Bovine tuberculosis lesion in retropharyngeal Fig. 17.8 Miliary bovine tuberculosis lesions in
lymph nodes. (© Crown Copyright 2017. Used with kind liver tissue. (© Crown Copyright 2017. Used with kind
permission of the Animal and Plant Health Agency.) permission of the Animal and Plant Health Agency.)
(not caseous) and can erode into airways, resulting in programmes, which will vary from country to coun-
rapid spread among housed goats. try depending on the level of infection and involve-
ment of wild life reservoirs. Most of these are aimed
Clinical presentation at controlling disease in cattle, but also include its
In countries where bovine TB occurs, clinical control in other susceptible species. There are no
signs reported include weight loss, drop in milk readily available treatments, and control is most
yield, coughing and other non-specific respira- often based on a test and cull policy. Sound biosecu-
tory signs such as lagging behind when driven. rity is important in keeping disease out, and when
However, many infected goats show few clinical wildlife sources are an issue, needs to be extensive
signs, with infection only being detected during and well adhered to.
PME or meat inspection or following surveillance
screening. Clinical signs associated with avian TB Anthrax
are more non-specific, with most cases being iden- Definition/overview
tified on PME. Anthrax is an overwhelming bacterial infection rec-
ognised in many livestock species worldwide. It is
Diagnosis endemic in many tropical and subtropical regions
The first cases in an incident are often detected of the world, and a sporadic problem in many
either at meat inspection or PME, with the typi- other countries where it may be notifiable (such as
cal TB granulomata and lung abscesses being in the UK). It is not a common problem in goats
identified. Microscopical examination may dem- compared with the number of cases reported in

onstrate the acid-fast organisms in ZN-stained other domestic and wild ruminants. Anthrax is also
smears, with confirmation by specialist laboratory of zoonotic importance.
cultures. In the live goat, the traditional diagnos-
tic test has been the single intradermal compara- Aetiology
tive cervical test (SICCT) – or ‘TB skin test,’ as Caused by Bacillus anthracis, a spore-bearing, anaero-
used in cattle. In the UK, as part of a coordinated bic, gram positive, rod-shaped organism. Spores can
effort to control TB, a number of other tests have remain dormant for 50 years or longer.
been applied. These include the gamma-interferon
test and, following the genomic sequencing of the Pathophysiology
M. bovis organism, molecular techniques linked to Infection is via the oral route, typically by grazing
individual and multiple antigen assays are being in areas in which the soil has become contaminated
developed. These latter techniques are showing by dormant spores (often brought to the surface
promising results in infected goat herds. The use by earth movement or flooding and soil erosion).
of Johne’s disease (M. avium subsp. paratuberculosis) This may be the reason the disease is less com-
vaccines may complicate the interpretation of some monly reported in goats, which tend to feed above
of these tests. ground level. Once ingested, the endospores ger-
minate at the site of tissue entry and then spread by
Differential diagnosis the circulation to the lymphatics, where the bacte-
Respiratory presentation needs to be differentiated ria continue to multiply, producing powerful tox-
from lungworm, pasteurellosis and mycoplasma ins resulting in an overwhelming septicaemia and
infections. If presented as weight loss without obvi- toxaemia.
ous respiratory signs, consider Johne’s disease, para-
sitic gastroenteritis and undernutrition. Clinical presentation
The disease is invariably peracute in its course and
Treatment/management/control many affected animals present as sudden death, often
TB is an OIE listed disease and is most often con- with blood exuding from mouth, nostrils or anus.
trolled by nationally operated coordinated control If alive, they are profoundly dull and depressed with
330 Chapter 17
severe pyrexia extending over a course of a few hours wear gloves and a facemask as a minimum protec-
to a few days. tive barrier.
To prevent wider spread within the herd, the
Diagnosis carcase should not be moved until anthrax is ruled
If anthrax is suspected, a PME is highly inadvisable, out, temporarily fencing it off from any herd
as this would potentially release spores thus fur- mates. If confirmed, potentially contaminated soil
ther contaminating the environment and acting as or bedding is removed and the area disinfected.
a severe zoonotic risk. Smears made from peripheral The water agency and milk buyer may have to be
blood (ear or tail) stained with McFadyens polychro- informed.
matic methylene blue will show the characteristic
pink staining capsules (Fig. 17.9). New and emerging diseases
Worldwide, a number of ‘new’ or ‘emerging’
Differential diagnosis diseases have been described in goats and in
For sudden death includes enterotoxaemia and other other ruminant livestock species. For example,
septicaemic conditions such as listeriosis and sal- bovine spongiform encephalopathy (BSE) and
monellosis, clostridial disease, plant and chemical Schmallenberg virus infection were both newly
toxicities, bloat or acidosis, hypomagnesaemia and recognised diseases in the UK and Germany, and
lightning strike. then much of Europe, respectively, neither hav-
ing been reported previously around the world.
Treatment/management/control Locally emerging diseases may be the result of
Treatment is often disappointing because of the movement of animals, animal (by-)products, per-
rapid course of the disease. High doses of anti- sonnel or vectors such as midges.
biotics such as penicillin or tetracycline may be As an example, at the time of publication there
tried, together with supportive care. In endemic is concern in Europe of a possible incursion of Rift
areas, livestock may be vaccinated annually with Valley fever. Its geographical distribution in 2016
some success. is shown in Fig. 17.10, essentially in sub-Saharan
The zoonotic potential of the disease cannot be Africa. One of the reasons for this concern follows
overemphasised. Anyone handling infected car- the incursion of BTV by an apparent leap from this
cases, their skins, or fixtures and fittings poten- same area in Africa to Northern Europe.
tially contaminated with infected blood should Many countries have strict legislation in place
to minimise these risks, including restrictions on
animal movements and strict policies for visitors
at entry points such as airports. The movement of
bluetongue infection into northern Europe from its
more traditional locations in southern Europe and
North Africa was a good example of midge-borne
infections which, being airborne, are more difficult
to prevent, with emphasis placed more on exami-
nation of meteorological and other data to predict
incursion of disease.
Underpinning prompt identification of these
types of disease is a comprehensive disease surveil-
lance gathering and reporting system, based on clin-
ical observation, routine laboratory testing, border
controls and import/export testing, PME and meat
Fig. 17.9 Positive anthrax blood smear. Note the inspection.
pink capsular stain.
Egypt
Saudi Arabia
Mauritania
Mali Niger
Sudan Yemen
Senegal Chad
Gambia Burkina
Guinea Faso
Nigeria Somalia
Ethiopia
Central African South Sudan
Cameroon Republic
Uganda
Congo Kenya
Gabon
Democratic Republic
of the Congo
Tanzania
Comoros
Angola Malawi
Zambia
Mozambique Madagascar
Zimbabwe
Namibia Botswana
South Africa
Fig. 17.10 Map showing the geographical distribution of Rift Valley fever virus in 2016. Blue: endemic areas
or with substantial outbreaks; green: few cases, periodic virus isolation or serological evidence; brown: status
unknown. (Source: Centers for Disease Control and Prevention, Atlanta.)
CHAPTER 18
ANAESTHESIA, FLUID THERAPY, EUTHANASIA

333
SEDATION under sedation, because the airway will not be pro-

tected by an ET tube. Blindfolding the animal often
General principles prolongs and deepens the level of sedation, and the
For surgical procedures, general anaesthesia (GA) is surroundings should be quiet. The risk of hypother-
preferable over sedation, because goats do not toler- mia must be addressed (see General anaesthesia).
ate physical restraint under sedation as well as cattle
and sheep. In addition, apnoea is relatively common, Sedatives
so it is an advantage having an endotracheal (ET) Drug licensing and prescribing restrictions limit the
tube in place. To reduce the risk of aspiration of number of available agents for goats in many coun-
saliva or regurgitated rumen fluid in a goat under tries. In the UK, for example, only the first three of
sedation, the animal is positioned with the nose the following sedatives can be used under the pre-
below the level of the throat or upper neck (e.g. by scribing cascade at the time of publishing:
placing a rolled up towel under its neck; Fig. 18.1).
Starvation, if possible (see General anaesthesia for •• Xylazine hydrochloride: 0.03–0.05 mg/kg
protocol), is particularly important for procedures i/v or up to 0.1 mg/kg i/m. Ruminants show
marked differences in sedative response.
Therefore, if a goat is likely to have repeated
procedures (e.g. wound dressing), a note of
the dose rate used and its effect should be kept
on the case file. ‘Topping-up’ can be difficult
with xylazine HCl, with often little noticeable
response to additional doses. Especially after
i/m administration, sufficient time (minimum
10 minutes) must be allowed for sedation to take
effect prior to disturbing the animal, otherwise
the full effect may not be achieved. Potential
side-effects include bradycardia, hypotension,
hypoxaemia and pulmonary oedema. Xylazine
HCl should be avoided in cases with urinary
obstruction, as it increases urine production.
It has oxytocin-like effects, potentially leading
Fig. 18.1 Some aspects of good anaesthesia practice. to abortion in late pregnancy or retained fetal
The nose is positioned below the larynx in case of membranes.
regurgitation; an i/v catheter enables fluid therapy and •• Detomidine hydrochloride: 0.02–0.04 mg/kg
provides immediate venous access if complications i/v. Potential side-effects are less likely
arise; the goat is on soft padding; the lowermost eye than with xylazine HCl, because of reduced
does not touch the table. Monitoring utilised here sensitivity to this sedative in ruminants and
includes pulse oximeter (on tongue), oesophageal the lack of oxytocin-like effects at low doses.
thermometer (grey tube) and electrocardiogram. Medetomidine has been used in goats at
334 Chapter 18
0.01–0.02 mg/kg i/m (or slow i/v to effect), but Preoperative starvation

is off-cascade in the UK. For elective procedures, the goat should be starved
•• Butorphanol: 0.05–0.2 mg/kg i/v or i/m. Potential prior to GA or sedation. A suitable protocol for
side-effects are not established in goats. morning surgery involves last concentrate meal
•• Diazepam: 0.2–0.4 mg/kg i/v. This is a useful 24 hours preoperative, forage removed early after-
agent in neonates or compromised patients. noon, and water removed between 10 pm and mid-
In combination with butorphanol, sedation is night. Exceptions to this protocol are neonates and
often deep enough to allow procedures such kids up to 3 months of age; they receive their last
as radiography. It appears to have an appetite milk feed at half of normal volume, or are allowed
stimulating effect in some goats. Similarly, to suckle, 2 hours prior to surgery. This reduces
midazolam is a useful agent, for example for the risk of hypoglycaemia. In peak lactation does,
premedication, and may be given i/m as well as supplementation with an energy precursor such as
i/v, at a dose rate of 0.3–0.6 mg/kg. propylene glycol may be indicated.
•• Alfaxalone: 2–3 mg/kg slow i/v to effect. Rumen tympany may develop during GA and can
be addressed by either passing a stomach tube or, in
Reversal an emergency, by advancing a 14–16 gauge hypoder-
•• Atipamezole: 0.02–0.125 mg/kg slow i/v mic needle into the rumen via the left flank.
may be given to reverse the alpha-2 agonists
(this constitutes off-cascade use in the UK). Preoperative assessment
•• Doxapram hydrochloride also partially reverses Thorough history taking and clinical examina-
the effects of sedatives. tion is vital to highlight any particular anaesthetic
concerns. The body weight of the patient is deter-
GENERAL ANAESTHESIA mined as accurately as possible. Body condition has
an influence on retention of lipophilic drugs and is
General principles noted. Where necessary, circulating volume deficits
Regardless of the type of GA, an intravenous cathe- and electrolyte imbalances are corrected as much as
ter should be placed to allow rapid intervention when possible prior to induction.
necessary (Fig. 18.1). The jugular, cephalic, saphe-
nous or ear veins are all suitable. Intraoperative support
For most surgical procedures, consideration Attention must be paid to positioning to prevent neu-
should be given to: ropathies or myopathies. Padding of prominent bony
points and supporting legs in their natural posture
•• Preoperative antibiosis (administered at least is advisable. Eyes are protected from trauma, reflux
30 minutes prior to the start of surgery to ensure material or surgical scrub by applying a suitable ocu-
tissue perfusion). lar gel and avoiding contact between the lowermost
•• Tetanus cover. Up-to-date vaccination cover eye and the operating table (Fig. 18.1). Placing the
(i.e. at least 14 days should have elapsed since head onto a 'doughnut-ring' is useful for this.
full primary course or last booster dose, but not Where possible, i/v fluids are administered
more than 6 months since last booster injection). throughout at a rate of 3–5 ml/kg per hour (unless
Alternatively, tetanus antitoxin or an antibiotic the goat is hypovolaemic, when a higher dose is
with activity against anaerobes may be given at required). Hartman’s or lactated Ringer’s solution
the point of surgery (e.g. procaine penicillin; is suitable for most patients. In neonates or hypo-
third-generation cephalosporin is also effective, thermic goats, the addition of 1–5% glucose can be
but subject to responsible use concerns). beneficial.
•• Fly control, depending on time of year. This
may be achieved by applying, for example, Hypothermia
Battles’ Summer Fly Cream to the wound edges Goats are very prone to hypothermia. For exam-
and the use of deltamethrin pour-on solutions. ple, rectal temperature may drop to 37.5°C within
A n a e s t h e si a , Flu i d Th e r a p y, Eu t h a n a si a 335
Inhalation anaesthesia
An ET tube is placed after induction, and the ani-
mal maintained on an isoflurane and oxygen mix
(in the UK, currently the prescription cascade can
be applied to isoflurane, but not other anaesthetic
gases). When using a closed circuit, a flow rate of
2–3 litres is usually sufficient.
A 9–12 mm cuffed ET tube is suitable for adult
goats and a 5.5–7 mm tube for young goats up to
a few months of age. Placement is easiest with the
goat in sternal recumbency, with an assistant fully
extending the neck and opening the mouth with the
aid of gauze straps. A laryngoscope with an extra
long blade is invaluable (Fig. 18.3). Lidocaine spray
may be applied to the larynx.
Fig. 18.2 Preventing hypothermia. Use of ‘hot
hands’ (disposable gloves filled with hot water) and Injection anaesthesia
a towel placed underneath and around the animal to This can be achieved by top-up doses of ketamine
soak up any fluids (e.g. from scrubbing, lavage). using one-third to one-half of the initial induction
dose at a time, or by using a ketamine drip (0.2%
solution consisting of 200 mg ketamine in 100 ml of
15 minutes of induction, and may easily fall to 35°C physiological saline; dose rate is 1 ml per minute for
during surgery. Countermeasures include a warm, a 60 kg goat; 50 mg of xylazine HCl can be added
draught-free operating environment, preventing to create a double drip). Propofol (5–7 mg/kg i/v)
the animal’s coat from becoming soaked with fluids,
using warm i/v and lavage fluids, covering as much
of the body as possible (e.g. using bubble-wrap or a
Baer Hugger™) and using heat pads, hot water bot-
tles or ‘hot hands’ (Fig. 18.2).
Induction
Induction can be achieved by a single drug or a
combination of the drugs listed above for seda-
tion. For example, xylazine HCl plus butorphanol
as premedication, followed 5–10 minutes later by
ketamine at 2–4 mg/kg i/v, given slowly to effect.
Additional increments of ketamine may be given if
the level of induction is not deep enough to allow
intubation. Other induction agents, such as propo-
fol, have been used in goats, but are off-cascade in
the UK.
The induction area should be quiet and offer
good footing. Premedication is highly recom-
mended. It reduces anxiety in the patient, thereby Fig. 18.3 Endotracheal intubation. The goat is in
facilitating catheter placement and induction, can sternal recumbency with its neck and head extended;
provide analgesia (depending on agent) and typi- the mouth is held open with the aid of gauze straps; a
cally reduces the required dose of induction and laryngoscope with a long blade is used. Note that the
maintenance agents. assistant is ‘topping-up’ the i/v induction agent.
336 Chapter 18
Fig. 18.4 For recovery, the goat is placed into sternal Fig. 18.5 The patient (on the right) is returned
recumbency and the head and neck supported. The into a well-bedded pen and a rug or blanket used as
goat is extubated once clear signs of chewing and necessary. The i/v catheter (here in the cephalic vein)
swallowing are present. Note the continued use of a is retained for several hours in case of late-onset
Baer-Hugger™ against hypothermia. complications during recovery.
is suitable for short procedures and where licensed If regurgitation occurred during surgery, the ET
for use in goats. Injection anaesthesia should only cuff is left inflated during extubation, otherwise it is
be considered for procedures of up to 1 hour dura- withdrawn partially deflated.
tion. An ET tube should be placed to ensure airway Ideally, a narrow gauge tube (e.g. a dog or cat
patency and allow rapid intervention if required. urinary catheter) is available, plus oxygen, to allow
intranasal oxygenation if required. A tracheotomy
Monitoring kit should be available for the rare cases that exhibit
Eyeball position and reflexes give an indication of laryngospasm on extubation.
anaesthetic depth. Circulatory function is monitored Hypothermia reducing measures are continued
through heart rate and rhythm, mucous membrane during recovery (Fig. 18.5) and the goat’s rectal
colour and capillary refill time. Respiratory rate temperature monitored for several hours postopera-
and character and core temperature are monitored tively. Offering kids milk or adults food and an elec-
(Fig. 18.1). Adjunct tools, such as pulse oximetry, trolyte solution containing sugars as soon as possible
capnography and an oesophageal thermometer, and after recovery aids thermoregulation.
blood gas, glucose and electrolyte analysis are useful
where available. LOCAL AND REGIONAL BLOCKS
Good communication between the anaesthetist
and surgeon is important. Anaesthetic depth can be General principles
deepened prior to a particularly painful stimulus, Local and regional blocks facilitate surgical proce-
the surgeon asked to temporarily stop if the patient dures in the conscious or sedated animal. However,
shows a response, and the anaesthetist can take the even when surgery is performed under GA, they
surgical manipulation into account when interpret- should be employed whenever possible, both to allow
ing patient parameters (e.g. bradycardia induced by a lighter level of GA, and to aid postoperative anal-
visceral traction). gesia management. Standard aseptic techniques must
be used when applying blocks. Prior to injecting the
Recovery local anaesthetic, one should always aspirate to ascer-
The goat is placed into supported sternal recum- tain that no blood or cerebrospinal fluid (CSF) is pres-
bency as soon as possible. Extubation is delayed until ent – if present, the needle is redirected. Sufficient
obvious signs of chewing are present (Fig. 18.4). time needs to be allowed for a block to take effect.
Drugs volume of anaesthetic rule as described above

