PATH-261 (SPO) L2SII Theory (Full)

Course Title: Systemic Pathology and Oncology (Theory)
Course code: PATH-261

Credit hour: 3
Level-2, Semester-II
Lectures: 1~ 6
Learning Objectives: The major learning outcomes/objectives of this course are to-
 Acquire knowledge about different terminologies in the different systems.
 Enrich knowledge on systemic diseases of livestock.
 Recognize the pertinent aspects of the diseases including etiology, pathogenesis and
pathological features which will help in the diagnosis of the diseases.
 Develop knowledge on comprehensive, state-of-the-art expertise and proficiency in
oncology.
Rationale:
 This course is designed for the details study of pathology of different systems.
 Oncology provides basic concepts on tumor.
How to do study systemic pathology? Approaches to good results…

 Lectures (audio/visual/pictorial) with questions and answers (Q/A)
 Textbooks
 Laboratory practices (gross specimen and glass slides)
 Postmortem demonstrations (real or video)
 Recommended internet websites
 Group discussion and/or peer-share/sharing knowledge
 Field practices
 Clinicopathological conferences/workshop/seminars
Books Recommended of the course:

1. Veterinary Pathology by Jones, T. C, Hunt. R. D. and king. NW 6th edition. Williams
and Wilkins, Philadelphia, USA1997.
2. Fundamentals of veterinary clinical pathology by Steven L. Stockham and Michael A.
Scott.
3. Text book of Veterinary Pathology by Prof. R.S. Chauhan. 1st edition, 2010.
Dr. Amina Khatun, Assist. Prof., Dept. of Pathology, FASVM, SAU, Dhaka-1207 1
Systemic pathology: Systemic pathology is the special branch of pathology, which deals with
the diseases of different systems of the body. e.g. Diseases of digestive system.
Systems of the body:

1. Digestive system
2. Respiratory system
3. Cardiovascular system
4. Haemopoietic and lymphatic system
5. Urogenital system
6. Musculoskeletal system
7. Nervous system
8. Endocrine system
9. Organs of special senses
10. Skin and appendages.
Oncology: Oncology is the branch of pathology or medicine, which deals with neoplasia
(cancer/tumor/neoplasm).
Diseases of Digestive System

Primary structures or parts of digestive system: (in consecutive order) as follows-
1. Mouth and Adnexa: (Teeth, tongue, lips, gum, palate)
2. Pharynx
3. Esophagus
4. Stomach
a. Simple stomach
b. Compound stomach
i. Rumen
ii. Reticulum
iii. Omasum
iv. Abomasum (true stomach)
5. Small intestine
a. Duodenum
b. Jejunum
c. Ileum.
6. Large Intestine
a. Caecum
b. Colon
i. Ascending colon
ii. Descending colon
iii. Transverse colon
c. Rectum
7. Anus.
Accessory/associated structures/organs of digestive system:
1. Salivary glands (3 pairs)
a. Parotid salivary glands
b. Submaxillary salivary glands
c. Sublingual salivary glands
2. Gastric and intestinal glands
3. Liver
4. Pancreas
5. Gall bladder
6. Nerves
a. Sympathetic
b. Parasympathetic
Digestive system of chicken: has following parts-

1. Tongue
2. Gullet
3. Crop
4. Proventriculus (glandular stomach)
5. Gizzard (muscular stomach)
6. Small intestine
7. Two caeca
8. Large intestine
9. Cloaca (common opening of digestive and genitourinary system)
10. Vent (External opening)
Pathological lesions/disorders in the mouth/oral cavity:

a. Inflammation:
i. Cheilitis: Inflammation of the lips.
ii. Gingivitis: Inflammation of gums.
iii. Periodontitis: Inflammation of the surrounding tissues of teeth.
iv. Glossitis: Inflammation of tongue.
v. Lampas: Inflammation of palate.
vi. Stomatitis: Inflammation of mucous membrane, lining of the mouth or buccal
cavity or oral mucosa.
b. Developmental anomalies:
i. Cleft lip (Cheiloschisis)
ii. Cleft palate (Palatoschisis)
iii. Brachygnathia superior: Shortness of the maxilla.
iv. Brachygnathia inferior (Macrognathia) Shortness of the mandibles.
v. Prognathism: abnormal prolongation of the mandibles.
vi. Agnathia: Mandibulofacial malformation characterized by absence of the lower
jaw.
vii. Epitheliogenesis imperfecta: Widespread defect in cutaneous epithelium and
also the lining of the oral cavity.
Stomatitis
Definition: Stomatitis is defined as an inflammation of mucous membrane of mouth, lining of
the mouth or buccal cavity or oral mucosa, characterized by partial or complete loss of appetite
by smacking of the lips and profuse salivation (ptyalism).
Causes of stomatitis:
1. Physical agents: e.g.-
i. Trauma while dosing.
ii. Foreign body injury.
iii. Malocclusion of teeth.
iv. Sharp awns.
v. Spines.
vi. Nails.
vii. Wires of grasses.
viii. Eating of frozen feed.
ix. Drinking of hot water etc.
2. Diseases caused by infectious agents:
a. Bacterial diseases: e.g.-
i. Nacrobacillosis.
ii. Actinomycosis (Actinomyces bovis) (Lumpy jaw in cattle)
iii. Actinobacillosis (Actinobacillus lignieresii) (Wooden tongue)
b. Viral diseases: e.g.-
i. Foot and mouth disease (FMD).
ii. Peste des petits ruminants (PPR)/ goat plaque.
iii. Rinderpest/ cattle plague.
iv. Bovine malignant catarrhal fever (BMCF).
v. Blue tongue.
vi. Vesicular stomatitis (VS).
vii. Bovine viral diarrhea/ bovine mucosal disease etc.
3. Fungal infections: e.g.-
a. Candida albicans.
4. Deficiency of essential vitamins: e.g.-
a. Hypovitaminosis
- Vit-C
- Riboflavin
- Niacin
- Vit-A etc.
5. Chemical agents:
i. Dosing of irritant drugs, e.g. chloral hydrate.
ii. Mistaken dosing of irritant substances, e.g. acid, alkaline, phenol etc.
iii. Counter irritants applying on skin, e.g. tincture of iodine.
iv. Manifestation of systemic poisoning, e.g. chronic mercury poisoning.
6. Secondary causes (o other diseases): e.g. autoimmune disorders.
Clinical signs of stomatitis:

1. Pain and discomfort in the mouth.
2. Dysphagia.
3. Burning sensation.
4. Irritability and restlessness.
5. Hyper salivation.
6. Partial or complete anorexia.
7. Smacking of lips.
8. Decreased/reduced production performance.
Pathology of stomatitis:
1. Gross lesions:
i. Formation of vesicles in oral mucosa.
ii. Erosion and ulceration.
iii. Sloughing off the mucosal epithelia.
2. Microscopic lesions:
i. Formation of varying degree of cavity.
ii. Hyperemia and congestion.
Tonsillitis: is the inflammation of tonsil. It is usually caused by viral or bacterial infections, and
characterized by sore throat, fever, enlargement of tonsils, difficult swallowing. Certain
hemolytic streptococci and coliforms that colonize in the tonsillar crypts cause an acute
inflammatory reactions. In such cases, the tonsils will be swollen and hyperemic, and the crypts
will exude a yellow-white purulent exudates.
Noma (orofacial gangrene): is derived from the Greek word “to devour” meaning destruction,
which denote the aggressive and destructive nature of the disease. Noma is a rapidly progressive,
gangrenous process that affects the gingiva and underlying bone, and the mucosa of the lips and
cheeks. Noma is mostly occurs in the children with malnutrition, poor oral hygiene and
debilitating concurrent illness found in the underdeveloped parts of Africa, Asia and South
America, and also in non-human primates (monkey, chimpanzee).
Cleft Palate: This is one of the most frequent congenital anomalies results from the failure of
the primitive oral and nasal cavity to be divided during embryonal life leading to a cleft (split)
of varying length in the approximate centre of the hard palate.
Neoplasms of oral cavity:

1. Viral papillomas: Papilloma virus induced benign neoplasm of the squamous
epithelium of the oral and labial mucosae. It occurs in dogs, cattle and rabbits.
2. Epulis: An epulis (pl: epulides) is a benign tumor or neoplasm derived from
periodontal ligaments or connective tissues. It occurs commonly in dogs, but
rarely in cats.
Types: based on the cellular and tissue composition, epulides are 3 types -
i. Fibromatous epulis
ii. Ossifying or cementifying epulis
iii. Acanthomatous epulis
3. Squamous cell carcinoma:
4. Malignant Melanoma:
5. Fibrosarcoma
6. Osteosarcoma
7. Odontogenic tumor.
Sialoadenitis: Inflammation of salivary glands.
Sialoliths: Sialoliths are salivary calculi, form in the ducts or in the gland itself, as a result of
chronic inflammation that provides desquamated cells or consolidated exudates as a minute
nidus formation upon which calcium salts precipitate.
Ranula: When the salivary duct is occluded for prolonged period, the gland undergoes atrophied.
But before this process is completed, a cyst may be formed in the obstructed duct due to dilating
effects of entrapped secretions. Such a cyst in the sublingual ducts, which is located in the
frenulum of the tongue is referred to as “ranula”.
Causes/mechanism/pathogenesis of Ranula:
1. Saliva is fluid formed primarily by three salivary glands on either side of the mouth:
- the parotid glands, the submandibular glands, and the sublingual glands.
2. If one of the salivary glands, usually the sublingual gland, is injured or diseased the
saliva will no longer reach the mouth where it can be swallowed.
3. The saliva leaks out of the injured gland and forms a bubble of fluid in the tissue around
the gland which is called a ranula.
4. A ranula usually is a 2-3 inch diameter painless soft swelling under the tongue or chin
that is easy to identify.
Salivary fistula: A salivary fistula occasionally forms when Injury creates an opening from the
ducts to the outside of the body, proper healing being prevented by the flow of saliva through
the opening.
Neoplasms of salivary glands:

1. Mucoepidermoid tumors
2. Squamous cell carcinoma
3. Adenoid cystic carcinoma (cylindroma)
4. Acinic cell carcinoma
5. Adenocarcinoma
6. Undifferentiated carcinoma
Diseases of Esophagus
A. Inflammatory degenerative lesions:
Esophagitis: Inflammation of esophagus resulting from foreign objects, wasting

medicine or corrosive drugs or infections.
Cause:
1. Rinderpest
2. Mucosal disease
3. Malignant catarrhal fever
4. Pox
5. Bovine rhinotracheatitis
6. Candidasis
7. Spirocercosis (Spirocerca lupi) in dog
8. Gongylonemiasis in ruminants
9. Gastrophilus Spp (Horse)
10. Hypoderma spp (cattle)
11. Sarcocystis spp (Protozoa) in sheep and goat
12. Toxoplasma spp
13. Caustic or irritating chemicals
14. Injuries
B. Obstructive lesions: e.g. Choke
Choke/ esophageal obstruction
Definition: Choke is a complete or partial impaction/ obstruction of the esophagus by foreign
bodies/ materials.
Pathogenesis: If the materials cannot pass through the esophagus then they occlude the passage.
1. In cattle: It is common in cattle as they try to swallow large and firm items of food
such as beets, turnips, apples, potatoes, sweet potatoes, mango seeds, jackfruit’s
residues, guava, tennis ball, polythene bag etc.
2. In horse: it is due to gradual accumulation of ground or wholegrains or tough grasses

that fails to continue their passage through the whole length of the esophagus and
ultimately results to form choke.
3. In dog and cat: choke results usually due to lodge of sharp piece of bones in the
thoracic esophagus.
4. Other Causes:
a. The adult nematode Spirocerca lupi in dog (They cause nodular growth >>
esophageal obstruction >> ultimately cause neoplasm)
b. Gongylonema spp (in cattle)
c. Bot fly: Gastrophilus spp., Hypoderma spp., Sarcocystis spp. (in human/
primates).
Pathological Lesions:
1. Vary with the causes.
2. The small foreign bodies produce localized laceration or necrosis, ulceration and
granulocytic response.
3. Complete obstruction and may cause death.
Effects and significance/ complications:
1. If choke is not relieved, death is likely to occur about in 3 days because of
pressure necrosis due to ischemia, followed by gangrene and resulting toxemia,
septicemia and sapraemia.
2. Sharp objects such as bones usually cause perforation.
3. Failure to regurgitation and to form gas in the rumen leading to ruminal tympany
or blot in ruminants.
4. In dog and cat, choke cause vomiting in few weeks by repeated distention on the
wall of the above partially obstruction usually unilateral known as esophageal
diverticulum.
Neoplasms of esophagus:
2. Adenocarcinoma,
3. Papilloma
4. Fibrosarcoma
5. Osteosarcoma
C. Motility disorders/ lesions: e.g. Reflux esophagitis.

Reflux esophagitis
It is a form of chemical esophagitis that occurs when reflux of gastric acid and pepsin
from the stomach, and bile salts and pancreatic juice from the intestine occur in the lower
esophagus.
Causes:
1. Chronic vomiting due to hyper acidity.
2. Loss of integrity of esophageal sphincter.
3. Esophageal diverticulum.
Grossly: there is hyperemia, erosion and ulceration.

Microscopically: infiltration of leucocytes that depends on the nature of the inflammation.
Stenosis or Stricture of esophagus: Narrowing the lumen of esophagus resulting from the
formation of excessive scar tissues in the wall of the esophagus during the healing process after
surgical operation, injuries, and infections.
Cricopharyngeal achalasia: When food particles is remained in the pharynx due to inadequate
relaxation of the cricopharyngeal sphincter, found in dogs.
Megaesophagus: Segmental non-localized dilatation of the esophagus due to neuromuscular

disorders found in puppies. The wall of the esophagus is atonic and flaccid. Pathogenesis is
poorly understood.
Diseases/ Disorders of Rumen (fore stomach of ruminants)
Diseases/disorders of rumen:
1. Ruminal tympany/bloat
2. Ruminal acidosis
Ruminal tympany/bloat
(Tympanic indigestion/Tympany/Ruminal bloat/Pasture bloat/leguminous bloat/ruminal
tympanites/bloat)
Tympany: Excessive accumulation of free gases separated from ingesta in the rumen is called
ruminal tympany.
Bloat: excessive accumulation of frothy gas (usually mixed with ingesta) in the rumen is called
bloat.
Gases are accumulated as –
 Methane
 CO2
 H2S
 Small amount of other gases.
The production of gases in the rumen is usually happened by the bacterial decomposition
of carbohydrate (CHO) and proteins, and the action of many kinds of saprophytic bacteria upon
ingested plant tissues. Normally, the gas is discharged in the form of belching or eructation
through the esophagus and mouth.
Etiology/causes:
1. Primary causes: due to dietary origin (usually), which causes frothy bloat. e.g.
i. Legume pastures
ii. Succulent grasses
iii. Over feeding of grains etc.
2. Secondary causes: may be because of eructation is infrequent/absent and
disorders of ruminal motility (vagus indigestion, diaphragmatic hernia).
Pathogenesis/mechanism of bloat:
1. In ruminants, normally gases are produced in the rumen by the microbial
fermentation/decomposition of carbohydrate (CHO) and proteins, and the action of
many kinds of saprophytic bacteria upon ingested plant tissues. These gas are expelled
out in the form of frequent belching or eructation through the esophagus and mouth.
2. Pathological bloating results from-
a. Any interference with the normal eructation or
b. The production of gas is in a quantities that exceed the capacity of esophageal
eructation to discharge it out.
A. The possible mechanisms which involves in the interference with the normal
eructation includes-
i. Physical obstruction of the esophageal or pharyngeal passage by firm items of
food such as beets, turnips, apple etc.
ii. Pressure on the esophagus by tumors, abscess, swollen lymphnodes and other
enlargement.
B. Ingestion of large quantities of fresh succulents, green legumes such as clover, alfalfa.
These succulent and legumes are rich in soluble proteins (saponins, pectins,
hemicelluloses, bacterial polysaccharides, microbial slime, and glucose) that become
denatured and insoluble in acidic ruminal fluid by bacterial degradation. These
denatured proteins acts as a foam stabilizing agents. As a results, the fermented gas is
dispersed in the form of small bubbles in the ruminal fluids and entrapped in the frothy
fluids that can’t be expelled out by eructation due to surface tension of liquid. Therefore,
progressively accumulation these gases cause massive distension of the rumen (frothy
bloat).
3. For eructation, active reverse peristalsis of the esophagus is required and this
mechanism is controlled by the autonomic nervous system. It is thought that sufficient
amount of toxic H2S gas is produced in the rumen during the fermentation of fresh green
legumes. These toxic gas may suppressed the function of local nervous structures. As a
result, the active peristalsis of the esophagus is hampered and the fermented gas
produced in rumen can’t be actively eructed, which causes distension of the rumen
(frothy bloat).
4. Some other mechanisms may also be involved in the development of pathological bloat.
Effect of bloat: it causes-

1. Forward displacement of the diaphragms that severely limit the respiratory capacity.
2. Rumen is expanded by pressure and compress the abdominal viscera and occlude the
caudal vena cava that causes shunts blood from the caudal to the cephalic parts of the
body. This is ultimately causes anoxia which leads the immediate death as well.
Ruminal Acidosis/Grain Overload/Acute Carbohydrate Engorgement