Goats are more sensitive to local anaesthetic agents, for lidocaine HCl); however, the true safe dose is
therefore a lower maximum dose rate compared with likely to be much below this level. Procaine HCl
cattle and sheep needs to be observed. Drugs may has lower tissue distribution, therefore it must be
be diluted between 1:1 to 1:3 drug to sterile saline more accurately placed to be effective.
to increase the volume available for injection (and •• Bupivicaine (off-cascade use in the UK): up to
thereby increase drug distribution across the tar- 2 mg/kg. Onset is within 20 minutes, with a
get tissue or site). Many veterinary preparations of duration of several hours.
lidocaine HCl and procaine HCl contain adrena-
line (syn. epinephrine) – these must not be used for Specific blocks
epidural blocks, intravenous regional anaesthesia The volumes stated in this section all refer to 2%
(IVRA) or distal limb ring blocks. It may be neces- lidocaine HCl and adult goats. To avoid overdos-
sary to source a human product that only contains ing in kids, similar volumes, but of 0.7–1% lidocaine
the anaesthetic agent. Anaesthetics that can be used HCl, may have to be used. In general, the smallest
for local or regional blocks include the following: gauge needle possible should be used.
•• Lidocaine hydrochloride 2% (under prescription Paravertebral

cascade in the UK): up to 6 mg/kg. As a rule of A paravertebral block is suitable for laparotomy,
thumb, a maximum of 0.3 times the animal’s body offering the advantage over regional infiltration of
weight can be given in millilitres (e.g. a 75 kg desensitising the entire flank, including the perito-
goat can receive 22.5 ml of 2% lidocaine HCl). neum. For an exploratory laparotomy, nerves T13,
Onset is within 10–20 minutes and duration about L1 and L2 are blocked. For a caesarean section,
60–90 minutes (up 120 minutes if the preparation blocking nerve L3 in addition is useful, but may lead
contains adrenaline). Signs of toxicity as a result of to moderate ataxia in the doe. Several techniques
overdosing include nystagmus, muscle twitching, may be employed.
convulsions, opisthotonus, hypotension and The proximal technique is described here. A 5 cm
respiratory arrest. If signs persist for more than (2 in) long, 18–20 gauge hypodermic needle is placed
1–2 minutes, diazepam is given at 0.1 mg/kg (off- at the cranial edges of the first to third lumbar ver-
cascade use in the UK) or thiopental at 5 mg/kg, tebrae (plus fourth for nerve L3, if desired), at the
plus fluid and respiratory support. mid-point between the spinal column and the tip
•• Procaine hydrochloride 5%: no information on of each vertebra. The needle is advanced through
maximum dose is available. The authors have the interarcuate ligament (syn. ligamentum flavum;
used it at up to 15 mg/kg without apparent located just ventral to the level of the bone), and 4 ml
side-effects (following the same body weight to instilled (Fig. 18.6). The needle is then withdrawn
(a) (b)
Fig. 18.6 Right lateral view of the lumber spine showing: (a) approximate course of the dorsal and ventral
branches of nerves T13 (white), L1 (yellow) and L2 (green); and (b) the position of the needle to anaesthetise the
ventral branch of L1.
338 Chapter 18
to above the ligament and 3–4 ml injected while recumbent, requiring assistance to stand during
withdrawing the needle further. recovery.
Successful blocking of the dorsal branches will For both blocks, the local anaesthetic is admin-
lead to loss of skin sensation. Curvature of the spine istered through the sacrococcygeal (young animals)
towards the blocked side (i.e. convex), sweating and or first intercoccygeal (mature animals) joint. While
rising steam are often observed in a successful block. moving the tail up and down, the most cranial mov-
ing joint is located. A 2.5 cm (1 in), 20 gauge needle is
Regional flank infiltration advanced midline, with the hub angled 10–15 degrees
The flank may be desensitised by injecting local caudally. The needle may be advanced to the ventral
anaesthetic subcutaneously and intramuscularly in a floor of the spinal canal, then slightly withdrawn and
linear fashion. A straight-line pattern along the line the local anaesthetic injected. There should be no
of incision requires less local anaesthetic (thereby resistance when injecting.
reducing the risk of toxicity), but may interfere with The tail becoming limp indicates a successful
wound healing. An alternative pattern is an inverted block.
L, with the downward arm towards the last rib and
the horizontal arm running parallel to the trans- Epidural – lumbosacral
verse processes. It is important with regional blocks This desensitises the flank, pelvis and hind leg.
to infiltrate all tissue layers. During onset of the block, loss of skin sensation
is monitored and, once the most caudal rib region
Epidural – caudal has been reached, the animal’s front is elevated to
A low caudal epidural block is achieved at a dose prevent further cranial migration of the block and
rate of 0.5 mg/kg, leading to desensitisation of the potential paralysis of the intercostal muscles. The
perineum, tail and usually scrotum. Xylazine HCl animal will become recumbent, requiring assistance
at 0.07 mg/kg may be added for prolonged effect. to stand during recovery.
A dose rate of 2–4 mg/kg leads to a high caudal Two to four mg/kg (equivalent to 1 ml/5–10 kg) is
block, desensitising the hind leg, udder, pelvis and injected into the lumbosacral space. The technique
caudal abdomen. For the high epidural, the animal’s is the same as for CSF collection (see Chapter 8);
hindquarters may be raised after administration for however, the needle is not advanced through the
5–10 minutes to aid drug distribution. If unilateral dura mater (i.e. it remains in the epidural space
tissue desensitisation is required, the desired side is (Fig. 18.7). If the subarachnoid space is inadver-
placed lowermost initially until the block has taken tently entered, there are two options: (a) the needle
effect. With the high block, the animal will become is withdrawn into the epidural space and the full
(a) (b)
Fig. 18.7 (a) Target area and landmarks for a lumbosacral epidural shown on a skeleton, and (b) needle in
position in the patient.
Fig. 18.8 (a) For a

mandibular block, a needle
is advanced on the medial
aspect of the mandible to a
point half-way between its
ramus and the mandibular
joint (indicated by
thumb and index finger,
respectively, here in an
alpaca). (b) Skull with a
blue marker inserted into
the target area (foramen of
(a) (b)
the mandibular nerve).
calculated volume administered; or (b) one-third of

the calculated volume is administered into the sub-
arachnoid space.
Mandibular
This is a useful block for dental work involving the Y
mandibular arcade. It also desensitises the intra- and
extraoral soft tissue rostral to the foramen. Three
to five ml are injected s/c on the medial aspect of
the mandibular ramus, half-way between its ventral
border and the mandibular joint (Fig. 18.8).
X
Mental
A mental block desensitises the rostral mandible, Fig. 18.9 Target positions for a mental nerve block
including the mandibular symphysis and incisors. It is (X) and infraorbital nerve block (Y, with needle
useful for dental procedures and repair of a fractured inserted), shown on an ovine skull.
symphysis. The mental foramen can be felt on the
lateral aspect of the mandible, half-way along the dia- 1–3 cm above the maxillary premolar teeth and 1–3 cm
stema between the incisors and cheek teeth (Fig. 18.9). cranial to the facial tuberosity, usually marked by a pal-
One to two ml is injected over the nerve as it exits the pable depression in the bone (Fig. 18.9). One to two ml
foramen or, for more reliable anaesthesia of the jaw and is injected over the nerve as it exits the foramen. One to
incisors, 1–3 ml is injected into the canal (with care). three ml injected into the canal (with care) may provide
anaesthesia of the first and second premolars.
Infraorbital
This block desensitises the upper lip and nose rostral Auriculopalpebral
to the foramen, and is useful to deal with traumatic An auriculopalpebral block is used to inhibit motor
injuries in this area such as dog bites. The landmark is function of the eyelids; for example, to facilitate
340 Chapter 18
Fig. 18.11 Insertion point and direction of the needle

Fig. 18.10 Approximate target points for an for a Peterson block (shown here on a bovine skull).
auriculopalpebral block (short arrow) and to block the
cornual branches of the lacrimal nerve (arrowhead)
and infratrochlear nerve (long arrow). Retrobulbar
A retrobulbar block is an alternative to desensitise
examination of the eye when blepharospasm is pres- intraorbital soft tissue structures. Some local anaes-
ent or to reduce movement during ocular surgery. thetic may be deposited superficially as the needle is
(Note: This block does not desensitise the eye- withdrawn, thereby blocking the eyelids.
lids – an additional block such as line infiltration A 5 cm (2 in) needle is in turn inserted at the 12,
is required.) One to two ml is injected s/c half-way 3, 6 and 9 o’clock positions around the orbit, through
along a line drawn from the lateral canthus to the the eyelid, and advanced to the back of the orbit.
base of the ear (Fig. 18.10). Two to three ml are deposited each time.
Peterson Cornual
A Peterson block will desensitise the intraorbital A cornual block may be suitable for disbudding kids
soft tissue structures; for example, for enucleation. (take care not to exceed the toxic dose – see above) or
(Note: The eyelids will not be desensitised by this as an adjunct to GA when dehorning adults. The cor-
block [i.e. they must be blocked separately]). The nual branches of both the lacrimal and infratroch-
risk of injecting local anaesthetic into the optic lear nerve must be blocked. One to two ml is injected
nerve is probably similar to the retrobulbar block, alongside the temporal ridge, one-third to half-way
but needle placement is away from the main ocular the distance from the lateral canthus of the eye to
structures. the lateral aspect of the horn base. Another 1–2 ml is
A 5 cm (2 in) hypodermic or spinal needle is injected at the dorsomedial aspect of the orbit, close
shaped into a moderate curve (about 30 degrees) to its margin (Fig. 18.10).
and, with the curvature pointing rostral, is
inserted in the corner formed by the zygomatic Intravenous regional anaesthesia
arch of the temporal bone ventrally and the supra- IVRA is useful for interventions involving the lower
orbital process rostrally (Fig. 18.11). The needle limb and foot, including claw amputation or joint
is advanced fully to its hub. It may become caught lavage. A tourniquet is placed either just below or
on the coronoid process of the mandible. If this above the carpus or, in the hind leg, just below or
is suspected, the needle is slightly withdrawn and above the tarsus. (Note: If above the tarsus, the
redirected. Five to seven ml are instilled at the depression either side of the Achilles tendon must
depth of the orbit. be padded to achieve adequate occlusion.) A short
ANALGESIA
General principles
The value of multimodal analgesia is well recog-
nised. By using different classes of analgesic drugs,
which act on different parts of the pain pathway, a
complimentary effect is achieved. This produces
a better level of analgesia and, potentially, the doses
of individual drugs can be kept lower, thereby reduc-
ing the risk of side-effects. An example combination
is the use of a local block, a NSAID and an opioid.
Ideally, analgesia is initiated pre- and perioperatively
to limit the amplification of the pain pathway and
central sensitisation. Limited information on effec-
tive dosing regimes is available in goats, but options
that are recognised as useful, either through phar-
macological studies or field observations, are listed.
Fig. 18.12 Intravenous regional anaesthesia using a Pain scales remain in their infancy for livestock
butterfly catheter (shown on a bovine limb). species and there is no well-validated score for goats.
Some aspects of the Glasgow Composite Measure
21–23 gauge needle or, preferably, butterfly cath- Pain Scale (CMPS) can be extrapolated to judge the
eter is placed into any discernible superficial vein likely presence of pain and discomfort. For exam-
below the tourniquet and 1 ml/15 kg of local anaes- ple, difficulty rising and abnormal gait, response to
thetic injected (Fig. 18.12). Care must be taken that gentle pressure onto surgical wounds, pain-related
the tourniquet remains tightly in place for at least vocalisation such as bruxism, restlessness or weight-
20 minutes to avoid local anaesthetic entering the shifting, or avoidance behaviour.
general circulation.
Opioids
Brachial plexus •• Butorphanol: 0.1 mg/kg i/v, or 0.1–0.2 mg/kg
The distal brachial plexus block desensitises the leg i/m. Suggested frequency is every 4–6 hours
from the elbow distally. From the cranial aspect of (extrapolated from other species). It is a less
the front leg, a needle is inserted horizontally at the potent analgesic than buprenorphine, but can
medial aspect of the shoulder joint, aiming at the cos- currently be used under the prescription cascade
tochondral junction of the first rib. Local anaesthetic in the UK. Potential side-effects are not known
is injected as the needle is withdrawn at a dose rate of in goats.
2–4 mg/kg lidocaine HCl or 0.5–1 mg/kg bupivacaine. •• Fentanyl: in other species, the target drug
A proximal block, which desensitises the leg from release rate is 1–5 µg/kg/hour (translating to
the mid-humerus distally, is possible, but technically a minimum of 1 × 5 mg patch, which delivers
challenging. 50 µg/hour for an adult goat). It takes up to
12 hours to reach peak plasma concentrations,
Teat blocks with a duration of about 72 hours. Apply to
Options to desensitise the teat include: ring block at hairless and well-cleansed and dried skin
the base of the teat (avoid adrenaline), IVRA using with the aid of a bandage (e.g. axilla, side of
a household rubber band as a tourniquet around the neck, lateral or medial antebrachium). Its use
base of the teat, line block in the shape of an inverted is currently off-cascade in the UK. Potential
V proximal to a teat wound, and infusion into the side-effects include bradycardia, respiratory
teat canal and cistern (to block the mucosal lining). depression, urinary retention and constipation.
342 Chapter 18
•• Morphine: 0.05–0.25 mg/kg i/v or i/m, titrated are regarded as adequate for analgesia in other
to effect. Analgesic duration is approximately species. For the use of oral meloxicam, it should
2–4 hours. Its use is currently off-cascade in the be noted that the calibration of the dispensing
UK. Potential side-effects include (as with most syringe provided with the product in the UK is
opioids) negative effects on the gastrointestinal 0.1 mg/kg for the dog solution and 0.6 mg/kg for
tract including ileus; however, the specific risk the horse solution.
and its scale in goats is not known.
•• Buprenorphine: 0.002–0.01 mg/kg i/v or i/m. It Corticosteroids
provides the longest duration of the injectable Corticosteroids, via their strong anti-inflammatory
opioids, with a possible duration of 6–8 hours. action, have some analgesic properties. They must
However, its use is currently off-cascade in the not be used in pregnant does, and other potential
UK. It is also relatively expensive. side-effects such as immunosuppression must be
taken into account. Betamethasone and dexametha-
Non-steroidal anti- sone are suitable for the purpose of analgesia, with
inflammatory drugs an anti-inflammatory effect of 36–72 hours.
NSAIDs should be used whenever possible.
Contraindications include hypovolaemic shock or NMDA receptor antagonists
renal compromise. Ideally, they are given at least Ketamine can be given at subanaesthetic doses as
30 minutes prior to surgery. Avoid administration part of a multimodal regime, providing good somatic
during surgery, as nephrotoxic effects may occur in analgesia. A single dose of 0.1–0.5 mg/kg i/v, i/m or
the sedated or anaesthetised animal because of com- s/c; or i/v infusion at 0.4–1.0 mg/kg/hour, with or
promised perfusion. Ketoprofen, flunixin meglu- without a loading dose of 0.1–0.5 mg/kg.
mine, carprofen and meloxicam have all been used in
goats without apparent side-effects. The recommen- FLUID THERAPY
dations stemming from pharmacological studies of
meloxicam in goats are summarised below. For the Assessing hydration status
other NSAIDs, the cattle doses are typically used in Skin tent is a useful measure in the field: when the
the absence of goat-specific information. upper eyelid is pinched, it should return to its nor-
mal position within 1–2 seconds. A delayed response
•• Meloxicam: 0.5 mg/kg i/v. Ideal dosing of 3–5 seconds indicates about 5–7% dehydration.
frequency is unknown, but for analgesia q8–12h With 10% dehydration, the skin turgor is typically
may be required. This is based on its rapid lost completely (i.e. the skin fold remains).
distribution and the plasma concentration As dehydration increases, the mucous membranes
believed to provide effective analgesia in the become drier. From about 8% dehydration, the eyes
horse being maintained in the goat for about become sunken; however, the animal’s body fat
8 hours. No drug was detectable 72 hours after reserves must be taken into account when assessing
administration in goat studies. Preliminary eye position (with loss of retrobulbar fat in emaci-
studies in goat kids (using the i/m route), showed ated animals).
slower clearance compared with adults (i.e. care Anuria sets in at 10% dehydration and above,
must be exercised with frequent dosing in young and the animal becomes weak and/or recumbent,
animals). with a weak pulse. From 12%, the animal becomes
•• Meloxicam: 0.5 mg/kg per os q24h. The drug moribund.
showed 79% (+/− 19) bioavailability after oral PCV increases with extracellular fluid (ECF) loss
administration. It takes about 15 hours to reach and, after several hours delay, blood loss. Total pro-
maximum plasma concentration, therefore tein tends to increase with ECF loss, unless there is
interim analgesia must be provided. Oral a protein-losing process present. Lactate can be used
dosing resulted in plasma concentrations that to assess hypovolaemia and tissue perfusion.
Fluid rates Choice of fluids

The maintenance rate is 2 ml/kg/hour (equivalent to Crystalloids
50 ml/kg/day), translating to 1 drop every 1.5–2 sec- Crystalloids are useful to replace ECF losses and as
onds for a 70 kg goat when using a giving set deliver- maintenance fluids. Examples and their characteris-
ing 20 drops per ml. Remember that fluids will be tics are:
excreted via the kidney. As a rule of thumb, of every
litre of i/v crystalloid fluid administered, only a •• Normal saline (0.9%): isotonic, acidic.
quarter remains in circulation after 1–2 hours. This •• Hartmann’s solution (syn. lactated Ringer’s
highlights the need for continued fluid administra- solution): isotonic, alkaline; contains potassium,
tion until the patient is fully stable. calcium and bicarbonate or lactate in addition to
Goats are relatively susceptible to pulmonary sodium and chloride.
oedema when being overhydrated. Care must be •• Glucose/dextrose solution (5% or 4% plus 0.18%
taken with ‘shock-doses’ of fluids (10–20 ml/kg/ NaCl): slightly hypotonic, acidic. (Note: The
hour). Once life-threatening hypovolaemia has been energy contained in these solutions is negligible
addressed, the remaining fluid deficit is best replaced in terms of the animal’s daily requirements.)
over 12–36 hours. During surgery, fluid rates may •• Hypertonic saline (7.2%): hypertonic, acidic.
be increased to 5 ml/kg/hour, providing the goat is Main indication is rapid restoration of
monitored for overhydration. circulating volume. In large animals, it is widely
used because of easier logistics compared with
Route of administration isotonic fluids. However, its effect is short-lived
If some rumen activity is present, oral fluids may be (<2 hours) and isotonic fluids are preferable.
considered unless the deficit needs to be restored Administer at 4 ml/kg over 10–20 minutes.
rapidly. They should ideally contain electrolytes. In Have clean, warm drinking water within reach
kids, absence of a suck reflex indicates likely gastro- of animal during administration. If the animal
intestinal tract stasis, and fluid should be adminis- does not drink voluntarily, administration via
tered i/v to ensure absorption. stomach tube is required.
For the i/v route, placement of an intravenous •• Potassium chloride: add at 10 mEq/litre main
catheter is highly advisable. For fluid therapy on fluid where hypokalaemia is present. Adjust fluid
farm, the catheter may be secured with superglue, rate so that it does not exceed 0.5 mEq/kg/hour.
thereby enabling the owner to remove it. Suitable •• Sodium bicarbonate (8.4%): for marked
veins include the jugular, cephalic, saphenous and metabolic acidosis. Ideally, the deficit is
ear veins (Fig. 18.13). calculated based on blood gas analysis.
The formula using total CO2 (TCO2) is:
(24 – measured TCO2) × 0.3–0.5 body weight

(in kg) = mmol of NaHCO3 required
The 8.4% solution is molar (i.e. 1 ml = 1 mmol)
(Note: The true fluid compartment that is affected

is 0.6 × body weight; using a factor of 0.3–0.5 pro-
vides a safety buffer, but may result in underdosing.)
Colloids
Colloids act as plasma volume expanders and are
useful to rapidly expand circulating volume. They
Fig. 18.13 Use of the jugular vein for intravenous fluid may also be considered in animals with hypopro-
therapy, and monitoring urine output, in a Pygmy goat. teinaemia (TP <35 g/l) to prevent oedema formation.
344 Chapter 18
Colloids remain in circulation longer than crystal- •• Method, including back-up option if first
loids. However, they do draw fluids from the inter- method fails.
stitial and intracellular compartments and therefore •• Safety, with potential risks considered from the
should be combined with isotonic fluids, especially in animal, the environment and the method of
patients already dehydrated. Products in this group euthanasia.
include: 6% hetastarch or pentastarch, Gelofusine®, •• Disposal of the cadaver.
Haemaccel®, dextran 40 or 70, 7.2% NaCl with •• Legal aspects (including animal welfare, drug and
starch, and Oxyglobin®. It is important to check the firearm regulations, environmental protection).
datasheet for potential side-effects (e.g. coagulopathy)
or contraindications prior to using these products. Animal welfare, in particular avoidance of undue
Colloids are given at 5–10 ml/kg and should not stress and discomfort, must be safeguarded during
be administered at more than 25% of the normal cir- the entire procedure. Signs of death include ces-
culating volume of the patient at any one time. sation of heartbeat and respiration, loss of corneal
reflex and full dilation of the pupils. Regardless of
Plasma method used, the animal should be monitored for
The two main indicators for a plasma transfusion 15–20 minutes after apparent death.
are: (1) failure of passive transfer in the neonate; and Sedation may be used where firearms are
(2) marked hypoalbuminaemia in mature animals. employed, but should be avoided for lethal injection
Goat blood does not separate out readily into solids as drug distribution is often adversely affected by the
and plasma, so a centrifuge is required. Despite goats cardiovascular effects of the sedative.
having several blood groups, adverse reactions to
plasma transfusion is rare. However, adrenaline and/ Lethal injection
or dexamethasone should be available in case of a reac- An overdose of barbiturates is suitable; for example,
tion. A blood transfusion set must be used and the flow pentobarbital sodium (available as a 20–40% solution)
rate set low for the first 10–20 minutes (1 drop/second) at a dose rate of 60–120 mg/kg given as a rapid bolus.
while the goat is observed for adverse reactions. The i/v route should be used whenever possible, pref-
erably through an indwelling catheter. In addition to
Blood transfusion the jugular, cephalic and saphenous veins, the milk vein
Severe blood loss during surgery may warrant a may be used in lactating does. For injection into the
blood transfusion (as a rough guideline, once >20% ear vein, the solution should not be stronger than 20%
of blood has been lost; see Chapter 7). to avoid a burning sensation (dilute with 0.9% NaCl,
if necessary). In kids and yearlings, the intraperitoneal
EUTHANASIA route may be effective. Intracardiac injection must
never be undertaken in a conscious animal.
While being a commonly performed procedure, A quinalbarbitone sodium/cinchocaine HCl
euthanasia should always be planned carefully. combination is available in the UK (Somulose™,
Aspects to consider include: Dechra). The dose rate of approximately 1 ml/10 kg
must be given over a defined time of 10–15 seconds
•• Owner’s consent and clear, unambiguous to avoid cardiac arrest prior to loss of consciousness.
instructions that euthanasia is requested.
•• Best timing in relation to assistance, disposal, Free-bullet firearms
facilities etc. (unless necessitated immediately by Suitable weapons are:
the animal’s condition).
•• Best place, to shield herd mates from procedure, •• 0.32 calibre ‘humane killer’ or 9 mm handgun,
allow easy access to cadaver, avoid undue used with round nose lead bullets and from a
discomfort by moving diseased animal etc. short distance (5–25 cm).
•• Assistance required and emotional impact on •• 0.22 calibre rim-fire rifle, used with round nose
people present. lead bullets and from a short distance (5–25 cm).
•• Shotgun of 12, 16 or 20 bore used with 4, 5 Captive bolt

or 6 birdshot, or 0.410 calibre, held at a short A 0.22 calibre trigger-fired penetrating captive bolt
distance (5–25 cm). is suitable for veterinary euthanasia. Care must
•• Larger calibre centre-fire rifle, used outdoors be taken to use a cartridge with a suitably high-
from a distance by a trained marksman. power charge. In contrast to free-bullet weapons,
the captive bolt is placed onto the goat’s head prior
The animal’s head must be firmly restrained to to discharge. The target point is the same for all
ensure accurate placement of the bullet, aided by seda- goats, regardless of whether horned or not: mid-
tion where required. A free bullet always carries the line behind the bony mass of the poll, in a direc-
risk of the bullet exiting the animal’s body. The risk tion towards the base of the tongue (Fig. 18.14). In
of being hit by a ricocheting bullet can be reduced by neonatal kids, the bolt may be placed on the inter-
placing the animal onto soft ground and away from section of two lines drawn between the lateral can-
solid walls, avoiding enclosed spaces such as small pens thus and the opposite horn bud. Exsanguination or
or trailers and limiting the number of people present. pithing must follow immediately after the stun to
In unhorned goats, the target point is midline ensure outright death.
just above the eyes in a direction down the line of
the spine. In horned goats, if the target point on the Conditionally acceptable methods
forehead is obscured, the animal is shot from behind A non-penetrating captive bolt may be used in ani-
the poll in a direction towards the angle of the man- mals less than 10 kg bodyweight.
dible (Fig. 18.14). This approach carries a high risk In animals that are unconscious (e.g. under GA or
of the bullet leaving the animal. A shotgun is pref- where the initial method of euthanasia did not result
erable over a pistol or rifle, and the animal must be in cardiac arrest), the following may be considered:
placed onto soft ground.
When firearms are used, after collapse tonic •• Potassium chloride at 1–2 mEq/kg i/v.
activity for 10–20 seconds is followed by involuntary •• Overdose of magnesium sulphate i/v.
kicking. (Note: Immediate kicking or paddling indi- •• Exsanguination.
cates an ineffective stun.) •• Combination drug containing tetracaine
HCl, mebezonium iodide and embutramid at
4–6 ml/50 kg (T 61™, MSD Animal Health).
Emergency on-farm slaughter

of neonatal kids
The UK’s Humane Slaughter Association describes
the use of external trauma in infant kids – but this
procedure must not be used at any other age, and
only when veterinary or other skilled intervention is
unavailable.
The aim is to humanely kill the kid by delivering
a heavy blow to the head. There are two variations
of this method:
1 Hold the kid by the back legs and deliver a

firm blow to the back of the head with a blunt
instrument; for example, an iron bar or hammer.
Fig. 18.14 Target point and angle of shot when 2 Hold the kid by the back legs and swing it
using a firearm (arrow) and when using a captive bolt through an arc to hit the back of its head with
or where horns obstruct the normal firearm target considerable force against a solid object; for
(arrowhead). example, a brick wall or metal stanchion.
346 Chapter 18
With both methods, it is essential that the blow Such a procedure is very much a last resort.
is delivered swiftly, firmly and with absolute deter- Veterinary surgeons developing health plans may
mination. If there is any doubt that the kid has not include this procedure under emergency slaughter.
been killed effectively, the blow should be immedi- Under no circumstances should it be used in any
ately repeated. other situation.
Death should be ensured by exsanguination,
cutting the throat from ear to ear to sever both Unacceptable methods
carotid arteries and both jugular veins. An alter- Methods that must never be used include drown-
native method is to insert the knife into the ven- ing or smothering, inducing hypothermia, expo-
tral base of the neck towards the entrance of the sure to thermal heat or chemicals, electrocution
chest to sever all the major blood vessels where or use of asphyxiant gases outwith commercial
they emerge from the heart. registered units.
CHAPTER 19
POST-MORTEM EXAMINATION AND SAMPLING

347
INTRODUCTION Case selection is of paramount importance:
Post-mortem examination (PME) is a useful tool •• It is important to consider whether a PME is

when investigating health and welfare issues in goats the best approach in investigating the disease
(Fig. 19.1). There are a number of reasons why such outbreak, rather than sampling live goats, which
an examination may be of value: may also be more cost effective. An example
is the investigation of a diarrhoea outbreak
•• To investigate why a goat has died or been found in young kids in which examination of faeces
dead. from a number of live animals may be a better
•• To investigate a problem affecting several approach.
animals, when a typical case can be euthanased •• The selected case has to be representative of the
for examination. problem under investigation.
•• To investigate a failure in either •• A goat with residual antibiotic levels following a
treatment or preventive medicine protocols, period of treatment may be useful to investigate
often in collaboration with a pharmaceutical the pathology, but be of limited value to identify
company. a possible bacterial cause.
•• To investigate welfare infringements instigated •• Severe autolysis can make accurate PME very
by an enforcement authority. difficult.
•• To target sample viscera for laboratory testing
such as liver tissue for copper assay. The practitioner’s skill as a pathologist may dic-
•• To undertake a specific examination as in the tate their decision whether to undertake the PME
investigation of an abortion outbreak. themselves or refer to a specialist laboratory or
pathology centre.
HISTORY
A comprehensive history is essential before embark-

ing on any PME, as this will have an influence on the
approaches taken, particularly with regard to sam-
pling. Such a history should include as a minimum:
•• Age, breed and gender.