(Impaction indigestion, Impaction, Rumen overload, Rumenitis, lactic acidosis, engorgement toxemia)
Definition: This condition associated with ingestion of excessive amounts of highly fermentable
carbohydrate rich feed causes an acute disease (lactic acidosis) due to production of excessive
amount of lactic acid in the rumen, which is characterized clinically by severe toxemia,
dehydration, depression and death. It occurs mostly in high production beef and dairy cattle, but
sheep and goats are also susceptible.
Pathogenesis or mechanisms:
1. Sudden ingestion of excessive amount of highly fermentable CHO rich diets.
2. The pH of rumen begins to decline due to the increased production of volatile fatty acids
(acetoacetic acid, propionic acid and butyric acid). (rumen pH= about 6.4)
3. When the pH approaches to approximately 5.0, then normal gram (-)ve bacteria and
protozoa of the rumen are died with a concomitant overgrowth of Streptococcus bovis
and other Streptococci.
4. These organisms (unlike the normal ruminal flora) produced large quantities of lactic
acid from the CHO substrates.
5. The pH of rumen further declined to the level less than 5.0, which kills the Streptococci.
6. At this point (time), the acid loving bacteria (lactobacillus acidophilus) rapidly
proliferated within the rumen contents and produced more lactic acid and resulting-
7. The pH of rumen dropped below 4.5, and the lactobacillus acidophilus and other
bacteria as well are died.
8. Excessive lactic acid increases osmotic pressure in the rumen contents that attracts fluid
from the circulation resulting diarrhea, dehydration, and shock. On the other hand, toxic
acidosis cause rumenitis and ruminal atony
Gross/microscopic lesions:
1. Nonspecific.
2. Erosion or ulceration of ruminal mucosa.
3. Desquamation of ruminal epithelia.
4. Presence of distinct odor of fermentation.
5. Microscopically rumenitis.
Traumatic reticulitis / Reticuloperitonitis
(Reticulopericarditis / Hardware disease)
It is a sporadic disease of ruminants caused by ingestion of sharp foreign materials and

characterized initially by an acute peritonitis. The penetration of the foreign body may proceed
beyond the peritoneum and caused involvement of other organs and produced different
pathological conditions.
1. Perforation of the fore stomach by foreign bodies eventually.
2. Always is a penetration of the reticular wall by sharp foreign bodies, usually a piece of
wire, screw or a nail 4cm or more in length.
Pathogenesis:
Ingestion of foreign / metallic sharp objects (e.g. wire) swallowed with feeds
Piercing of reticulum by metallic or sharp objects during contraction
Can pierce and carry infection to the peritoneum, diaphragm, pericardium,

Myocardium, and produce Traumatic reticuloperitonitis-pericarditis and
myocarditis (Shaggy Heart Disease/ hardware disease)
Can pierce and carry infection to the pleura to lungs and can produce
pleuritis and pneumonia.
Can pierce the reticulum and carry infection to the Liver, Spleen and can
produce abscess in these organs.
The most commonly associated bacteria are pyogenic bacteria:

 Actinomyces pyogenes,
 Fusobacterium necrophorum
Parasites in fore stomach of ruminants: Mostly Rumen flukes (Paramphistomum spp.).
Immature stage can cause damage to the mucosa that may cause rumenitis.
Diseases in omasum: rare
Diseases of stomach and abomasum

1. Pyloric stenosis- Delayed gastric emptying resulting frequent vomiting, gastric dilation
etc.
2. Torsion
3. Displacement
4. Impaction
5. Gastritis
6. Tumors.
Gastritis
Definition: Inflammation of the mucous membrane of the stomach/abomasum.
 Transmural gastritis is called when inflammation involved all layers of the stomach.
Causes of gastritis:
1. Bacterial diseases-
- Colibacillosis
- Salmonellosis
- Tuberculosis
- Campylobacteriosis
- Streptococcosis
- Staphylococcosis
- Clostridium perfringens etc.
2. Fungal diseases-
- Histoplasmosis
- Candidiasis.
3. Parasitic diseases-
- Hemonchosis
- Bunostomiasis
- Trichostrongylosis
- Habronemiasis
- Gnathostomiasis etc.
4. Viruses.
Symptoms: Anorexia, vomiting and abdominal pain.
Gross lesions:
1. Erosion and ulceration in the entire mucosa.
2. Presence of excess mucous in the gastric.
3. Blood mixed ingesta in the gastric lumen with hemorrhagic spot in the gastric mucosa.
4. Nodulation with thickened gastric wall.
Microscopic lesions:
1. Increased number of goblet cells.
2. Hyperemia and congestion in the underlying tissues.
3. Presence of extravascular erythrocytes.
4. Presence of pink colored fibrin network.
Types of gastritis:
1. Acute Catarrhal gastritis
2. Acute Hemorrhagic gastritis
3. Catarrhal or hemorrhagic gastritis
4. Chronic hypertrophic gastritis
5. Gastritis glandularis & gastric cystica profunda.
6. Eosinophilic gastritis
7. Lymphocytic gastritis
1. Acute Catarrhal gastritis: Characterized by the increased mucus secretion.

Grossly, increased reddening and thickening of the mucous surfaces.
Microscopically, there is hyperemia, increased number of goblet cells and
desquamation of the epithelial cells, infiltration of leucocytes, mostly neutrophils and
eosinophils.
2. Acute hemorrhagic gastritis: characterized by presence of free blood (without inflammatory

reactions) in the gastric lumen.
a. The lesions consist of multiple mucosal hemorrhages, erosion and edema, may be
localized or diffused.
b. Necrosis of the surface epithelium with extravasations of the blood and plasma
from the damaged blood vessels in the lamina propria.
c. There is infiltration of leucocytes in the affected area.
Clinically, acute hemorrhagic gastritis is characterized by discomfort, pain,
anorexia, and nausea and vomiting.
In severe cases, the vomitus contains coffee ground like materials or blood tinged
materials.
The causes includes-
a. Poisons, e.g. Cyanide, Mercuric chloride, etc.
b. Infectious disease: e.g. Anthrax, Rinderpest, Leptospirosis, Hog cholera etc.
c. Helminths: e.g. Trichostrongylus, Haemonchus, Mecistocirrus, Ostertagia,
Gastrophillus, Habronema spp. (horse) etc.
d. Toxic chemicals: Carbolic acid, disinfectants, uremia, etc.
4. Chronic hypertrophic gastritis (Giant rugal gastritis/ gastritis hypertrophia gigantica):

It is mostly found in man and sometimes in dog.
Etiology not Known.
Symptom include: lethargy, emaciation, vomiting, prolong anorexia, hepatic disease,
anemia, protein loss.
Lesions include –
Grossly, elevation and folding of the mucosa and severe rugae due to local epithelial
hyperplasia in the fundus.
Microscopically: Loss of partial cells with compensatory hyperplasia of goblet cells,

mononuclear infiltration in the lamina propria.
5. Gastritis glandularis & gastric cystica profunda:
In nonhuman primates: Hyperemia and petechae on the mucosa.
Occasionally, ulcer, hyperplasia of the mucosa.
Cause not known.
6. Eosinophilic gastritis: Frequent infection with Toxocara canis. Presence of large number of
eosinophil with fibrosis stomach wall.
7. Lymphocytic gastritis: Due to chronic infection with intracellular bacteria, e.g. Helicobacter
pylori. Most common in Dog, Cat and ferret.
Tumors stomach and abomasum:

1. Adenocarcinoma.
2. Squamous cell carcinoma.
3. Leiomyoma/ Leiomyosarcoma.
4. Signet ring adenocarcinoma.
Diseases of the Intestine:
A. Congenital anomalies
1. Atresia jejuni
2. Atresia ilei
3. Atresia ani (more common)
4. Aplasia
5. Hypoplasia
B. Inflammation
1. Enteritis: Inflammation of the Intestine.
2. Duodenitis: Duodenum
3. Jejunitis: Jejunum
4. Ileitis: Ileum.
5. Typhlitis: Inflammation of the Caecum (also called cecitis)
6. Colitis: Colon
7. Proctitis: Rectum.
C. Intestinal Obstruction
Causes:
1. Rubber ball
2. Rubber nipples
3. Nut
4. Piliconcretion (formation of hair balls in calves and sheep)
5. Hernias and strangulation
6. Torsion- (twisting upon itself)
7. Volvulus-in which a loop of intestine passes through a tear in the mesentery or similar
abnormality.
8. Intussusceptions-ln this condition, excessive peristaltic motility forces a segment of
the bowel inside the segment just below it, much like the parts of telescope.
9. Meckel’s diverticulum: Persistence of omphaloenteric duct of the embryo. It is a few
centimeters long, small tube branching from the ileum, sometimes cause strangulation
of the intestine.
Causes of inflammation of intestine:

A. Infectious cause
Bacteria
1. Vibrio cholerae
2. Salmonella spp.
3. Shigella spp.
4. Campylobacter jejuni
5. Yearsina enterocolitica
6. Escherichia coli (E. coli)
7. Clostridium perfringens
8. Other Clostridial spp.
9. Mycobacterium paratuberculosis (now it is called Mycobacterium avium sub spp
paratuberculosis)
10. Bacillus anthrasis
11. Mycobacterium tuberculosis.
Virus
1. Rota virus
2. Rinderpest virus
3. Canine distemper virus
4. Canine hepatitis virus
5. Hog cholera
6. Bovine viral diarrhea virus (BVDV).
Protozoa
1. Entamoeba histolytica
2. Giardia spp
3. Coccdia spp.
4. Toxoplasma spp
5. Balantidium coli.
Fungus
1. Histoplasmosis
2. Coccidioidomycosis.
Helminth Parasites
1. Hookworms
2. Nodular worms
3. Tape worms.
B. Non-infectious causes:
1. Vascular disturbances as in congestive heart failure, portal hypertensions.
2. Toxins from decomposed foods (food poisoning)
3. Chemical poisoning e.g. Arsenic, uremic products, lead, Mercury, Cyanide, Nitrate etc.
4. Drugs, e.g. over dose of anthelmintic, certain antibiotics etc.
5. Nutritional deficiencies, e.g. deficiency of vitamin B complex.
Types of enteritis:
A. Catarrhal enteritis
B. Hemorrhagic enteritis
C. Purulent enteritis
D. Fibrinous enteritis
E. Granulomatous enteritis
F. Chronic proliferative enteritis
G. Lymphocytic or plasmacytic enteritis.
H. Eosinophilic enteritis
Catarrhal enteritis: is the most common form of enteric infection.
Clinical symptoms- profuse diarrhea which may turns to death.
Lesions- it is characterized by hyperemia, desquamation increased goblet cells
proliferation and leucocytic infiltration.
Hemorrhagic enteritis: Most severe form of acute enteritis.
Clinical symptoms- Diarrhea with bloody discharges.
Causes- are poisons (cyanide, Arsenic); bacteria, virus etc.
Purulent enteritis:
Infrequent but occasionally occurs in association with mechanical injuries from foreign bodies
and helminth parasites which become complicated with pyogenic bacteria.
Fibrinous enteritis:
Common in cattle. Fibrinous exudates is often pseudomembranous type. When inflammation
subsides, the pseudomembrane become detached and passed out through feces in the form of
hollow cast that seems to be the part of intestine. It is caused by Salmonella spp, Spherophorus
necrophorus.
Granulomatous enteritis:
Found in granulomatous diseases, e.g. Tuberculosis, Histoplasmosis etc.
Chronic Proloferative enteritis:
Mycobacterium paratuberculosis in ruminants, Lawsonia intracellularis in pigs etc.
Lymphocytic/ Plasmacytic enteritis:
Common in dog and cat. Common causes are chronic diarrhea and vomition. In the lamina
propria, there is well differentiated lymphocyte, plasma cell and erythrocyte can be found.
Eosinophilic enteritis: Common in dog and cat due to repeated episode of diarrhea associated
with peripheral eosinophilia. The mucosa, submucosa and lamina muscularis are infiltrated with
eosinophil, mast cell and macrophages.
Neoplasm of the intestine:
1. Adenoma
2. Adenocarcinoma
3. Signet ring adenocarcinoma
4. Undifferentiated carcinomas
5. Leiomyoma/ Leiomyosarcoma
6. Cavernous haemangioma
7. Lymphosarcoma (lymphoma)
8. Lipoma / Sarcoma
9. Secondary tumors.
Malabsorption Syndrome
It is due to failure of absorption of nutrients from the intestinal tract results in clinical
manifestations that collectively called malabsroption syndrome.
Clinical signs: include-
1. Gastrointestinal upset (vomiting, diarrhea)
2. Loss of weight
3. Changes in eating habit
4. Steatorrhea, (the excretion of abnormal quantities of fat in feces due to
insufficiency of pancreatic juices, there is deficiency of lipase enzyme that
ultimately hampers the absorption and digestion of fat. As a result, fat comes out
with feces).
Causes:
1. Pancreatic insufficiency due to chronic pancreatitis and malignant neoplasms.
2. Diseases involving the mucosal epithelium-
 Non-tropical sprue (gluten-sensitive enteropathy): It is characterized by
villous atrophy, elongated crypts and increased cell turnover of epithelial
cells.
 Tropical sprue: Caused by folic acid deficiency.
 Transmissible gastroenteritis (TGE) in swine- a viral disease of pigs.
 Protein losing enteropathy of unknown cause.
3. A combination of pancreatic insufficiency and mucosal absorption.
4. Intolerance to lactose.
5. Gastric malfunction due to neoplasm or gastritis.
6. Hepatic malfunction.
7. Specific disease condition, e.g. proliferative enteropathy.
Lesions: Depend on causes.
Diseases of the peritoneum
Peritonitis: Inflammation of the peritoneum usually due to secondary numerous diseases

or disease conditions (typically caused by bacterial infection either via the blood or after
rupture of an abdominal organ).
Causes:
1. Noninfectious: Urine, uremia, acids, trauma etc.
2. Infectious: Most of the peritonitis is infectious.
 Streptococcus spp.
 Staphylococcus spp.
 Corynebacterium spp.
 Tuberculosis of serous membrane (pearly disease)
 Actinobacillus spp.
 Clostridium spp. etc.
Route of Infection:
 Operative incision through abdominal wall
 Perforated peptic ulcers
 Perforated intestinal ulcers
 Perforated uterus
 Direct extension from the necrotic visceral organs
 Hematogenous route
 Fallopian tube
 Omphalitis (infection of the naval in newborn)
Tissue reactions: As peritoneum is lined by secretory serous epithelium, it produces huge

amount of serofibrinous or fibrinous exudates.
Outcome: Peritonitis may heal rapidly within 24 hours but sometimes it may takes 6 - 10
days, where there is a possibility of adhesion (peritoneal adhesions is condition in which
pathological bonds form between the omentum, the small and large bowels,
the abdominal wall, and other intra-abdominal organs).
Some special note:

1. Peritonitis always fatal to horse.
2. Cattle may have due to generalized peritonitis.
3. Peritonitis seldom occurs in dogs.
Hydroperitoneum (inflammatory) /Ascites (noninflammatory)

Definition: Defined as accumulation of body (watery) fluids in the peritoneal cavity,
which is caused by the usual causes of edema. Other causes are also include as - passive
congestion of the portal vein, Neoplasm of the peritoneum etc.
Tumors of the peritoneum
1. Mesothelioma (a type of cancer of mesothelium).
2. Fibrosarcoma.
3. Lipoma.
4. Liposarcoma.
Disease of Liver and Biliary System

A. Circulatory disorders:
1. Passive congestion (congested liver).
2. Acute passive congestion.
3. Chronic passive congestion (nutmeg liver)
4. Telangiectasis
Telangiectasis: Dilatation of functional blood vessels in anywhere of the body. In liver, a small
group of sinusoids within any part of the lobule are greatly dilated. The cells of hepatic cords
between the dilated sinusoids have partially or completely disappeared. Grossly, a dark red spot,
irregular in shape, from one to several millimeters in diameter and slightly depressed from
surface of the organs.
Liver Telangiectasis
B. Degeneration and Deposits in the liver:

1. Fatty liver.
2. Glycogen infiltration.
3. Hydropic degeneration.
4. Pigments: bile pigments (icterus), lipofuscin, blood pigments, and melanin (very
occasional).
5. Amyloids.
6. Acidophilic crystalline intranuclear inclusions ((in dogs and cats).
C. Congenital defects:
1. Intrahepatic congenital cysts.
2. Congenital portosystemic vascular shunts.
D. Hepatic encephalopathy:
Hepatitis
Definition: Defined as the inflammation of the liver parenchyma.
- When inflammation involved in the portal area, then it is called portal hepatitis.
- If it includes the peri-portal area, then it is called periportal hepatitis.
- Hepatitis may be acute or chronic.
Types of hepatitis: Based on severity, there are three types of hepatitis-

1. Acute hepatitis: due to the congestion in the sinusoids and characterized by -
a. Edema in portal traits
b. Neutrophil infiltration in bacterial hepatitis
c. Lymphocytes and plasma cells in viral hepatitis
d. Degenerative changes in the hepatocytes
e. Necrotic changes
f. Stasis of bile pigment
Hepatic necrosis / Necrotic changes: The necrosis is most often coagulative type recognized
by pyknotic nucleus and acidophilic cytoplasm. According to the location, necrosis in the liver
may be classified as-
a. Diffuse/massive necrosis- characterized by necrosis of entire lobules and
contiguous lobules. It may only affect several lobules or entire lobes of the liver
(spread over considerable areas without regards to lobular boundaries).
b. Focal necrosis- in which, minute or small necrotic areas or foci, of sub-lobular
size, appears here and there, are occupying any part of any lobule. The focus may
consist of one cell to one group of cells.
c. Zonal necrosis- characterized by hepatocyte necrosis is restricted to a particular
part of the lobule or acinus. They are 4 types-
i. Centrilobular- characterized by necrosis of hepatocytes nearest the
central vein. It is the usual form of necrosis as seen in hypoxic condition
(passive congestion and severe anemia) and acute toxic hepatitis.
ii. Midzonal- characterized by necrosis of hepatocytes half way between the
periphery and center of the lobule.
iii. Periportal (peripheral) - characterized by necrosis of hepatocytes
surrounding triads (peripheral zone of lobule, the hepatocytes are
regularly necrosed).
iv. Paracentral-in which, the entire acinus becomes necrotic wherein the
necrotic tissue may extend as a band from the central vein (only one side)
to the periportal areas or triad to triad (known as bridging necrosis).
2. Chronic Hepatitis: Characterized by the
a. Predominantly lymphocytic infiltration mainly in the portal area
b. Proliferation of the fibrous connective tissues (FCT)
 Some form of hepatitis originates from the biliary tree and entered into the
portal tissues and ultimately the lobules.
 These are initially classified as cholangitis (when limited in the biliary tree)
and with progression cholangiohepatitis or biliary hepatitis.
 This may result from extrahepatic or intrahepatic bile duct obstruction or
infectious causes.
3. Toxic hepatitis or toxic liver disease:

a. Many drugs and toxin cause hepatic injuries which accompanied with acute or
chronic inflammation and hence it is called toxic hepatitis.
b. Some hepatic lesions lack inflammatory components, e.g. fatty change to
neoplasia, and hence it is called toxic liver disease.
Mechanism of Toxic Liver Disease:

There are two mechanisms of toxic liver diseases:
1. Direct toxicity to the liver by the toxins
2. Toxicity arising during detoxification process by the toxic metabolites,
e.g. Phylloerythrin from chlorophyll.
Causes of Hepatitis / Toxic Liver Disease:
A. Noninfectious Causes-
1. Chemical poisons: Copper, Arsenical drugs, Chloroform, etc.
2. Plant toxins: Senecio, Crotalaria, Cynoglossum, Lantana, etc.
3. Mycotoxins: Aflatoxins, Phomopsin and Sporidesmin.
B. Infectious causes-
1. Viral Diseases:
a. Hepatitis virus B & C infection.
b. Infectious Canine Hepatitis infection.
c. Rift Valley Fever
d. Infectious Bovine rhinotracheitis (IBR)
e. Feline infectious peritonitis
f. Duck viral hepatitis
g. Feline viral Rhinotracheitis
h. Adenovirus infection etc.
2. Bacterial Diseases-
a. Black Disease (Clostridium novyi)
b. Tularemia (Pasteurella tularensis)
c. Listeriosis
d. Leptospirosis
e. Salmonellosis
f. Tuberculosis
g. Pasteurella hemolytica
h. E. coli
i. Yersiniosis
j. Helicobacter hepaticus etc.
3. Protozoal disease-
a. Toxoplasmosis
b. Neosporosis
c. Leishmaniasis
d. Hepatic coccidiosis
e. Amoebiasis.
4. Fungal diseases-
a. Histoplasmosis
b. Coccidioidomycosis
5. Metazoan parasites-
a. Fascioliasis
b. Dicrocoelium
c. Larvae of migratory nematodes
d. Hydatid cysts etc.
Cirrhosis
The word ‘cirrhosis’ comes from the Greek, ‘kirrhos’ meant tawny or orange-colored.
Cirrhosis is not a primary disorder, but rather represents the end stage of liver diseases from
any of several causes, which is generally considered as progressive, irreversible and ultimately
fatal.
Cirrhosis is resulted from a series of pathological events leading to form increased dense
fibrous connective tissues (FCT) in the liver. Depending upon the cause, the FCT may surround
each lobule, run from portal area to portal area, and extend from portal area to central vein or
course from central vein to central vein.
Characteristics: Cirrhosis is characterized by-

i. Diffuse hepatic fibrosis resulting in altered reconstruction of the lobular
parenchyma with widespread connective tissue septa.
ii. Circumscribed regenerative nodules of hepatocytes.
iii. Anastomosis between vascular channel, linking portal and central vessels.
Special note: In ruminants, cirrhosis accompanied with bile duct proliferation.
Gross lesions:
1. The color of the liver is fawny or orange.
2. The liver is hard or firm to touch, and surface is smooth and uneven.
3. Hepatomegaly in earlier stage but reduced in size at later stage.
1. Proliferation of fibrous CT tissues begins at the island of portal area (Glisson’s) and
increases to surround the lobule (within or around the hepatic lobule).
2. Interstitial FCT are more than the parenchymal tissues of the lobules.
3. The FCT may be immature and cellular, but usually matured.
4. Newly formed bile ducts are often found in the proliferative FCT, which are recognized
as tiny circle of small epithelial cells with dark staining nuclei.
Types of cirrhosis:
1. Parasitic cirrhosis: Connective tissue proliferates along with migratory tracts. The
migration of the larvae of swine kidney worm (Stephanurus dentatus), liver flukes
and Ascaris lumbricoides (in human).
2. Central or cardiac cirrhosis: Connective tissue proliferates along with central
veins (around) resulting from chronic passive congestion due to chronic/congestive
heart failure.
3. Postnecrotic cirrhosis: when cirrhosis is followed by extensive hepatic necrosis,
which may be focal, multi-focal to bridging.
4. Pigment cirrhosis: cirrhosis occurs in connection with pigment
(hemochromatosis).
5. Biliary cirrhosis: Chronic cholangitis followed by biliary cirrhosis. Well advanced
biliary cirrhosis present in perilobular fibrosis. The FCT which encircle various bile
duct. Newly formed bile ducts may be prominent and there is infiltration of
inflammatory cells (neutrophils) if there is secondary bacterial infections.
Causes of cirrhosis:
A. Infectious cause-
1. Hepatitis B and C virus in human.
2. Infectious canine hepatitis virus in dog.
3. Parasites (liver flukes, larvae of migratory parasites etc.)
B. Toxic cause:
1. Drinking excessive alcohol.
2. Chronic poisoning by toxic plants.
3. Mycotoxins- Aflatoxin.
4. Chronic copper poisoning.
Effects of cirrhosis:
1. Anemia (As liver produces RBC maturing factors).
2. Edema (due to hypoproteinemia).
3. Photosensitization (If there is liver disease, there will be dermatitis).
4. Ascites.
5. Hemorrhage (As liver produce prothrombin).

6. Digestive disturbances (As liver involved in metabolism).
Neoplasm of liver:
1. Hepatocellular adenoma.
2. Hepatic cell carcinoma.
3. Intrahepatic bile duct adenoma.
4. Intrahepatic bile duct carcinoma.
5. Hepatoblastoma.
6. Hemangioma.
7. Hemangiosarcoma.
Diseases of Bile Duct & Pancreas
Cholangitis: Inflammation of the bile duct.
Cholecystitis: Inflammation of the gall bladder.
Cholelithiasis: Formation of stone in the gall bladder or bile duct. The stones are called
gallstone or biliary calculi or choleliths. Gall stone is very rare in domestic animals.
Pancreatitis: Inflammation of the pancreas. It is very rare in domestic animals.
Tumors:
1. Insulinoma.
2. Adenoma.
3. Adenocarcinoma.
Credit hour: 3
Level-2, Semester-1I
Lectures: 8~13
Cardiovascular System
Intended Learning Outcomes/Objectives (ILOs): The students will be able to -

1. Know the name of developmental anomalies and express pathological conditions of
cardiovascular system.
2. Describe the pathogenesis and pathology of
 Cardiac failure
 Myocarditis
 Cardiomyopathy
 Pericarditis
 Endocarditis\
 Arteriosclerosis
 Arteritis
 Phlebitis
3. Investigate the diseases of cardiovascular system
4. Recall neoplasms of cardiovascular system
Cardiovascular system: consists of the heart, blood vessels and blood. Lymphatics are the
important component of circulatory systems.
1. The Systemic Circulation:

 O2-rich blood is pumped from the left ventricle through the arteries of the systemic
circulation to the capillaries in the periphery of the body.
 CO2-containing blood is transported by the veins back to the right atrium of the
heart.
2. The Pulmonary Circulation: Blood is pumped from the right ventricle through the lungs
where it is enriched with oxygen before returning back to the left atrium.
3. Fetal circulation:
 The lungs are functionally inactive during fetal development. Oxygenation of fetal
blood occurs in the placenta. Oxygenated blood travels to the right atrium via the
umbilical vein, which joins the caudal vena cava.
 The majority of blood bypasses the heart and lungs and travels directly into the
systemic circulation via the foramen ovale and ductus arteriosus.
Important points to be considered:

 Right side contains oxygenated blood before birth.
 Right side pump is stronger than left side before birth.
 Left side pump/flow of blood is stronger after birth.
Congenital Cardiac Anomalies/heart diseases: they can be divided into the following major
groups-
1. Defects that allow shunting of blood from right to left or the reverse.
2. Defects that lead to obstruction of blood flow.
3. Valvular defects that may lead to obstruction of flow or regurgitation.
4. Abnormal arterial and venous connections or positionings.
5. Malposition of the heart.
1. Shunts: A hole or a small passage, which allows movement of fluid from one part of the
body to another. Or it is an abnormal communication between chambers and/or blood
vessels.
a. Left to right shunt: When blood enters from the left side to right side of the heart.
i. Patent ductus arteriosus.
ii. Atrial septal defects.
iii. Ventricular septal defects.
iv. Atrioventricular septal defects.
b. Right to left shunt: When blood enters from the right side to left side of the heart.
i. Transposition of the great vessels.
ii. Tetralogy of Fallot.
iii. Truncus arteriosus
iv. Tricuspid atresia
In this group paradoxical embolism can occur.
2. Obstructive congenital anomalies:
a. Subaortic stenosis.
b. Coarctation of the aorta.
c. Pulmonary stenosis.
3. Others:
a. Valvular defects. e.g. congenital or acquired.
i. Defects in aortic valve lead to left ventricular hypertrophy and left-sided heart
failure (LSHF).
ii. Pulmonary valve leads to right-sided heart failure (RSHF).
iii. Tricuspid valve leads to RSHF.
iv. Mitral valve leads to enlargement of left atrium, LSHF and “brown induration
of lung”.
b. Endocardial fibroelastosis.
c. Malposition of the Heart. e.g. ectopia cordis.
d. Portocaval (portosystemic) venous shunts.
e. Abnormal arterial and venous connections or positioning. e.g.
i. Persistent right aortic arch.
- Aorta normally develops from left 4th aortic arch. If persistence of
right 4th aortic arch, the ligamentum arteriosum forms a vascular ring
around esophagus and trachea
Effect: Megaesophagus i.e. dilatation above the ring.
ii. Double aortic arch
- Persistent of both right and left aortic arches. The effect is same as
persistent right aortic arch.
iii. Interruption of the aortic arch- No aorta formation and life is incompatible.
f. Congenital hereditary lymphedema.
Short description on congenital cardiac anomalies:
1. Shunts:
i. Left to right shunts:
i. Patent ductus arteriosus:
 In fetal stage, oxygenation of blood occurs in placenta rather in the lung
(after birth).
 So, there is no need of entering the blood into the lung.
 Oxygenated blood that enters into the pulmonary artery drains into the aorta
through a duct called ductus arteriosus.
 After birth, this duct is closed and is called Ligamentum Arteriosum.
 If this duct remains opened after birth, oxygenated blood passes from aorta to
pulmonary artery (deoxygenated blood) - left to right shunt.
Effect:
 Murmur sound (abnormal sound) in heart.
 Right ventricular hypertrophy leading to right-sided heart failure (increased
pressure on the pulmonary artery, so right ventricle undergoes excess
pressure).
 Late cyanosis or Blue Baby due to anoxia (if right to left shunts occur).
ii. Atrial Septal Defect [patent foramen ovale (PFO)]:

 In fetal stage, oxygenated blood from placenta passes from right atrium to left
atrium via a channel called foramen ovale.
 After birth, this foramen is closed and is called fossa ovalis.
 If this foramen remains opened after birth, oxygenated blood passes from left
atrium to right atrium (deoxygenated blood)-left to right shunt.
Effect:
 Right ventricular hypertrophy due to pulmonary hypertension (increased
pressure on the pulmonary artery, so right ventricle undergoes excess
pressure).
 Late cyanosis or Blue Baby (if right to left shunts occur).
 Stroke.
iii. Ventricular Septal Defect (VSD):

 In embryonic life, ventricle has one chamber. Then the chamber is divided
into right & left ventricle by the development of septum.
 Failure of perfect closure may occur and results ventricular septal defect.
Effect:
 Small defect may close spontaneously and has no clinical importance.
 Larger and multiple defect may leads to pulmonary hypertension and
eventually right-sided heart failure-Left to right shunt.
 Late cyanosis or Blue Baby. (if right to left shunts occur)
 Thickened and roughened orifice, and thickened endocardium due to
“Jet Stream” of blood.
iv. Atrioventricular septal defect (AVSD):
About 2,118 babies (1 in 1,859 babies) are born with AVSD every year in the
United States (CDC).
 Results from incomplete fusion the endocardial cushions, which help to form
the lower portion of the atrial septum, the membranous portion of the
ventricular septum and the septal leaflets of the tricuspid and mitral
(bicuspid) valves.
Effect:
 Late cyanosis.
 Congestive heart failure (in infancy) - is when the heart cannot pump enough
oxygen-rich blood to meet the needs of the body.
 Recurrent pulmonary infections.
 Exercise intolerance, easy fatigability.
b. Right to left shunts:

i. Transposition of great vessels:
 Usually pulmonary arteries arise from the right ventricle and aorta from the
left ventricle.
 But in this case pulmonary arteries arise from the left ventricle and aorta
from the right ventricle.
 This situation can only be survived when mixing of O2 via a shunt can take
place:
 Patent Foramen Ovale (PFO) or Atrial Septal Defect (ASD)
 Ventricular Septal Defect (VSD)
 Patent Ductus Arteriosus (PDA).
ii. Tetralogy of Fallot: it has present 4 features

 Ventricular septal defect
 Pulmonary/Subpulmonic stenosis
 Biventricular origin of aorta/ dextroposition of the aortic valve (semilunar
valve)
 Right ventricular hypertrophy
Effect: Cyanosis
Eisenmenger’s complex/syndrome: it is the Tetralogy of Fallot without pulmonary
stenosis.
iii. Truncus arteriosus: Failure to divide of the aorta and pulmonary artery each other.
 Failure of the spiral ridge to divide the truncus arteriosus and conus cordis
into the pulmonary artery and aorta.
 Seen most frequently in the horse.
 Animal may survive up to a year.
Effect:
 Cyanosis
 RV hypertrophy
 Pulmonary hypertension
iv. Tricuspid atresia: It is the obliteration of the right atrioventricular orifice

and characterized by absence of the fusion of the tricuspid valves.
2. Obstructive congenital anomalies: These are may be isolated or combined disorders.
i. Subaortic stenosis:
 Formation of a fibrous connective tissue band below the aortic semilunar
valve
Effect:
 Left Ventricular (LV) hypertrophy.
 Aorta above valve becomes dilated.
 Intramural arteries in the adjacent myocardium are thickened and fibrotic.
ii. Coarctation of the aorta:
 Narrowing (FCT proliferation) of a segment of aorta near or immediately
before the attachment of ductus arteriosus.
- Preductal/ Infantile coarctation: Narrowing below the attachment
of ductus arteriosus.
- Postductal/ Adult coarctation: Narrowing above the attachment
of ductus arteriosus.
iii. Pulmonary stenosis:
 Obstruction (FCT proliferation) in the region of either the pulmonary valve
or the subpulmonary ventricular outflow tract.
Effect:
 Right ventricular (RV) hypertrophy
iv. Aortic stenosis:
 Obstruction (FCT proliferation) to the outflow from the left ventricle at or
near the aortic valve.
Effect:
 Left ventricular (LV) hypertrophy.
 Aorta above valves become dilated.
3. Others:
a. Abnormal arterial and venous connections or positioning:
i. Persistence of right aortic arch: If persists, then the ligamentum arteriosus
forms a vascular ring around esophagus and trachea. Megaesophagus (difficulties
in breathing & swallowing) is the effect.
ii. Double aortic arch: Persistence of both right and left aortic arch.
Megaesophagus (difficulties in breathing & swallowing) is the effect.
iii. Interrupted aortic arch: Obliteration of the fourth aortic arch on the left side.
b. Abnormalities of the Position of the Heart

i. Ectopia cordis: if the Heart is outside of the thoracic cavity. Some animals can survive for
several days to months.
ii. Dextrocardia: if the Heart is on the right side rather than the left. Usually fatal.
iii. Acardia: congenital absence of the heart.
iv. Diplocardia: Two hearts are present (a cardiac condition in which the right and left
halves of the heart are separated by a fissure).
c. Portocaval (portosystemic) venous shunts:
 Persistent ductus venosus: Passing of deoxygenated venous blood by ductus

venosus instead of passing through the liver. As a result, toxemia, hepatic
encephalopathy and hepatic atrophy occurs.
d. Endocardial fibroelastosis: The endocardium of the ventricles is thickened due to

increase in elastic fibers of the subendothelial connective tissues. Death occurs
soon after birth.
Compensatory mechanism of heart: If patient is able to survive the initial results then following
conditions may occur-
 Cardiac dilatation: Increased diastolic volume and tries to increase stroke volume.
 Cardiac hypertrophy: Individual myocyte increase in size.
Sequelae: At first the effect is beneficial and later it contributes to heart failure.
Heart Failure/ Cardiac Failure

Definition: It is the inability of the heart to pump an adequate supply of blood (circulation) to meet
the body’s needs or demands.
 It is the leading cause of death in adult human, owing to high incidence of ischemic heart
disease due to coronary atherosclerosis and the high incidence of hypertension (high
blood pressure).
Types/ Classification of cardiac failure:
1. Acute Heart Failure:
 It is resulting from a sudden cessation of effective cardiac contraction leading to
“brain death” within minutes.
Causes of Acute Heart Failure:
 Ischemic heart disease
 Acute myocarditis
 Hypertrophic cardiomyopathy
 Cardiac tampnade
 Sudden occlusion of pulmonary artery or aorta
 Severe electrolytes imbalance
 Certain toxicities.
2. Chronic/ congestive Heart Failure:
 It is resulting from inability of the heart to maintain venous return.
 It is the result of failure of the heart to maintain adequate circulation as a result of
diminished output (forward failure) and backing up of blood (backward failure).
a. Left-sided heart failure
b. Right-sided heart failure
c. Other types
- Both left and right-sided heart failure
- Forward heart failure: Inadequate cardiac output.
- Backward heart failure: Pulmonary venous congestion
- Low output heart failure
- High output heart failure.
Causes of Chronic Heart Failure:

 Myocarditis
 Aortic or mitral valve disease
 Congenital cardiac detects
 Hypertension.
Left-sided Heart Failure
 Left-sided heart failure is the most common type of heart failure.
Causes:
1. Hypertension
2. Aortic valvular disease
3. Mitral valvular disease
4. Congenital Heart Disease
5. Ischemic heart disease, especially myocardial infarction (MI)
6. Myocardial diseases- Cardiomyopathies, myocarditis, myocardial degeneration etc.
7. Nephritis in dogs.
Gross Lesions of LSHF:

 Lungs and Pleura:
 Venous congestion, hemorrhage and edema,
 Macrophage laden with golden shiny color haemosiderin pigment called “Heart
failure cells”.
 Hypertrophied alveolar lining cells and fibrosis of alveolar walls called “Brown
indurations of lungs”.
 Kidney:
 Edema in the lower part of the body due to retention of salt and water.
 Brain:
 Cerebral anoxia (absence of oxygen)
Right-sided Heart Failure

 Right-sided heart failure occurs when the right side of the heart can’t perform its job
effectively.
 It’s usually triggered by left-sided heart failure. The accumulation of blood in the lungs
caused by left-sided heart failure makes the right ventricle work harder.
Causes of RSHF:
 The primary diseases of lungs or pulmonary vasculatures.
 Pulmonary hypertension.
 Tricuspid or pulmonary valvular disease.
 Also, those mentioned in the left-sided heart failure.
Gross Lesion:
 Chronic passive congestion in kidney, liver and spleen
 Nut-meg liver (centrilobular necrosis).
 Splenomegaly.
 Cardiac cirrhosis.
 Dilatation of caudal venacava.
 Dilation of RV.
Pulmonary hypertensive heart disease

(Cor pulmonale)
 It is the Heart failure due to abnormalities in lung, which is not related to left sided heart
failure or congenital cardiac defects, is termed as Cor pulmonale.
Causes:
 The primary diseases of lungs or pulmonary vasculatures.
 Pulmonary hypertension
 Chronic fibrosing pneumonia
 Pulmonary embolism
Thromboembolic disease
Dead Dirofilaria
 Emphysema that causes the compression of pulmonary arterioles
 Hypoxia, is another important cause of pulmonary hypertension due to reduced atmospheric
O2. It occurs in animals and human when reside at high altitudes.
When cattle resides above 7000 feet called “high altitude disease/ brisket disease”
When human resides at much higher elevation above 12000 feet called “Monge
disease”/ chronic mountain sickness.
Effect
Polycythemia
Increased viscosity of blood
Edema (brisket region)
Right-sided heart failure
Diseases or Disorders of Myocardium
Hypertrophy
Cardiomyopathy
Myocardial degenerative changes
Myocardial necrosis
Myocarditis
Hypertrophy: Reversible increase in the mass but not number of myocardial cells.
1. Concentric Cardiac Hypertrophy (Pressure Overload Hypertrophy): An increase
in the mass of the ventricle without accompanying increase in end diastolic volume.
2. Eccentric Cardiac Hypertrophy (Volume Overload Hypertrophy): An increase in
myocardial mass accompanied by an increase in end diastolic volume (8ventricular
volume).
Causes:
 Adaptive response due to increase workload on the heart

o Congenital anomalies
o Heart failure
o Cor pulmonale
o Valvular diseases
o Hypertension
o Hyperthyroidism
o Chronic renal disease
o Idiopathic cardiac hypertrophy
o Equine laminitis
 Individual muscle fibers increase in thickness
 Nuclei enlarged
Cardiomyopathy: Acute, subacute, or chronic generalized disorder of heart muscle.
1. Hypertrophic cardiomyopathy: Increased heart weight as a percent of body.

2. Congestive cardiomyopathy: Progressive cardiac dilation and contractile
dysfunction.
3. Restrictive cardiomyopathy: Due to restriction of ventricular filling.
Myocardial degenerative changes:

 Atrophy (Brown atrophy of the heart)
Cause:
o Wasting disease (TB)
o Malnutrition
 Mucoid degeneration of fat.
 Fatty infiltration.
 Fatty change
 Hyaline degeneration
 Calcification.
Myocardial Necrosis:
Causes:
 In human, coronary vascular disease is the main cause.

 In animals
Nutritional deficiencies: Poisonings:
Vitamin E & Gossypol
Selenium Coffee senna
Thiamine (Vit-B1) Coyotillo
Carnitine Vetch
Potassium Bracken fern
Copper Causes of myocarditis
Myocarditis: Inflammation of myocardium having leukocyte infiltration and degeneration
or necrosis of myocytes.
Causes:
1. Virus:
 Canine parvo virus
 Encephalomyocarditis virus
 Canine Distemper virus
 Aujezky's disease
 Cytomegalovirus
 Foot and mouth disease virus (Tiger heart disease)
 Bluetongue virus
 West Nile Virus
 Malignant catarrhal fever virus
 Newcastle disease virus
 Avian encephalomyelitis
 Eastern and western equine encephalomyelitis
 Human causes – Coxsackie virus, influenza, HIV, cytomegalovirus.
2. Bacteria:
 Clostridium chauvoei
 Listeria monocytogenes
 Fusobacterium necrophorum
 Mycobacterium bovis
 Corynebacterium pseudotuberculosis
 Actinobacillus equuli
 Staphylococcus spp.
 Pseudomonas aeruginosa
 Streptococcus pneumoniae
 Bacillus piliformis
 Haemophilus somnus
Protozoa:
 Toxoplasma gondii
 Sarcocystis spp.
 Encephalitozoon cuniculi
 Trypanosoma cruzi
4. Metazoan parasite:
 Trichinella spiralis
 Cestode larvae
5. Rickettsia
6. Chlamydia
7. Fungi: Rare
 Blastomyces dermatitidis
 Coccidioides immitis
 Cryptococcus neoformance
Diseases of Endocardium
Endocarditis/Infectious endocarditis: Inflammation of the endocardium, usually
bacterial in origin.
1. Valvular endocarditis:
 Valves are affected.
2. Vegetative endocarditis:
 The heart valves with proliferative lesions appear like the head of a
cauliflower.
3. Mural endocarditis:
 Only the wall of the heart (atria and ventricles) (endocardium) other than
valves affected.
Causes of endocarditis:
Infectious causes:
Pig:
Erysipelothrix rhusiopathiae
Streptococcus suis
Staphylococcus aureus
Cattle & Sheep:
Actinomyces pyogenes
§Streptococcus spp.
Horse: uncommon
Streptococcus equi
Actinobacillus equuli
Migrating larvae of Strongyle
Cat & Dog:
Beta hemolytic Streptococcus spp.
Erysipelothrix rhusiopathiae
Staphylococcus spp.
Fungus:
Candida spp.
Histoplasma spp.
Aspergillus spp
Mucor etc.
Noninfectious causes:
 Uremic endocarditis- edema, necrosis, reactive cells, thrombus and
mineralization are found in endocardium and myocardium (common in dog).
 Valvular endocarditis (myxomatous or mucoid degeneration of mitral
valve): common in dog; resemble to Marfan syndrome (mitral valve prolapse
and aortic changes); effect is left-sided heart failure.
 Valvular blood cyst: (cattle, dog)- hematoma found in tricuspid valve with
chondrogenic and osteogenic metaplasia; no interference with function.
Pathology/ Lesions of endocarditis:
Gross:
1. Yellow-red or yellow-gray proliferative lesions (vegetation) covered by a thin clot of
blood, which can be easily peeled off at necropsy.
2. The surface is friable, small lesions can be broken off leaving a granular, eroded
surface on the valve.
Microscopic:
1. Numerous bacterial colonies.
2. Accumulations of fibrin, neutrophils and variable amounts of granulation material.
Sequela of endocarditis:
3. Chronic lesions may organized by granulation from the base of the valve.
4. May undergo mineralization.
5. Complete resolution is uncommon.
 Right Heart
Valvular distortion = right heart failure
Pulmonary thrombosis and abscessation (embolic pneumonia)
 Left Heart
Valvular distortion = left heart failure
Thromboemboli (kidney, spleen, myocardium, brain, joints)
Diseases of the Arteries
Arteriosclerosis:
 Definition: "hardening of the arteries".