•• Homebred or purchased (and when).
•• Numbers affected, number dead and size of
group (morbidity/mortality).
•• Clinical signs exhibited prior to death or
Fig. 19.1 A goat carcase ready for post-mortem euthanasia, and any signs of potential relevance
examination and sampling. in rest of group.
348 Chapter 19
•• Treatment history (e.g. anthelmintics, If any of these infectious agents (particularly

antibiotics). ACDP Hazard group 3) are suspected, it may be
•• Kidding date (if applicable). preferable to refer the carcase to a laboratory that
•• Management – housed/outdoors. can undertake the PME in containment facilities.
•• Management – diet fed, any recent changes.
•• Management – vaccination status. PREPARATION
•• Management – any recent handling or
procedures (e.g. transport, disbudding). Prior to the PME itself, it is important to have all
the instruments and sampling equipment required,
HEALTH AND SAFETY including one or more sharp knives or disposable
PME scalpels, a hack saw or garden loppers (useful for
Anyone undertaking, assisting with or observing cutting through ribs), scalpel and forceps for any fine
a PME should be aware of the health and safety dissection, swabs and sampling pots. These should be
implications. There is a potential risk of cuts or stab readily available with the tops taken off the pots for
wounds, and it is advisable to wear a cut proof glove ease of access, reducing the risk of external contamina-
on the non-cutting hand (under waterproof gloves). tion of containers. A camera, smartphone or tablet to
Suitable protective overclothing and wellington take images of relevant pathology is useful, and some
boots should be worn. These may either be dispos- form of means to record findings, ensuring that notes
able or easily cleaned and disinfected on completion are made at the time of the examination, and at the end
of the PME, and between PMEs to avoid potential of each carcase if more than one PM is being under-
cross contamination between carcases. Care should taken (this will ensure that findings are not mixed-up).
also be taken to avoid injury while lifting heavy
carcases. POST-MORTEM EXAMINATION
In addition, there are the risks associated with a APPROACH
number of zoonotic pathogens potentially infect-
ing the carcase or contaminating the environment. It is important to develop a systematic approach to
In the UK, for example, these are classified by the each and every PME undertaken. This will ensure
Advisory Committee on Dangerous Pathogens that no organ system is overlooked. There may be
(ACDP) as: a tendency, particularly if the clinical signs suggest
(e.g. diarrhoea), to examine the gastrointestinal tract
•• Hazard group 2 pathogens. These can first; this, however, will release gut content thus con-
cause human disease and may be a hazard taminating the entire carcase and potentially mask-
to employees, but are unlikely to spread to ing other significant pathology.
the community and there is usually effective One author’s (DH) approach is as follows:
prophylaxis or treatment available. Salmonella
spp. and Cryptosporidium spp. are examples of 1 External examination. Entire carcase, then
hazard group 2 pathogens. partially skinned to allow access to internal
•• Hazard group 3 pathogens. These can viscera:
cause severe human disease and may be • Note down any identifying ear tag or other
a serious hazard to employees. They may identification.
also spread to the wider community, but • Describe the coat covering, including any
there is usually effective prophylaxis or evidence of ectoparasites.
treatment available. These pathogens • Attribute a body condition to the carcase.
include Coxiella burnetii (Q fever), Avoid condition scoring a carcase; instead
Mycobacterium bovis (tuberculosis) and use descriptive terms such as emaciated,
Escherichia coli O157. thin, moderate, good, overfat condition etc.
Pos t - Mor t e m E x a m i n at ion a n d Sa m pl i ng 349
• Examine the umbilicus in young kids. Describe any pathology, and whether
• Examine the udder in females. bilateral. Examine any focal lesions by
• Examine the feet for visible lesions. excision.
• Examine the external mucous membranes – Excise into the lumen of the oesophagus
for evidence of anaemia. and then the larynx and trachea down
• For ease of PME activity, cut down through past the bronchial bifurcation.
each axilla to lie the front legs flat on – Examine the bronchomediastinal lymph
the working surface, and cut down and nodes.
disarticulate through the two hip joints. – Excise the pericardial sac. Describe the
This should ensure the carcase remains quantity and consistency of any fluid
stable and does not move sideways as the present.
examination continues. – Examine the heart including each
• As the carcase is skinned, note any signs chamber and heart valve.
of dehydration (subcutaneous tissue has a 4 Examine the renal system:
‘tacky’ feel) or jaundice. • Remove each kidney. Incise through the
• Take a sample of blood (into a plain capsule, renal medulla and cortex to section
container; for example a vacutainer) from the kidney into two halves lengthwise.
any free blood flowing from the carcase for Can the capsule be easily peeled back?
possible testing. Describe any changes evident (subcapsular
2 Open the abdominal cavity – leave viscera in haemorrhage, infarct, pale cortex in
carcase initially: nephrosis). Repeat with the opposite kidney.
• Have a superficial look at the intact viscera, • Examine the ureters, incise into the bladder
but do not open the gut at this stage. and examine the penis in males.
• Note any evidence of spatial displacement, any 5 Examine the reproductive system:
fluid present (describe nature and quantity). • Pregnant – number of fetuses and stage of
3 Open the thoracic cavity and examine the pregnancy.
contents. • Recently kidded – any evidence of retained
• This can be easily achieved in young kids by placenta, endometritis.
cutting along the costochondral junction. • Note any kidding injuries to birth canal.
In mature animals cut through ribs/sternum • Examine the testicles – if castrated recently,
using a hacksaw or garden loppers. note any evidence of infection.
• Try not to damage the underlying 6 Examine the remaining abdominal cavity
pericardial sac attached to the sternum. contents systematically:
• Examine initially for excess fluid in • Remove the liver and examine grossly.
the thorax, describe the quantity and Describe colour, shape, margins and
consistency, and take a swab or pipette consistency (firm/friable) and incise any
aliquot into a sample container if considered superficial lesions.
significant. • Serially section the liver for evidence of
• By digital palpation, assess whether there are deeper lesions.
adhesions between the lung and the thoracic • Examine the gallbladder. Describe content –
wall. Note if fibrinous and easily broken note any evidence of liver fluke.
down, or firm and fibrous. • Examine the caudal vena cava for necrotic
• Remove the complete pluck including the change or thrombus formation.
tongue and examine systematically: • Examine the intestinal tract grossly.
– Examine the lung tissue, initially Describe any changes in colour of
comparing one lung with the other. the serosal surface (e.g. congested).
350 Chapter 19
Palpate between finger and thumb along two opposing hemi-brain portions). If
its length for the subtle thickening often neuropathological examination is required,
identified in Johne’s disease. Incise into the place the brain tissue in a container of
jejunum, ileum and large intestine. Describe formol saline intact (i.e. do not section at
any mucosal lesions present. Describe the this stage). Fixation can be achieved by
colour and consistency of the contents, ensuring a minimum 10:1 ratio of fixative to
and take a sample if deemed necessary. brain tissue.
Strip content into a bowl if parasitic 9 Examine the spinal cord if necessary. Removal
gastroenteritis suspected. of the spinal cord itself can be achieved either
• Take a sample of faeces to test for potential by skilfully sawing down the length of the
pathogens (e.g. cryptosporidia, coccidia, spinal column after all the muscle and viscera
salmonella, nematode ova). have been removed, or by systematic use
• Examine associated mesenteric lymph nodes. of bone cutters. This examination may be
• Examine the fore-stomachs – note any necessary if swayback is suspected.
evidence of cranial abdominal peritonitis 10 Finally, give an overall assessment of the
(e.g. reticulitis). carcase quality: fresh or decayed.
• Examine the abomasal contents – wash into
a bowl to examine for nematode infestation,
specifically Haemonchus contortus, which
can often be seen with the naked eye when
contents are swirled around the bowl.
• Examine rumen contents. Describe the
quantity and consistency (liquid or dry
and impacted). Examine specifically for
any extraneous material such as leaves of
potentially toxic plants (e.g. rhododendron).
7 Examine joints/musculature:
• Excise into joints. Describe the quantity and
consistency of synovial fluid, and the joint
surface.
• If conditions such as trauma or white muscle
disease are suspected, continue to skin the
carcase and incise into major muscle masses.
8 Remove the head to examine the oral cavity
and brain (if deemed necessary):
• The tongue will have been examined with
the pluck.
• Examine the oral cavity for ulceration or
diphtheria.
• Examine the dentition, particularly in
elderly goats for evidence of tooth loss,
overgrowth and gum disease.
• If facilities allow, gain access to the
brain either by removing the overlying Fig. 19.2 The roof of the cranial cavity removed
skull by placing it in a vice and making following diamond-shaped cuts through the skull after
a diamond-shaped cut (Fig. 19.2), or by skinning. The head must be held firmly for this to be
sagittally sawing the head in half (obtaining undertaken accurately and safely.
Pos t - Mor t e m E x a m i n at ion a n d Sa m pl i ng 351
SAMPLING PROTOCOLS be placed in 10 times its own volume of formol saline

fixative. Normal lung tissue will float in fixative. It
Sample collection will vary depending on the path can be kept below the surface (thus ensuring com-
ology identified or the disease/condition suspected. plete perfusion) by placing a piece of paper towel on
top (Fig. 19.7).
Bacteriology If fresh gut is available (from very freshly dead or
Many organisms are very labile, and may be euthanased goats), then 1 cm lengths of gut should
destroyed by the pH change in tissue as it autoly- be sampled, and opened up such that the mucosa is
ses in transit to a laboratory. If there is to be a delay bathed in fixative (at 10 times the volume of tissue;
in testing samples, then swabs taken aseptically and Fig. 19.8). Sample pots should be clearly labelled
placed in transport media at the time of the PME or and allow easy removal of the fixed tissue.
immediately afterwards are far preferable over tissue
submission (Fig. 19.3). Ideally, samples should only
be taken from goats that have not received any antio-
biosis prior to death or euthanasia. Once a tissue or
specific lesion has been identified for bacteriologi-
cal sampling, the surface should be seared with a hot
spatula (Fig. 19.4) and then, using a sterile scalpel,
a small nick made in the tissue into which the swab
is then inserted (Fig. 19.5). Swabs should be clearly
labelled.
Histopathology
Any tissue sampled must be fresh to be of any real
value: autolysis and freezing/thawing of tissue ren-
ders it unsuitable. Sample selection is important. Fig. 19.3 A plain swab placed into a transport
Small cubes of tissue measuring 1–1.5 cm3 should be medium prior to sending to a laboratory is ideal
taken (except brain), including both abnormal and for ensuring bacterial stability. It should be taken
normal tissue for comparison (Fig. 19.6). It should aseptically to avoid contamination.
Fig. 19.4 The surface of the tissue (in this case liver) Fig. 19.5 A swab can be plunged directly into softer
is seared with hot metal (such as a spatula). This will tissue. This may be facilitated by making a small nick
kill off surface contaminants. with a sterile scalpel.
352 Chapter 19
Fig. 19.6 A small portion of tissue placed in 10 times Fig. 19.7 A paper towel has been placed over lung
its volume of fixative in a suitable wide-mouthed, leak- tissue to prevent it from floating, which could result in
proof container. poor fixation.
Aborted goat kids

Unless the entire kid and placenta can be sent to
a diagnostic laboratory for testing, then during a
PME:
•• With a pipette or syringe, take a sample of any

free fluid in either the thoracic or abdominal
cavity into a plain vacutainer or other sterile
container.
•• Take a sample of stomach content aseptically
using a vacutainer and needle, or a swab of fluid
taken aseptically if minimal amount.
Fig. 19.8 One cm lengths of gut, placed into fixative,
•• Take a portion of placenta with at least one
ensuring the mucosa surface is in contact with the
cotyledon.
fixative. This can be achieved by placing the gut over
the open ends of a pair of forceps.
APPENDICES
353
1 LABORATORY REFERENCE INTERVALS
The figures in the tables below are given for guidance only. Laboratories should indicate their own reference
intervals with any test results provided. Reference intervals may vary slightly depending on the test proce-
dure, age and type of goat and the geographical location.
Table 1 R
ed blood cell parameters. (With permission Table 2 W
hite blood cell parameters. (With permission
Animal and Plant Health Agency UK) Animal and Plant Health Agency UK)
REFERENCE REFERENCE PERCENTAGE OF

TEST UNITS INTERVAL TEST UNITS INTERVAL TOTAL WBCC
Red blood cell count × 1012/l 10–18 White blood cell × 109/l 6–14
Haemoglobin g/dl 8–15 count (WBCC)
Packed cell volume l/l 0.24–0.39 Neutrophils × 109/l 1.2–7.2 30–48

(mature)
Mean corpuscular pg 7–9
haemoglobin Neutrophils × 109/l Rare Rare
(band/immature)
Mean corpuscular g/dl 31–42
haemoglobin content Lymphocytes × 109/l 2.0–9.0 45–70
Mean corpuscular fl 16–34 Monocytes × 109/l 0–0.5 0–4

volume. Eosinophils × 10 /l
9 0.05–0.5 1–8
Platelets × 10 /µl (or 10 /l)
3 9 300–600 Basophils × 10 /l
9 0–0.1 Rare
Table 3 E
nzyme assays at 37°C. (With permission
Animal and Plant Health Agency UK)
REFERENCE
TEST UNITS INTERVAL
ALP IU/l 0–300
AST IU/l 0–300
CK (CPK) IU/l 0–100
gGT IU/l 0–30
GLDH IU/l 0–10
LDH IU/l 0–400
Pepsinogen IU/l 0–1.0
GSH-Px U/ml RBCs >60
354 A ppe n dic e s
Table 4 O
ther blood biochemistry tests. (With Table 6 Cerebrospinal fluid.
permission Animal and Plant Health
Agency UK)
TEST UNITS REFERENCE INTERVAL
TEST UNITS REFERENCE INTERVAL Protein g/l <0.4

Nucleated cells cells/µl 0–8
Albumin g/l 29–43
Red blood cells Nil
Beta-hydroxybutyrate mmol/l 0–1.2
Bacteria Nil
Bilirubin – total µmol/l 0–7
Beta-hydroxybutyrate mmol/l <0.5
Calcium mmol/l 2.3–2.9
Chloride mmol/l 98–110
Copper (plasma) µmol/l 9–19
Creatinine µmol/l 54–123
Globulin g/l 23–46 Table 7 Synovial fluid.
Glucose mmol/l 2.4–4.0
Haptoglobin g/l <0.1
Magnesium mmol/l 0.8–1.3 Protein g/l Mean 20
Phosphate mmol/l 1.0–2.4 Nucleated cells cells/µl Mean 50 (mostly lymphocytes

and monocytes)
Potassium mmol/l 3.4–6.1
Total protein g/l 62–79
Sodium mmol/l 135–156
T4 nmol/l 43–90
Urea mmol/l 4.0–8.6 Table 8 Peritoneal fluid.
Vitamin B12 pmol/l >221

(cyanocobalamin)
Zinc µmol/l >12 adequate Protein g/l 20–25
<6 deficient Nucleated cells × 10 /l
9 0.2–0.3
Table 5 Aqueous/vitreous humour. Table 9 Urinalysis.
TEST INTERPRETATION TEST UNITS REFERENCE INTERVAL

Calcium <1 mmol/l suggests hypocalcaemia pH 7.0–8.0
Magnesium Aqueous humour <0.33 mmol/l or Specific gravity 1.020–1.040
vitreous humour <0.65 mmol/l
Osmolarity mOsm/kg 800–1200
suggests hypomagnesaemia
Electrolytes Low
Beta- >2.5 mmol/l suggests ketosis
hydroxybutyrate (Na, Cl, P, Ca, Mg)
Urea Levels of urea in aqueous humour of Protein Trace
>30 mmol/l in ruminants are consistent Ketones Trace (lactating does)
with significant renal disease, although
kidney histopathology is needed for a Bacteria per ml <10,000 = contamination
definitive diagnosis >100,000 = infection
A ppe n dic e s 355
2 CONVERSION FACTORS
To convert from SI units to old/conventional units, divide by the conversion factor
SI UNITS CONVERSION FACTOR OLD/CONVENTIONAL UNITS
HAEMATOLOGY
PCV l/l 0.01 %
RBCs × 1012/l 1 × 106/µl
Erythrocytes × 109/l 1 × 103/µl
Nucleated cell count × 10 /l
9 1 × 103/µl
Eosinophils × 109/l 1 × 103/µl
Fibrinogen g/l 100 mg/dl
MCV fl n/a fl
MCH pg n/a pg
MCHC g/l 10 g/dl
BIOCHEMISTRY
ALP U/l 1 IU/l
ALT U/l 1 U/l
ACTH pmol/ml 0.22 pg/ml
Albumin g/l 10 g/dl
Ammonia (NH4) µmol/l 0.587 µg/dl
Amylase U/l 1 U/l
AST U/l 1 U/l
Bilirubin µmol/l 17.1 mg/dl
Calcium mmol/l 0.2495 mg/dl
Carbon dioxide mmol/l 1 mEq/l
Chloride mmol/l 1 mEq/l
Cholesterol mmol/l 0.0259 mg/dl
Copper µmmol/l 0.157 µg/dl
Cortisol nmol/l 27.59 µg/dl
Creatine kinase (CK) U/l 1 IU/l
Creatinine µmol/l 88.4 mg/dl
GGT U/l 1 U/l

GLDH U/l 1 U/l
Globulin g/l 10 g/dl
Glucose mmol/l 0.0555 mg/dl
Iron, binding µmol/l 0.179 µg/dl
Iron, total µmol/l 0.179 µg/dl
Lipase U/l 1 IU/l
U/l Cherry-Crandall U
Continued
356 A ppe n dic e s
SI UNITS CONVERSION FACTOR OLD/CONVENTIONAL UNITS

Magnesium mmol/l 0.4114 U/l
Osmolality mmol/l 1 Osm/kg
Phosphorus mmol/l 0.323 mg/dl
Potassium mmol/l 1 mEq/l
Protein, total g/l 10 g/dl
SDH U/l 1 IU/l
Selenium µmol/l 0.1266 µg/dl
Sodium mmol/l 1 mEq/l
Triglycerides mmol/l 0.0113 mg/dl
Triiodothyronine (T3) nmol/l 0.0154 µg/dl
Thyroxine (T4) nmol/l 12.5 µg/dl
Urea nitrogen mmol/l 0.357 mg/dl
Uric acid mmol/l 59.48 mg/dl
Vitamin E µmol/l 2.322 mg/ml
Smith MC, Sherman DM (2009) Goat Medicine. Wiley-

3 FURTHER READING
Blackwell, Ames.
Solaiman SG (2010) Goat Science and Production. Wiley-
Textbooks Blackwell, Ames.
Cannas A, Pulina G (2007) Dairy Goats – Feeding and Wolfe DF, Moll HD (1998) Large Animal Urogenital
utrition. CABI Publishing, Wallingford.
N Surgery, 2nd edn. Lippincott Williams and Wilkins,
Clarke KW, Trim CM (2013) Veterinary Anaesthesia, Philadelphia.
11th edn. Saunders/Elsevier, St. Louis.
Constable P, Hinchcliffe KW, Done SH, Gruenberg W
Review article
(2016) Veterinary Medicine: A Textbook of the Diseases of
Harwood DG (2016) Goat health planning. In Practice
Cattle, Horses, Sheep, Pigs and Goats, 11th edn. Saunders/
38(8):387–98.
Elsevier, St. Louis.
Dugdale A (2010) Veterinary Anaesthesia – Principles to
Practice. Wiley-Blackwell, Ames. Further information
Fubini SL, Ducharme NG (2016) Farm Animal Surgery, British Goat Society - https://www.britishgoatsociety.com/
2nd edn. Saunders/Elsevier, St. Louis. Goat Veterinary Society - http://www.goatvetsoc.co.uk/
Gordon I (2017) Reproductive Technologies in Farm Animals, National Research Council (2007) Nutrient Requirements
2nd edn. CABI Publishing, Wallingford of Small Ruminants: Sheep, Goats, Cervids, and
Harwood DG (2006) Goat Health and Welfare: A Veterinary New World Camelids. The National Academies
Guide. Crowood Press, Marlborough. Press Washington DC. (www.nap.edu), doi.
Hendrickson DA, Baird AN (2013) Turner and McIlwraith’s org/10.17226/11654
Techniques in Large Animal Surgery, 4th edn. Wiley- OIE (World Organisation for Animal Health) (2017)
Blackwell, Ames Listed diseases, infections and infestations in force in
Matthews JG (2016) Diseases of the Goat, 4th edn. Wiley- 2017. http://www.oie.int/en/animal-health-in-the-
Blackwell, Chichester. world/oie-listed-diseases-2017/
Mowlem A (2001) Practical Goat Keeping. Crowood Press, Various guides on milk quality, out-of-season breed-
Marlborough. ing and building design available from: The Dairy
Pugh DG, Baird N (2011) Sheep and Goat Medicine, Practices Council (www.dairypc.org): Small Ruminant
2nd edn. Elsevier Health Sciences, London. Task Force. (Follow link to ‘Guidelines’, then to ‘Small
Smith BP (2014) Large Animal Internal Medicine, 5th edn. Ruminants’)
Elsevier, St. Louis.
INDEX
357
Note: Page numbers in bold refer to figures and in italics to tables
abdominal distension 109–10, 129, 129, 145 anaesthesia see general anaesthesia; specific regional blocks
abdominal examination 109–11, 110 anal/perineal reflex 197
abdominal fluid 111, 111 analgesia 341–2
abdominal pain 110 Anaplasma phagocytophilum 42
abdominal wall, closure 74–5, 75 Anglo-Nubian goat 115
abdominocentesis 112, 112, 354 Angora goats 13, 44
abiotrophy 202 angular limb deformity 217, 218
abomasum anoestrus 22, 23, 24–5
bloat (abomasitis) 128–30 anthelmintic resistance 156–7, 158–9
displacement 126–7 anthelmintics 157–9
emptying defect 125–6 anthrax 329–30, 330
examination of contents 350 aphthous fever 323–6, 325
nematode parasites 154, 156 apnoea 333
normal structure and function 125 primary 87
ulceration 127–8, 127 aqueous humour, analysis 300, 354
abortion 34–44 arbovirus infections 42, 330
enzootic 36–38 arterial thrombosis 187
habitual 44 arthritis
infectious causes 35–43 bacterial (joint ill) 227–8
induced 28, 67 CAE infection 226, 226
non-infectious causes 43–4 Mycoplasma 228–9
sample collection 34–5, 352 arthrocentesis 216, 354
accessory sex glands, disorders 52 arthrogryposis 99–100
acetonaemia (lactational ketosis) 303–4 artificial insemination 26–7, 26, 27
acidosis artificial rearing 104–6, 104–6
metabolic 245, 302, 304, 343 artificial respiration 87–8
neonatal 100 ascites 111, 179, 184, 308
rumen 122–3, 122, 186 Aspergillus fumigatus 176
Actinobacillus lignierisi 126, 169 asphyxia, neonate 86–8
adenovirus 163 aspiration pneumonia 170, 333
adrenaline 88, 92 ataxia 102, 196, 198, 198, 202, 210, 211, 303, 307, 317, 320
agalactia enzootic (swayback) 306–7, 307
contagious 173, 228, 229, 274–5 atelectasis 87, 87
post-partum 273 atipamezole 334
air-hunger signs 165–6, 166 atresia ani, recti, coli 96–7, 96, 129
airways, clearing in newborn 87 atrial septal defect 181–2
Akabane virus 42 atropine 88, 290, 293
albendazole 214 Aujeszky’s disease (pseudorabies) 212–13
alfaxalone 334 aural see ear
allergic pneumonitis 176–7 auriculopalpebral block 339–40, 340
alopecia 250–3, 257, 260, 264 axillary nerve 205
Alpine goat 22
aminoglycosides 82, 245, 247 babesiosis 193–4
amitraz solutions 258 Bacillus anthracis 329
ammonium chloride 242 bacteriology 351, 351
ammonium tetrathiomolybdate (antidote) 319 bacteriuria 238
ampicillin 279 Bacteroides spp. 82
anaemia 155, 155, 156, 187–9, 258, 307, 310 balanoposthitis 33, 33, 54–5
358 I n de x
base deficit 343 breeding

behaviour 4–7 natural service 25–6
benzimidazoles 157–8, 157 out-of-season 23, 45
Besnoitia caprae 260 synchronisation 23–4
besnoitiosis 260 breeding soundness examination 45–9, 46
17-beta oestradiol 273 breeds 3, 5
beta-hydroxybutyrate (BHB) 302 British Goat Society 2
beta-mannosidosis 101 browsing behaviour 7, 7, 301, 305, 313
betamethasone 342 Brucella abortus 40
bezoar 126, 126, 132 Brucella melitensis 40,50
biliuria 314 brucellosis 39–40
biochemistry 353–4 buck
biosecurity 18–20, 227, 275 behaviour 25–6, 26
biparietal diameter (BPD) 62, 63 body weight 14
birth canal 69, 69 breeding soundness 45–9, 46
birth weight 103–4, 104 doe:buck ratio 25
blackleg 229 intersex 24, 24
bladder, urinary reproductive tract, normal structure and function 45, 45
eversion/herniation 84 teaser 57
rupture 240 temporary suppression of fertility 59
ultrasonography 239, 239 bunny hopping gait 195
bleating 6 bunyaviruses 42, 99, 102
bleeding diathesis 244 bupivacaine 337
blepharospasm 288, 289, 292, 292 buprenorphine 342
blindfolding 198 burns 253
blindness 196, 196, 198, 203, 210, 214, 295, 302, 303 butorphanol 72, 334, 335, 341
blood, abnormal colour 314 butylscopolamine bromide 71
blood collection and analysis 180–1, 181
blood donation 189 Cache Valley virus 42
blood groups 189 caesarean section 72–5, 337
blood parasites 193–4 calciferol 187, 217–8
blood transfusion 189, 344 calcium:phosphorus ratio 242
blood vessel disorders 185–7 calcium
blowfly 259–60, 259 blood and humour levels 299
bluetongue 163, 263, 326–7 deficiency 217, 218, 299–300
body condition scoring 8–9, 9, 47 requirements in lactation 300
body reflexes 197 calcium borogluconate 81, 300, 302
body truss 65, 66 calcium oxalate 316
body weight 14 California mastitis test 277, 277
at breeding 21 campylobacter infection 42–3
at weaning 106 C. fetus fetus 42
birth 103–4, 104 C. jejuni 42
Boer goat 5 capillary refill time 179
bone marrow biopsy 189 caprine arthritis encephalitis (CAE) 225–7
bone marrow disease 188 mastitis 226, 276, 277
bone sequestrum 221–3, 222 pneumonitis 176, 176, 226
borborygmi 110, 132 caprine arthritis encephalitis virus (CAEV) 225
border disease virus 43 caprine herpesvirus 1 (CpHV-1) 32–3, 43, 163
bottle feeding 105, 105 capripox viruses 262–3
‘bottle jaw’ 159 captive bolt 345
Bovicola limbata 257, 257 carbetocin 82
bovine somatotropin 302 carbohydrate overload 113, 122–3, 122–3, 136, 229–30
bovine spongiform encephalopathy (BSE) 210–11, 330 carbon dioxide toxicity 314
bovine viral diarrhoea virus 43 carbon monoxide toxicity 314
brachial plexus block 341 cardiac dysrhythmias 180
brachygnathia 115 cardiac murmurs 181, 182
bracken toxicity 237, 314 cardiac neoplasia 185
brain cardiomegaly 184, 185
post-mortem examination 350, 350 cardiomyopathies 184–5, 185
regions/functions 195, 195 cardiotoxins 181, 316, 317
brain injury, disbudding 201, 202, 208, 209 cardiovascular disease 88, 181–5
breath, abnormal smell 314 signs of 179–80
I n de x 359
cardiovascular system, examination 15, 179–81 computed tomography (CT) 112

carprofen 279, 342 congenital disorders 24, 28–9, 85-6, 96, 97–8, 98–100,
cartilage disorders 224–5 101, 102, 115, 181, 187, 253, 281, 306, 310
caseous lymphadenitis (CLA) 176, 177, 191–3, 192 conjunctival membranes, colour 155, 156, 156, 187, 189
cashmere 3, 14 conjunctival pedicle flap 294
cast 219, 220, 220 conjunctivitis 162, 162, 166, 262, 274, 293, 295
hanging pin 220 contagious agalactia 173, 274–5
castration 56–7, 56, 57 contagious caprine pleuropneumonia (CCPP) 172–3
cats 35, 35, 36 contagious ecthyma (orf) 260–1, 261
cefquinome 279 contagious ovine digital dermatitis (CODD) 232–3
ceftiofur 247 contagious pustular dermatitis (orf) 260–1, 261
central nervous system (CNS), regions and functions 195, 195 Cooperia 154
cephalosporins 82, 278 copper analysis, liver biopsy 113
cerebellar abiotrophy 202 copper deficiency 102, 306–8
cerebellar hypoplasia 102 copper, dietary levels of 307
cerebellum 195 copper, toxicity 314, 318–19, 318, 319
cerebral oedema 210 cor pulmonale 185
cerebrocortical necrosis (polioencephalomalacia) 202–4 cornea 285
cerebrospinal fluid (CSF), collection/analysis 199–201, damage 286, 286, 288, 289
200, 354 oedema 286, 293
cerebrospinal nematodiasis 214 ulceration 286, 289–90, 289, 290, 292
cervix 21, 21 cornual block 340, 340
dilation failure (ringwomb) 70–1 corticosteroids
laceration 77–8 analgesia 342
prolapse 65–6 induction of lactation 274
cestodes 160–1 induction of parturition 67
Chlamydia abortus (C. psittaci) 37, 50, 293 necrotic laryngitis 170
chlamydiosis 36–8 pemphigus foliaceus 250
Chlamydophila pecorum 292 peripheral nerve injuries 206
chlorate 314 Corynebacterium spp. 50, 54, 177, 191–3, 192, 246,
choke 121 247, 275, 298
chorioptic mange 253–5, 254, 255 cough 172–3, 175
Chorioptes spp. 253–4, 255 cowdriosis 181
chromosome count 3 cows milk 13
circling 203, 203, 213 Coxiella burnetti 35, 38, 38, 348
claws, lesions 229–35, 230, 231, 233 cranial nerves 286
claws, overgrown 233, 234 cranial nerve reflexes, normal 196
cleft palate (palatoschisis) 97 creatine kinase 308
clenbuterol 71 creatinine, peritoneal fluid 240
clinical examination, basic 14–15 critical temperature, lower/upper 12
colic, signs 110 cryptorchidism 51–2, 52
cloprostenol 67, 71 cryptosporidiosis 142–4, 348
clostridial metritis 82, 83 Cryptosporidium parvum 143
clostridial myositis 229 crystalloid fluids 343
Clostridium perfringens 81, 93, 128, 149–51, 149, 210 Culicoides midges 260, 326
Clostridium septicum 81, 229 cyanide 314
Clostridium tetani 209 cyanocobalamin (vitamin B12) 309–10
cloudburst (pseudopregnancy) 63–4, 63, 64 cyanogenic glycosides 315
coagulopathies 188 cyanosis 179
coat 13–14 cypermethrin 258
cobalt deficiency 309–10 cystic ovarian disease 25, 25
cobalt, dietary levels of 310 cystitis 237, 245–7, 246
coccidiosis 144–6 cystocentesis 241
coenurosis (gid) 213–14 cystoscopy 239
Coenurus cerebralis 213 cystotomy 243–4, 243, 244
collagenase inhibitors 290
colloid fluids 343–4 death, acute/sudden 119, 149, 172, 174, 184, 185, 186, 300,
colostrum 90 308, 316, 317, 317, 319, 329
CAE transmission 225, 225, 227 death, signs of 344
storage and feeding 91, 91 decoquinate (Deccox) 36
colostrum bank 92–3, 93 degenerative joint disease (DJD) 224–5
complement system 90 dehorning (adult goat) 267–9, 267–269
360 I n de x
dehydration 342 ear

deltamethrin 258, 259 clinical examination 295
demodectic mange 256 haematoma 296–7, 297
Demodex caprae 256 infectious disease 297–8
dental injuries 295–6, 296
disease 115–18 mange (psoroptic) 257
formula 114 tagging 296, 296
radiography 116, 116, 117 ear tip necrosis 298
dentition 114 Echinococcus granulosus 161
eruption 114 eclampsia 229–300, 299
dermatitis Ehmer sling 220, 223
fly bite 259, 259 Eimeria spp. 144–6
malassezia 264 Elaphostrongylus cervi 214
mycotic (dermatophilosis) 264 electrocardiography (ECG) 180, 180
seborrhoeic 251–2, 252 electroejaculation (EEJ) 47–8, 48
staphylococcal 263–4, 263 electrolytes, fractional excretion 239
dermatophilosis 264 electromyography (EMG) 201
dermatophytosis (ringworm) 265, 265 embryo transfer 27, 28
dermatosis, zinc responsive 250–1 embryonic loss, early 33–4
detomidine hydrochloride 72, 333–4 emerging diseases 330, 331
developmental abnormalities 85 encephalitis
dexamethasone 67, 206, 274, 342 bacterial 208–9
diabetes 136 listerial 206–8
diamidine derivatives 194 viral 213
diazepam 334 endocarditis 182–3
Dichelobacter nodosus 231 endometritis 30–1, 30
diclazuril 146 endotracheal extubation 336, 336
Dicrocoelium dendriticum 160 endotracheal intubation 335, 335
Dictyocaulus filaria 175, 175 energy requirements 8, 301
digestive system enilconazole 265
examination 15 enrofloxacin 247
infectious diseases 142–61 enteritis, haemorrhagic 145, 147, 149–51, 162, 207, 244
digital dermatitis, contagious ovine 232–3 enteritis, parasitic 153–9
diminazine 194 enterotoxaemia 149–51, 210, 210
dinoprost 67 entropion 287–8, 288
diphenhydramine 92 enucleation 294–5, 294
disbudding environmental enrichment 6, 6
complications 201, 202, 208, 209, 267 enzootic ataxia (delayed swayback) 306–7
local anaesthesia 340, 340 enzootic calcinosis 218
surgery 267, 267 enzootic haematuria 237
disuse atrophy 221 epididymitis 50–1, 50
dog tapeworm 213–14 epidural anaesthesia 338–9, 338
dog-sitting posture 199, 301, 301, 307 epiphora 166, 288, 288, 289, 289, 293
dogs 42 equine chorionic gonadotropin (eCG) 23
domestication 1 Eric Williams test 110
doramectin 157, 158, eructation, failure 121
doxapram hydrochloride 87, 334 erythema 252, 252, 255, 260
drenching gun injuries 119–20, 119 erythromycin 132
dropped elbow 205 Escherichia coli 82, 93, 142, 146–7, 208, 227, 246
dropped hock 205, 205 mastitis 275, 276
dropped stifle 205 O157:H7 146, 348
drug administration 15–9 estimated breeding values (EBVs) 4
dry goat therapy 279 euthanasia 344–5, 345
dry matter intake 303–4, 304 exercise intolerance 175, 179, 181, 183, 329
dry period nutrition 300, 303–4 exophthalmos 291, 291
ductus arteriosus 88, 182 exsanguination 346
‘dummy kid’ (neonatal malformation syndrome) 102 external coaptation 221
duodenum 130 external skeletal fixation 220, 221
dyspnoea 122, 159, 165, 169, 170, 171, 172, 175, 180, 190, extracellular fluid (ECF), loss 342
212, 229, 262 eye
dystocia 30, 68–72, 204 clinical examination 285–7, 285, 287
dysuria 29, 52, 240 foreign bodies 287, 288–9, 288
I n de x 361
eye (continued) first aid

infectious disease 291–3 fractures 219, 220
non-infectious disorders 287–91 ocular trauma 287
normal structure and function 285 fistula
regional nerve blocks 339–40, 340 discharging 222, 222
surgery 290, 290, 293–5, 294 recto-vaginal 78–9, 78
systemic disease affecting 295 rumen 124, 125
ultrasonography 286–7, 287 flank anaesthesia 338
eyelids flank incision 72, 73
entropion 287–8, 288 flexion tests 216
suturing (tarsorrhaphy) 293 flies 258–60
tears/lacerations 287 floppy kid syndrome 100–1, 304
florfenicol 247
flukicides 160
facial nerve paralysis 197, 197, 207 fluid therapy 342–4
facial sensation 196 general anaesthesia 334
faecal egg counts (FECs) 155, 155, 156, 157, 187, 189 septicaemic kid 94, 94
faecal examination 111 flunixin meglumine 27, 94, 279, 342
faecal oocyst count 145 fluorescein staining 289–90, 290
failure of passive transfer 91–3 fluorogestone acetate 23
FAMACHA© system 155, 156, 156 fly control 259, 260, 334
Farquharson technique 66 fly strike (myiasis) 259, 259
Fasciola spp. 159–60 Foley catheter 243, 244, 244
fascioliasis (liver fluke) 159–60, 159 follicle stimulating hormone (FSH) 27
fat stores 8, 9 follicular cyst 25, 25
fatty liver necrosis 303–4, 303 foot abscess 235, 235
fecundity 22 foot disease 229–35
feed storage 10, 10 foot examination 13
feed supplements 305–6, 305, 306 foot and mouth disease (FMD) 181, 263, 323–6, 325
feeding foot overgrowth 233
dry period 300 foot trimming 233–4, 234, 235
fibre levels 118, 123, 123 footbaths 232
forage 303–4, 304 footrot 230–2
lactation 303–4, 304 forage 7, 8, 123
prevention of pregnancy toxaemia 302–3 fungal spoilage 320, 321
see also artificial rearing; nutrition toxic plants 313, 313
feeding behaviour 7, 7, 301, 305, 313 foramen ovale, closure 88, 182
female reproductive system 21 foreign bodies
congenital disorders 97–8, 97 abomasum 126, 126
femoral head, erosion 224 foot 235
femoral nerve 205, 205 ocular 287, 288–9, 288
fencing 5, 5, 12 forestomach disorders 121–4
fentanyl 341 forestomach, normal structure and function 121
fertility fostering 104, 104
buck 46, 47–9 foxes 213
doe 21 fractures 201, 219–21
herd problems 32 fractures, first aid 219, 220
temporary suppression 59 freemartinism 24
fetal maldisposition 70 frenulum, persistent 52, 53
fetal membranes, retained 67, 81–2, 81 fungal pneumonia 176–7
fetotomy 75–7, 76 furosemide 245
fetus Fusobacterium spp. 82, 169, 186, 231
age calculation 62, 63
maceration 43 gag reflex 196
mummification 35, 36, 42, 43, 44, 44 gait assessment 195–6, 198, 215–6
sexing 62 gallbladder 111, 113, 136
signs of distress 70 gallbladder, fascioliasis 160, 160
signs of life 69–70 gamma-glutamyl transferase (gGT) 92
fibre, dietary 118, 123, 123 gastroenteritis, parasitic 153–9
fibre break 253 general anaesthesia (GA) 334–6
fighting 25–6, 26 dehorning 268
figure-of-eight bandage 268–9, 269 disbudding 267
362 I n de x
general anaesthesia (GA) (continued) head butting 4, 5

exploratory laparotomy 134 head, regional nerve blocks 339–40, 339, 340
induction 335 head tilt 197, 197, 298
monitoring 333 health plan 18
pre- and intraoperative considerations 333, 334–5 health and safety, post-mortems 348, 351
recovery 336 heart, examination 179
genetic abnormalities 85, 86, 202, 281, 287–8 heart failure 179–80, 183, 184, 185
genomics 3–4 heart rate 179
gestation 61 heart sounds 179
see also pregnancy heart valves 179, 182–3
gestational age 62, 63 see also cardiac valves
giant cell tumour, oral 118, 118 heartbeat, absent in newborn 88, 88
giardiasis 163 heartwater 181
gid (coenurosis) 213–14 ‘heat box’ 90, 90
glucose hepatic see liver
intraperitoneal 18, 89 hepatic lipidosis 136, 301, 302, 303, 303
intravenous 302 hepatotoxins 314, 320
glucose/dextrose solution 343 hernia
glutathione peroxidase 308 inguinal 50, 51, 132, 132
goat keeping, evolution 1–3 umbilical 137–8, 137, 140–2
goat meat 3, 4, 4 hip dysplasia 224–5, 224
goat plague (peste des petit ruminants) 161–3, 176 histopathology 351, 352
goat pox 262–3, 262 Histophilus somni 183
goitre, congenital 101, 310–11 history taking 14
goitre, milk 189–90 horns 13
goitrogens 310 removal in adult 267–9
Golden Guernsey goat 7 housing 11–12, 11
gonadotrophin-releasing hormone (GnRH) 25, 27 and fly worry 259, 260
goose-stepping 205 goatlings 107, 107
gousiekte 184 ventilation 11–12, 165, 165, 166
grass tetany (grass staggers) 300–1 human chorionic gonadotropin (hCG) 27
grazing 7 humane killer 344–5, 345
griseofulvin 265 husbandry systems 2
growth, poor 145, 155, 182, 187, 310 hydration status, assessment 342
growth rate, post-weaning 107 hydrometra 63–4, 63, 64
gynaecomastia 59 hydronephrosis 240, 241
hydrops uteri 64–5, 64
haematocrit 181, 189 hygiene 19–20
haematology 180–1, 181, 353, 355 hymen, persistent 28, 29
haematoma hyperaesthesia/hypersensitivity 208, 209, 211, 213, 300, 316
aural 296–7, 297 hyperkeratosis 251, 251, 252
penile 53–4 hypermetria 198, 199, 202
sporadic 266 hyphaema 295
traumatic 219 hypocalcaemia (milk fever) 299–300, 299, 302
haematopoiesis 187 hypocalcaemia, atypical/secondary 245, 299, 316
haematuria 237, 238, 314 hypocupraemia 306–7
haemoglobinuria 237, 238, 314 hypoglycaemia, neonate 95–6, 95
haemolysis 188 hypomagnesaemia (grass tetany) 300–1
Haemonchus contortus 154, 155, 187, 350 hypometria 198
haemoptysis 186 hypoproteinaemia 181, 181
haemorrhage 188 hypopyon 295
after castration 57, 57 hypospadias 24, 24
post-parturient 77, 77 hypothermia
haemothorax 171 general anaesthesia 334–5, 335, 336, 336
hair follicles 13 neonate 89, 89
hair plucks 249, 249 hypotrichosis 253, 253
handling 12–13
hanging pin (transfixation pin) casts 220 identification, individual goats 20
‘hard udder’ 226 ileal obstruction 111
Hartmann’s solution 343 ileocolonic junction 130
hay, toxic plants 313 ileus 132
haylage 7, 8 illness, signs of 6
I n de x 363
imidocarb 194 joints (continued)

immune response, stimulation 92 cartilage disorders 224–5
immune system 90–5 congenital contracture 99–100
immunoglobulin (Ig) 90, 91 dislocation 223
impetigo, udder 263, 263 mycoplasma infection 228–9
impression smears 249–50 palpation 216
infectious keratoconjunctivitis (pink eye) 291–2 radiography 216, 217
infiltration anaesthesia 336–41 jugular veins 179
infraorbital block 339, 339
inguinal hernia 50, 51, 132, 132 kale 314, 317
inhalation anaesthesia 335 keratin 251, 252
injection anaesthesia 335–6 keratitis 295
injection site abscesses 266, 266 keratoconjunctivitis 262, 262, 274
injections keratoconjunctivitis, infectious (pink eye) 291–2
intramuscular 16, 17 ketamine 335, 342
intraperitoneal 18, 19 ketones 301, 302, 303
intravenous 17–18, 18, 185–6 ketoprofen 342
needle sizes 18 ketosis 301–4
subconjunctival 18, 19, 292 kidneys 237
subcutaneous 16, 17 biopsy 239
injury risks 215 lymphosarcoma 245, 245
insect bite reactions 260 ultrasonography 239, 239
insulin 302 see also renal
intensive dairy farming 2 Klebsiella spp. 246
intention tremor 202 knuckling reflex 197
interdigital dermatitis (scald) 230–2, 231 kyphosis 218
intersex 24, 24
interstitial pneumonitis 226 labour 67–8
intestines lactation 13, 271
disorders 111, 128–32, 135 calcium requirements 300
normal structure and function 130 drying off 272–3, 279
parasites 153–9 induction 273–4
ultrasonography 111, 111, 131 lack of post-partum 273
intramammary tube 279 in non-bred females 272–3
intramedullary pins 220 lactational ketosis 303–4
intramuscular injection 16–7 lambing snare 70, 70
intraperitoneal injection 18 lameness
intraocular pressure (IOP) 286, 287 assessment 215–17
intravenous catheter 17–18, 18 foot 216, 229–35, 230, 324–5
intravenous fluid therapy 334, 342–4 laminitis 229–30
intravenous injections 17–18, 18 lancet fluke 160
venous thrombosis 185–6 laparotomy
intravenous regional anaesthesia (IVRA) 340–1, 341 exploratory 134, 135
intussusception 111, 130, 131 insemination 26–7, 27
iodine deficiency 101, 310–11 paravertebral block 337–8, 337
Ipomoea spp. 202 laryngeal infections 169–70, 169, 170
iris 285, 285 legislation 20
adhesions (synechiae) 290, 293, 293 leptospirosis 43
iritis 293 lethal injection 344
iron deficiency anaemia 188 leucoencephalomyelitis 226
isolation 20, 20 levamisole 157–8, 157
ivermectin 157, 214, 298 libido, deficiency 46
Ixodes ricinus 42, 258 lice 249, 249, 257–8, 257
lidocaine hydrochloride 337
jaundice 136, 179, 314, 317, 318, 318 lifespan 14
Johne’s disease (paratuberculosis) 151–3 lighting, artificial 23
joint blocks 216–17 limb reflexes 196
joint fluid 216, 229, 354 limbs
joint ill (bacterial arthritis) 227–8 angular deformity 217, 218
joints nerve blocks 340–1, 341
abscess, pedal 235, 235 palpation 216
CAE infection 226, 226 Linognathus spp. 257
364 I n de x
Listeria monocytogenes 40, 206, 292, 293 mandibular block 339, 339
listeriosis 40–1, 206–8 mange 253–7, 297–8
litter size, determination of 62 Mannheimia haemolytica 174
liver mannosidosis, acquired 201–2
abscess 136, 136 beta 101
biopsy 112–13, 113 marching soldier gait 196, 198
examination 110–11, 112 mastectomy 283–4
fatty necrosis (hepatic lipidosis) 136, 301, 302, 303, 303 mastitis 275–81
metastatic tumours 136, 137 acute 276, 278
normal structure and function 136 aetiology 275
tuberculosis lesions 328 CAE 226, 276, 277
white muscle disease, ovine 310 chronic 276, 276, 279
liver fluke 159–60, 159 clinical presentation 276, 276
local anaesthesia 216–17, 336–41 control 279–80
local anaesthetic agents 337 diagnosis 277–8, 277
lochial secretions 83, 83 FMD associated 324–5
locoweeds 202 gangrenous 271, 276, 277, 278–9
longevity 14 milk appearance 271
lordosis 218 pathophysiology 275–6
louping ill 213 prevention and control 279–81
lower motor neurons (LMN) lesions 195 subclinical 277
lucerne (alfalfa) 7, 250 treatment 278–9
lungs tuberculosis associated 275
abscesses 167, 176, 177 meat 3, 4, 4
adaptation in newborn 86 meconium retention 96, 96
atelectasis 87, 87 medetomidine 333–4
auscultation 166–7 median nerve 205
consolidation 174, 174 mediastinal neoplasia 190
premature kid 103 medication 15–9
tuberculosis 328 megaoesophagus 120–1, 120
lungworm 174–5 megestrol acetate 23
luteal cyst 25 melanoma 266
lymph nodes 187, 188 melatonin 23
enlargement 262–3 meloxicam 279, 342
neoplasia 190 menace reflex 101, 195, 196
tuberculosis lesions 328 meningeal worm 214
lymphadenitis, caseous (CLA) 176, 177, 191–3, 192 meningitis, bacterial 208–9
lymphoma 190 mental nerve block 339, 339
ocular 290–1, 291 mental state 195, 199
uterine 31 mesenteric torsion 131, 131
lymphosarcoma 190, 190, 191 metacestode disease 161
kidneys 245, 245 metamizole 71
oral 118, 118 metatarsal fracture 219, 220, 221
methaemoglobin 314, 317
maceration 43 methylene blue (antidote) 318
macrocyclic lactones 157, 158, 254–6, 258 metritis 82–4, 83
topical 254–5 miconazole 264
magnesium Microsporum spp. 265
blood and humour levels 300, 354 midges 260, 326
deficiency 300 milk
dietary levels 301 artificial feeding 104–6, 105
magnetic resonance imaging (MRI) 112, 214 bulk sample culture 278
maiden milkers 272–3 composition 13, 13
Malassezia spp. 264, 298 conductivity testing 278
male reproductive tract 45, 45 in mastitis 271
disorders 52–5 pasteurisation 227
examination 47–9 quality testing 278
malignant oedema 229 sampling 272
mammary gland see udder somatic cell count (SCC) 271, 277, 278
mandible see also lactation
brachygnathia/prognathia 115, 115 milk fever (hypocalcaemia) 299–300, 299
swelling 117, 117 milk goitre 189–90
I n de x 365
milking machines 280–1 neomycin 245

milking regime 279–80 neonate
mineral deficiencies 10, 44, 86, 217, 218, 305–11 artificial rearing 104–9
mineral supplements 305–6, 306 cardiac function 88, 88
misalliance 28 emergency slaughter 345–6
mites hypotrichosis 253, 253
ears 297–8 immune system 90–5
skin (mange) 253–7 metabolic disorders 100–1
modified Ziehl–Neelsen (MZN) smears 37, 38 musculoskeletal function 98–100
mohair 13 neonatal maladjustment syndrome (‘dummy kid’) 102
monepantel 157, 158 neurological assessment 101–2, 199, 199
monorchism 52 premature 103, 103
Moraxella spp. 292 respiration 86–8
Morel’s disease 265 rotavirus infection 142
morphine 342 septicaemia 93–5, 93, 94
moxidectin 157–8, 157 thermoregulation 89–90
mucous membrane colour 155, 156, 156, 179, 187, 189 urinary function 97–8
Muellerius capillaris 175, 175 weak 85–6, 306, 310
mummification 35, 36, 42, 43, 44 neoplasia
muscle atrophy 198, 204 heart/cardiac 185
muscular dystrophy, nutritional (white muscle kidney/renal 245
disease) 308–9 liver/hepatic 136
musculocutaneous nerve 205 lung 172
musculoskeletal system lymph nodes 190
clinical examination 215–17 male reproductive tract 55, 55
infectious disorders 225–9 ocular 290–1
non-infectious diseases 217–25, 308–9 oral 118, 119
Mycobacterium avium 176, 328 skin/cutaneous 265–6
Mycobacterium avium subsp. paratuberculosis (MAP) 151–3 udder/mammary gland 272, 273
Mycobacterium bovis 176, 275, 328, 348 uterine 31–2, 31, 32
Mycoplasma spp. Neospora caninum 42
arthritis 228–9 neosporosis 42
contagious agalactia 274 neovascularisation 286, 286, 289
Mycoplasma agalactiae 228, 274, 292 nephrotoxicity 245
Mycoplasma arginini 176, 228, 292 nerve blocks 216–17, 337, 337, 339–41, 339, 340, 341
Mycoplasma capricolum subsp. capricolum 274 ‘nest box’ 90, 90
Mycoplasma capricolum subsp. capripneumoniae 172–3, 228 neurological assessment 101–2, 199, 199
Mycoplasma conjunctivae 292 neurological disease
Mycoplasma mycoides subsp. capri 228 infectious 206–8
Mycoplasma mycoides subsp. mycoides 188, 228, 274 neonatal kid 102
Mycoplasma ovipneumoniae 176 non-infectious 201–6, 317, 320
mycotic dermatitis 264 ‘New Zealand’ position 80, 80
mycotoxins 245, 319–21, 320 nitrate/nitrate toxicity 314, 317–18
myelography 201, 201 nitrous fumes 171–2, 313, 314
myiasis ‘nits’ 249, 249, 257
dermal/skin 258–9 non-steroidal anti-inflammatory drugs (NSAIDs) 41,
nasal 169 224, 225, 230, 279, 342
myoglobinuria 238, 308 norgestomet 23
myositis, clostridial 229 notifiable diseases 323, 323
nutrition 7–10, 11, 304
nasal cavity, normal structure 165 and abortion 44
nasal discharge 162, 162, 165, 166, 169 calcium/magnesium requirements 300, 301
nasal passages, narrowing/obstruction 169 dry period 300, 303–4
nasolacrimal duct 285, 286 trace element deficiencies 250–1, 305–11
natamycin 265 vitamin deficiencies 203, 204, 217–18, 311–12
navel, disinfection 95, 95
necropsy see post-mortem examination oak poisoning 245, 314
nematodes obturator nerve 205
cerebrospinal 214 ocular see eye
intestinal 153–9 oedema, dependent 151, 155, 179, 184, 191, 244, 260, 310
life cycle 154 oesophageal feeder 15, 16
Nematodirus battus 156 Oesophagostomum 154
366 I n de x
oesophagus parasites (continued)

dilation 120–1, 120 gastrointestinal 153–60
obstruction (choke) 121–2 lung 174–5
oestrogens 82 parasitic gastroenteritis 153–9
oestrus paratuberculosis (Johne’s disease) 151–3
behaviour 22–3 paravertebral block 337–8, 337
control 23–4 Parelaphostrongylus tenuis 214
cycle 22–3, 22 paresis (weakness) 198, 198, 213, 299–300, 301, 306–7, 308
OIE (World Organisation for Animal Health) 323 parturient paresis 299–300, 299
omentum 130 parturition
omeprazole 128 correction of fetal maldisposition 70
omphalitis 138, 139 dystocia 68–72
open farms 143 induction 67, 302
ophthalmoscopy 286 normal 67–8
opioids 341–2 post-parturient problems 77–84, 299–301, 303–4
opisthotonus 203, 210, 213 parturition kit 69, 69
oral cavity, examination 109, 109, 116–17 passive transfer 90–1
oral lesions Pasteurella multocida 174
bluetongue 327, 327 pasteurellosis 173–4
drenching gun injuries 119–20, 119 patellar reflex 196
FMD 325, 325 patent urachus 139, 140–2
orf 261, 261 pedal joint abscess 235, 235
peste des petits ruminants 162 pemphigus foliaceus 250
tongue 120 penicillins 31, 82, 209
tumours 118–19, 118 penis
oral medications 15–16, 16 deviation 52–3
orchitis 50 examination 45, 47, 48
orf 260–1, 261 phimosis/paraphimosis 54
orogastric tubing 15–6, 16 trauma 53–4
osteochondrosis (OC) 224–5 pentobarbital sodium 344
osteodystrophy, mature bone 218–19 pericardial effusion 183–4, 183
osteomalacia 218 pericardiocentesis 180
osteomyelitis 217, 221 pericarditis 183–4
osteoporosis 218 peripheral nerve disorders 204–6, 205
Ostertagia 154 peritoneal fluid 134, 135, 354
otitis 197, 297–8 peritonitis 78, 79, 109, 112, 124, 127–8, 128, 134–5
ovary peroneal nerve 205
disorders of 24–5, 24 peste des petit ruminants (goat plague) 161–3, 176
normal structure and function 21, 21 Peterson block 340, 340
superovulation programme 27, 28 phenacetin 314
over-milking 280 phenols 314
oviduct (fallopian tube), patency test 28, 28 phenolsulphonphthalein (PSP) excretion 239
ovine white liver disease (OWLD) 310 phimosis 54
oxalate toxicity 316–17 phlebitis 185, 186
oxytetracycline 245, 279 phosphate, serum 240
oxytocin 82, 278 phosphorus deficiency 217, 218
photosensitisation 237, 252–3, 317
pain, signs of 6, 110, 110, 341 phytobezoars 126, 126
palatoschisis (cleft palate) 97 pink eye 291–2
pancreas 136 placenta 61, 61, 62
panniculus reflex 197 plants
pantoprazole 128 causing photosensitisation 252
paper slide test 197 containing goitrogens 310
papillomas (warts) 265–6 containing swainsonine 202
paralysis toxic 181, 184, 245, 252, 313, 315, 316, 314–17, 317
flaccid 195, 199 plasma transfusion 92, 92, 344
spastic 196, 199, 09 pleural effusion 170–1, 190
paralysis, peripheral nerve 204–6 pleuritis 171
paraphimosis 54 pleuropneumonia, contagious caprine 172–3
parasites pneumonia
blood 193–4 aspiration 170
external 253–60 bacterial 173–4, 174
I n de x 367
pneumonia (continued) pseudorabies (Aujeszky’s disease) 212–13

fungal 176–7 Psoroptes cuniculi (P. caprae) 257, 298
parasitic 174–5 Psoroptes ovis 297
pneumonitis psoroptic mange 257
allergic 176–7 puberty 21, 45
CAE 176, 176 pulse 179
pneumothorax 113, 171 punch biopsy 250, 250
poisoning see toxicities pupillary light reflex (PLR) 196, 196
polioencephalomalacia (cerebrocortical necrosis) 202–4 pyelonephritis 237, 245–7
polledness 13 pygmy goat syndrome 251–2, 252
population size 1 Pygmy goats 3
portosystemic shunts 187 pyloric stenosis 125–6
positive pressure ventilation (PPV) 88 pyometra 30, 64
post-mortem examination 347–52 pyothorax 171
approach 348–50 pyrethroids 258, 259
case selection 347
health and safety 348 Q fever 35, 38–9, 38, 348
history of case 347–8 quarantine 20, 20
sampling 351, 351, 352
value of 347 rabies 212
posture radial nerve 205
abnormalities 198 radioimmune diffusion 92
assessment 215–16 ‘rag-doll’ neonate 199, 199
potassium, dietary 300 ragwort 252, 313, 317
potassium chloride 343 Raillietia caprae 297
potassium iodide 118, 311 rape, oilseed 314, 317
pregnancy rearing, kids 104–7, 105–7
abdominal contour 109, 110 record keeping 20
ante-natal preparation 67 rectal prolapse 132–4, 133
behaviour 6–7 rectal temperature 12
diagnosis 61–2, 63 recto-vaginal fistula 78–9, 78
embryonic loss 33–4 rectoanal mucosa-associated lymphoid tissue
prepartum problems 63–7, 301–2 (RAMALT) test 211
rate 26 recumbency
pregnancy toxaemia 44, 301–3 hypocalcaemia 299, 299
prematurity 103, 103 neurological assessment 199
premedication 335 reflexes 195–7
preoperative preparation 334 regional anaesthesia 336–41
prepuce, examination 47, 48 renal
prion diseases 210–12 artery, embolism 237
procaine hydrochloride 337 biopsy 239
procaine penicillin 210, 247 function tests 239
progesterone 23, 273 infarct 237, 244, 244
prognathia 115, 115 insufficiency/failure 244–5
prokinetics 132 reserpine 274
prolapse respiratory disease
rectal 132–4, 133 infectious 172–5, 226, 328–9
uterine 79–81 non-infectious 169–72
vaginal/cervical 65–6, 65 treatment principles 167
propofol 335–6 respiratory rate 165
proprioception, assessment 197 respiratory stertor 169
propylene glycol 302 respiratory system
prostaglandin-F2-α (PGF2α) 23, 31, 67, 82 examination 15, 165–7
prostate gland 47 neonate 86–8
protein requirements 8 normal structure and function 165
proteinuria 238 restraint
Proteus spp. 246 CSF collection 199–200, 200
protozoal infections 142–6, 163 dehorning 268
pruritus 212, 251, 254, 255 disbudding 267
pseudolactation 272 foot trimming 234
Pseudomonas spp. 246, 275 mastectomy 283
pseudopregnancy 63–4, 63 teat surgery 282
368 I n de x
resuscitators 88, 88 silage clamp 8, 313, 314

reticuloperitonitis, traumatic 124 sinusitis 169
retinol 311 skin
retrobulbar block 340 examination 249–50
Rhododendron 314–15, 315 skin necrosis 252, 253, 262, 320
rib fracture, newborn 86, 86 non-infectious disorders 250–3
rickets 217–18 parasitic diseases 253–60
Rift Valley fever 43, 330, 331 skin biopsy 250, 250
ringwomb 70–1 skin innervation, autonomous zones 205
ringworm 265, 265 skin scrape 249, 249
Robert-Jones bandage 220 small ruminant lentivirus (SRLV) 225
rock salt 305 smartphone technology 180
rotavirus 142 smoke bomb test 166
routine procedures 18 smooth muscle relaxants 71, 241
rubber ring castration 56, 56 snake bites 172, 188, 253
rumen sodium bicarbonate 101, 123, 343
acidosis 122–3, 122, 136, 203 sodium iodide 118
contractions 119 somatic cell count (SCC) 271, 277, 278
examination of contents 350 space requirements 11, 107
fistula 124, 125 sperm
trocarisation 124 abnormalities 46, 47
tympany (bloat) 121–2, 129, 209, 210 examination 49
rumen fluid 113–14, 114, 122, 123 spermatic cord, ligation/clamping 56, 57
rumenitis 122–3, 186, 186 spermatogenesis 45, 59
rumenocentesis 113–14 spinal abscess 204, 204
rumenotomy 124–5 spinal cord lesions 197, 201
spleen 187
Saanen goat 3, 6 splinting 219, 220
St John’s Wort 252, 317 squamous cell carcinoma (SCC) 290–1
saline, hypertonic 343 stance, abnormal 91, 101, 197, 199, 202, 205, 205
Salmonella spp. 93, 147, 348 staphylococci, coagulase-negative 275
salmonellosis 41, 147–8 Staphylococcus aureus 258, 263, 263, 275, 276
salpingitis 82 Staphylococcus aureus subsp. anaerobius 263, 265
sample collection Staphylococcus hyicus 263
aborted kid 34–5, 352 Staphylococcus intermedius 263
post-mortems 351, 352 ‘star-gazing’ 203
Sarcina spp. 128, 128, 129 starvation, pre-operative 334
sarcocystosis 120 sticky kid disease 104
Sarcoptes scabiei var. caprae 255–6 stomach contents, abnormal 314
sarcoptic mange 255–6, 256 stomach tube 15–16, 16, 122
scald (interdigital dermatitis) 230–2, 231 stomatitis see oral lesions
Schirmer tear test 286, 286 strabismus 196, 196
Schmallenberg virus 42, 99, 330 straw, feeding 123
scrapie 210–12 Streptococcus spp. 82, 93, 227, 246
scrotal circumference 47, 48 group D 183
seborrhoeic dermatitis (pygmy goat syndrome) streptothricosis 264
251–2, 252 stress 13
sedation 72, 333–4 Stromal abscess 289–90, 289
reversal 334 Strongyloides 154
selenium deficiency 184, 308–9 subacute rumen acidosis (SARA) 122–3
selenium sulphide washes 252, 254, 264 subconjunctival injection 18, 19, 292
semen suck reflex 196
collection 26, 47–8 subcutaneous injection 16
evaluation 47–9 sudden death 119, 149, 172, 174, 184, 185, 186, 300, 308,
seminal vesiculitis 52 316, 317, 317, 319, 329
septal defects 181–2, 182 sulphonamides 245
septic shock 93 supernumerary teats 281–2, 281
septicaemia, neonatal 93–5 superovulation programme 27, 28
sigmoidoscope, human 27, 27 suprascapular nerve 205
silage 7, 8 surgery, general principles 334–5
listeriosis 40–1, 41, 206, 208 swainsonine 202
I n de x 369
swayback tick pyaemia 258

congenital 102, 306–7 ticks 42, 258, 258
delayed 306, 307, 307 tocopherol 184, 191, 308–9, 312
swelling disease 191, 191, 312 toclopramide 132
synechiae 290, 293, 293 Toggenburg goat 3
synovial fluid 216, 354 toltrazuril 146
tongue lesions 120
Taenia multiceps 213 tooth eruption 114–5, 114
tail flagging 22, 22 total bacterial count 278
tape strips 249 total protein (TP) 91, 181
tapetum lucidum 285 toxicities 313–21
tapeworms 160–1 causing abortion 44
carnivore 213–14 causing nephrosis 245
tarsorrhaphy 290, 292, 293 causing neurological disease 202
taxine 315–16 gases/fumes 171–2, 313
Taxus baccata 315–6, 315, 316 investigation 313, 314
tear apparatus 285 treatment approach 313
teat biting 272, 272 water 321
teat blocks 341 see also plants, toxic and specific toxins
teat feeders 105, 106 Toxoplasma gondii 35, 293
teat lesions 260–1, 263, 263, 265, 280, 325 toxoplasmosis 33, 35–6, 35, 36
teats trace element deficiencies 305–11
fishtail 282 trachea, narrowing 167, 167
supernumerary 281–2 tracheotomy 167–9, 168
surgery 282–3 transcervical intrauterine insemination 27
trauma 272, 272, 280, 280, 283 trauma
washing/disinfection 280 blood vessels 187
Teladorsagia/Ostertagia nematodes 154 drenching gun 119–20, 119
tendonectomy 98–9, 99 ears 295–7, 296
tendons eye 287
contracted 98–9, 99 fractures 219–21
injuries 223–4 horns 267, 268
laxity 99, 103 joint dislocation 223
terminology 3 tendon 223
testes udder/teats 272, 272, 280, 280
absent/incomplete descent 51–2, 52 uterine tract 29–30, 29
degeneration/atrophy 49–50, 51 traumatic reticuloperitonitis 124, 183
examination 47 treponeme-associated foot disease 232–3, 233
hypoplasia 49 trichobezoars 126
neoplasia 55, 55 Trichophyton spp. 265
normal structure and function 45, 45 Trichostrongylus 154
retained 51–2 Trichuris 154
tetanus 209–10, 334 trimethoprim/sulphonamides 82, 247
tethering 12 triplets 75
tetracyclines 31, 38, 82, 229 trough space 7
tetralogy of Fallot 182 Truperella pyogenes 82, 119, 169, 170, 183, 186, 227
thermoregulation 12, 89–90, 103 mastitis 275, 276
thiamine (vitamin B1) 203, 204 tube cystotomy 243–4, 243, 244
third eyelid flap 290, 290, 293 tuberculosis 176, 177, 275, 328–9, 328
thorax tylosin 229
auscultation 166–7, 179 udder
radiography 167, 167 atrophy 274
tumours 172 bluetongue lesions 327, 327
thrombosis 185–7 enlargement 272, 272
thymus 187 examination 271–2
enlargement 189–90, 266 fibrosis 276
neoplasia 172, 190, 191 impetigo 263, 263
thyroid gland 310–11 induration 271
thyroxine (T4) 310, 311 infectious disorders 274–81
tibial nerve 205, 205 non-infectious diseases 272–4
tick-borne diseases 42, 181, 193–4, 213, 258 surgery 281–4
370 I n de x
ulnar nerve 205 vaginal discharge 30, 43

umbilical hernia 137–8, 137 vaginal speculum 27
repair 140–2 vaginitis, necrotic 84
umbilical stump valethamate bromide 71
bleeding 77, 77 vas deferens, ligation 58, 58–9
care 95, 95 vasculitis 187
umbilicus vasectomy 57–8, 58, 59
infections 138–9, 139 Velpeau sling 220, 223
normal structure and function 137 vena cava thrombosis 177, 180, 186–7, 186
surgery 139–42 venereal disease 59
underbite 115, 115 venous thrombosis 185–6
upper motor neuron (UMN) system/lesions 195–7, 198 ventilation 11–2, 165, 165, 166
urachitis 138–9 ventricular dilation 184, 185
urachus, patent 139, 140–2 ventricular septal defect (VSD) 181–2, 182
uraemia 98, 240, 244–5 vestibular syndrome 197, 197, 198
urea:creatinine ratio 239 vitamin A 311
urea, dietary levels 319 vitamin B group 203, 204, 309–10
urea poisoning 319 vitamin D 187, 217–18
ureters 237 vitamin E 184, 191, 308–9, 312
urethra 237 vitreous humour, analysis 299, 300, 354
obstruction 240–1, 240 vomiting 315
urethral process (filiform appendage) 45, 45, 237 vulva
removal 241 acquired disorders 29, 29, 30
urethrotomy 242–3, 243 congenital disorders 97–8, 97
urinalysis 237–8, 238, 238, 314, 354 sutures 29, 80, 80
urine, abnormal colour 314 vulvoplasty 66
urinary tract vulvovaginitis 32–3, 43, 54, 59
bladder, calculi 240
examination 237–9 Walpole’s solution 244
neonate 97–8 warble fly 258
normal structure and function 237 water provision 9, 10, 251
urination, frequent 29, 246 water quality 305, 321, 321
urine acidification 242, 247 wattles 14, 22, 22
urine output 94, 94, 237 weakness (paresis) 195, 198, 198, 214, 299–300, 306–7,
urine retention 97–8, 97 308
urolithiasis 237, 240–1, 240 weaning 106–7
uroperitoneum, diagnosis 240 Weingart frame 125
uterine artery, thrombus 187 white line disease 234–5
uterus white muscle disease 308–9, 309
acquired disorders 29–30 Winkler’s cervicoplasty 66
amputation 81 withdrawal reflex 196
congenital disorders 28–9 world goat population 1–2
endometritis 30–1, 30 World Organisation for Animal Health (OIE) 323
neoplasia 31–2, 31 worm burden 187, 189
normal structure and function 21 wounds, non-healing 222, 222
post-partum infection 82–3, 83
prolapse 79–81 xylazine hydrochloride 65, 72, 133, 333, 335, 338
rupture 66–7, 79
torsion 71, 72 yersiniosis 148
uveitis 290, 293, 295 yew 315–16, 315, 316
vagal indigestion 121, 125–6 zinc deficiency 250–1

vagina zinc sulphate turbidity test 91
laceration 78 zoonotic pathogens 35, 37–40, 43, 142, 143, 146–8, 161,
prolapse 65–6, 65, 79 163, 191, 212, 255, 261, 265, 328, 329, 348
vaginal dilation, failure 70

Goat Medicine and Surgery

Uploaded by

Copyright:

Available Formats

Goat Medicine and Surgery

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Goat Medicine and Surgery

Uploaded by

Copyright:

Available Formats

Goat Medicine and

KARIN MUELLER MVSC DCHP DIPECBHM MRCVS

© 2018 by Taylor & Francis Group, LLC

No claim to original U.S. Government works

Printed on acid-free paper

International Standard Book Number-13: 978-1-4987-4863-6 (Hardback)

Library of Congress Cataloging‑in‑Publication Data

Names: Harwood, David, BVM, author. | Mueller, Karin, author.

Visit the Taylor & Francis Web site at

and the CRC Press Web site at

CHAPTER 2 REPRODUCTIVE SYSTEM 21

Non-infectious causes of abortion 43

CHAPTER 3 PREGNANCY AND PARTURITION 61

CHAPTER 5 DIGESTIVE TRACT AND ABDOMEN 109

NON-INFECTIOUS DISEASES OF THE DIGESTIVE TRACT AND ABDOMEN 114

Umbilical infections 138

CHAPTER 6 RESPIRATORY SYSTEM 165

Caseous lymphadenitis 176

CHAPTER 7 CARDIOVASCULAR DISEASE AND DISORDERS OF

CHAPTER 8 NERVOUS SYSTEM DISORDERS 195

Inherited central nervous system disorders 202

CHAPTER 9 MUSCULOSKELETAL DISEASE INCLUDING FOOT DISORDERS 215

Pedal joint abscess 235

CHAPTER 10 URINARY TRACT DISEASE 237

CHAPTER 11 SKIN DISEASES 249

CHAPTER 12 MAMMARY GLAND DISORDERS 271

CHAPTER 13 SENSORY ORGAN DISEASE 285

CLINICAL EXAMINATION OF THE EYE 285

CHAPTER 14 METABOLIC DISORDERS 299

CHAPTER 15 TRACE ELEMENT AND VITAMIN DISORDERS 305

CHAPTER 16 POISONING AND TOXICITIES 313

CHAPTER 17 EXOTIC AND EMERGING DISEASES 323

CHAPTER 18 ANAESTHESIA, FLUID THERAPY, EUTHANASIA 333

CHAPTER 19 POST-MORTEM EXAMINATION AND SAMPLING 347

ACDP Advisory Committee on Dangerous CT computed tomography

i/m intramuscular OIE World Organisation for Animal Health

EVOLUTION •• Provision of shelter from predators and the

This background information gives the reader

GOAT BREEDS AND THEIR PURPOSES

The goat is a member of the family Bovidae and is

Source: United States Department of Agriculture.

It is important to ensure that top performing

Goat behaviour can be interesting, unusual and at

translates to about 8.5 MJ of ME for a 50 kg goat and

Fig. 1.28 When using the neck for intramuscular

The gluteal muscles may be used in well-­

Fig. 1.29 Intravenous injection into the jugular vein.

Using the non-dominant hand, the kid is held

Intraperitoneal injection Biosecurity is defined as ‘the prevention of disease-­

Fig. 1.31 Intraperitoneal

from entering or leaving a property and being spread.

•• Prevent the introduction of infectious diseases.

NORMAL STRUCTURE AND FUNCTION

The goat has a bicornual uterus, with a short uter-

FECUNDITY polyoestrus breeders. In Northern Europe they are

Fig. 2.3 Wattles, here in a British Alpine goat, are

with single service or insemination at 40–48

•• Prepubescent because of suboptimal growth

•• Failure to stand: not being in oestrus; fear of the Treatment/management/control

The gluteal muscles may be used in well-

Intraperitoneal injection Biosecurity is defined as ‘the prevention of disease-

ring-electrode one, and the unit should allow grad-