 Common in human, but also in dog, cat, swine and monkey.
 Characterized by intimal thickening following proliferation of connective tissue,
hyaline degeneration, infiltration of lipids (not seen in dog) and finally calcification.
1. Atherosclerosis:
 Greek word “Athere” means a soft, mushy, gruel like substance and “Skleros” means
hard.
 In this condition such a substance is formed in the intimal layer.
 This condition affects larger to medium sized elastic and muscular arteries –
e.g. Aorta and its branches; Coronary arteries and cerebral arteries.
 Degeneration in the wall of an artery in which lipids (cholesterol,
triglycerides, etc.) are the primary components of the degenerative response.
 Atheromatous plaques may occlude the vessels, producing ischemic necrosis

of the tissue which supplied by the involved artery.
How to develop/mechanisms of atherosclerosis:

 Atheroma deposition of lipid materials in the intimal layer (inner layer) of arteries.
 Deposition of lipids in the cytoplasm of smooth muscles of tunica intima,
macrophages or extracellular.
 Fibrous plaque formation.
 Fibrous connective tissue/ “fibrous plaque” surrounds the lipid laden cells (clearly
empty space).
 Thrombus formation may be found that may lead to thromboemboli formation.
 Hyalinization of FCT, leads to necrosis, calcification.
 Then, necrosed tissues could be replaced by osseous tissues
Effect of atherosclerosis:
 Thrombus formation in coronary artery may lead to myocardial infarction (M.I.).
 If in cerebral artery then cerebral ischemia, infarction, hemorrhage, hemiplegia,
aphasia etc.
 If in aorta then aortic aneurysm
Causes:
 Unknown, but may also be due to-
Senility
Hypertension
High blood cholesterol and lipid content
Intramural haemorrhages
Endocrine deficiency
Heredity, obesity, stress, physical activity and smoking habits are contributing
factors.
2. Monckeberg medial sclerosis or calcification:

 This condition affects medium sized muscular arteries (tunica media)
 The muscular tissues undergo hyaline and fatty degeneration followed by necrosis
and calcification.
Causes:
 Senility but not necessarily with hypertension
 Prolonged action of epinephrine and nicotine
 Hypervitaminosis (vit- D)
 Chronic interstitial nephritis in dog.
3. Arteriolosclerosis: This condition affects small arteries and arterioles.
a. Hyaline arteriolosclerosis: A homogenous pink collagenous fibrosis and thickening
of the wall of the arteries. No cellular details.
Cause:
Diabetic angiopathy
Senility
Hypertension.
b. Hyperplastic arteriolosclerosis:
An “onion skin” appearance is found due to the hyperplastic proliferation and
concentric arrangement of arteriolar wall
Cause:
Hypertension
Chronic renal disease
Hyperthyroidism
Hyperadrenocorticism
Cor pulmonale
High altitude diseases in cattle.
Arteritis: Inflammation of the arteries.
 Causes: Not really known. It’s believed to be an autoimmune disorder.
 Causal agents may be virus, bacteria, protozoa, fungus etc.
 Arteritis may be acute or chronic.
 Polyarteritis nodosa/ Periarteritis nodosa: Inflammation involving all layers of

the wall.
Cause:
Bacteria
Virus
Sensitivity to some drugs/chemicals: sulphonamides, arsenic,
deoxycorticosterone etc.
Sarcosporidia spp in some animals
Malignant catarrhal fever in cattle
Equine infectious anemia in horse.
Lesions:
Edema
Fibrinoid necrosis
Leukocytic infiltration
Intimal and medial fibroplasia
Thrombosis
Nodular appearance of the arteries.
Aneurysm: An aneurism is the localized dilatation of the artery or a cardiac chamber.
Types of aneurysms:
1. True aneurysm
1. Intima and media have wholly or partially ruptured due to weakness &
2. Artery can not resist the blood pressure causing the development of aneurysm.
2. False aneurysm / Dissecting aneurysm
1. Due to medial necrosis, blood can enter to necrotic area through vasa vasorum
or through inner coat and may exit through other end.
2. Due to flowing of blood, inner coat is separated from outer coat. That’s why it
is called dissecting aneurysm
Causes: Weakening of the wall is due to

 Syphilis in man
 Infected embolus
 Polyarteritis nodosa
 Trauma
 Parasites- Strongylus vulgaris (blood worm)
 Infection with abscess or tuberculosis
 Congenital weakness of the walls
Hypertension:
1. High blood pressure/systemic hypertension is the most important disease of human
2. Clinically, persons having persistently high blood pressure than the normal is called
high blood pressure/systemic hypertension
Normal blood pressure range
Age BP
20 yrs 140/85 mm Hg
20-50 yrs 160/105 mmHg
50-70 yrs 170/115 mmHg
Types: Clinically
1. Mild high blood pressure 150/105 mm Hg
2. Moderate high blood pressure 170/115 mmHg
3. Severe high blood pressure >170/115 mm Hg
On the basis of cause Hypertension
1. Essential hypertension/ primary hypertension/ idiopathic hypertension : causes
and pathogenesis are not known
2. Secondary hypertension : hypertension may also develop secondarily to other
diseases
3. In dog
a. Chronic renal disease causes activation of renin-angiotensin system and also
causes retention of Na and H2O.
b. Hyperadrenocorticism
c. Pheochromocytoma
d. Hyperthyroidism
e. Hyperparthyroidism
Effect of hypertension:
a. Heart failure
b. Renal failure (Nephrosclerosis)
c. Cerebral lesions: infarction and hemorrhage leading to hemiplegia and
aphasia
Diseases of the Veins
Phlebitis: Inflammation of the veins.
Varicose Veins:
 Veins are dilated, irregular and tortuous.
 Leg veins and hemorrhoidal brain veins are most commonly affected (human)
 Veins of scrotal plexus in horse and supramammary veins in cow are mostly
affected.
Causes:
 Any interference to the return of venous blood- mitral stenosis, pulmonary
emphysema and liver cirrhosis
 Pressure on vein by- tumor, pregnant uterus, increased abdominal pressure
 Standing for a long time.
 Muscular exertion in athletes.
 Aging
 Post inflammatory weakness of vessel wall.
Telangiectasis: Markedly dilated cluster of blood vessels (capillary and veins).
Lymphangiectasis: Dilatation of the lymphatic duct.
Lymphangitis: Inflammation of the lymphatic channel/system.
Pericardium
Some conditions of pericardium:
Conditions Definition Causes
Hydropericardium/ Excessive accumulation of serous  Cachectic diseases
Pericardial effusion fluid in the pericardial space.  Congestive heart failure
 Renal diseases
 Chronic stomach worm infection
 Damage to capillary
endothelium by anoxic
conditions
 Liver insufficiency
 Tumors
Hemopericardium/ Accumulation of blood in the  Trauma and rupture of the heart,

Cardiac tamponade pericardial cavity aorta or coronary artery.
 Hemorrhagic pericarditis
 Mesothelioma
Hemo- Transudate with addition of  Causes of both hydro and
Hydropericardium erythrocytes and/or hemoglobin hemopericardium.
serosanguinous fluid.
Pneumopericardium Entry of air/gas into the  Entry of gas producing
pericardial cavity organisms into the pericardium
through penetration.
Pyopericardium Pus in the pericardium.  Tuberculosis
 Secondary infection of purulent
pleuritis, purulent pneumonia
and rupturing of myocardial
abscess.
Chylopericardium Lymph (milky-white fluid) in the  Rupture or tumorous damage to
pericardial cavity. the thoracic duct.
Serous atrophy of fat Fat present in the grooves of the  Cachectic diseases
heart become transformed into a  Inadequate nutritional supply.
gelatinous mass.  Secondary to starvation or
inanition.
 Occurs relatively rapidly in a
sick cow.
Pericarditis: Inflammation of the pericardium is commonly seen in animals.
1. Serous Pericarditis: is characterized by the accumulation of protein-rich fluids with

varying numbers of inflammatory cells in the fluids and pericardium.
 Usually, it is caused by viral infection.
 The clear serous fluid must be distinguished from a transudate, which
typically accumulates in the pericardial sac in heart failure or anasarca.
2. Serofibrinous and Fibrinous pericarditis:

Causes:
Cow: Horse:
 Black quarter  Pneumonia
 Bovine encephalomyelitis, pasteurellosis  Influenza
 Contagious bovine pleuropneumonia  Strangles
Coliform septicemias.  Streptococcal infection.
Swine: Sheep:
 Mycoplasma pneumonia  Pasteurellosis
 Pasteurellosis  Salmonellosis
 Salmonellosis  Streptococcal infections
 Glasser's disease (Haemophilus suis)
Dog:
 Streptococcal infection
 Hog cholera  Canine distemper
 Canine leptospirosis
Birds: Psittacosis Cat: Feline infectious peritonitis (FIP)
Lesions:
Gross:
 Accumulation of fluid and fibrin within pericardial space.
 Surfaces of epicardium and pericardial sac may be slightly opaque.
 Fibrinous adhesions which can be broken down (torn apart) easily are
occasionally referred to as "Bread and Butter." Or “Shaggy Heart”.
Microscopic:
 Usually only mild inflammation with fibrin on the surface involving the
 Pericardial sac and epicardium in acute disease processes.
 Variable numbers of neutrophils and macrophages are seen.
3. Purulent or Suppurative Pericarditis
Cause:
 Associated with various pyogenic bacteria.
 Often complication of traumatic reticulopericarditis.
 Salmonellosis in poultry
 Nutritional anaemia in pigs.
Lesions:
Gross: Fluid and liquefied inflammatory debris accumulated within the pericardial sac,
usually very malodorous.
Microscopic:
 Moderate accumulations of neutrophils and other inflammatory cells on the
surface of the pericardial sac and epicardium.
 Fibrous connective tissue present beneath the layer of inflammatory cells, but
dependent upon the time frame of the disease process.
Sequelae: Either fibrinous or suppurative pericarditis may undergo organization which
produces fibrous adhesions of the pericardium to the epicardium.
4. Traumatic Reticulopericarditis ("Hardware Disease")

 Due to extension of a sharp object through the wall of the reticulum, diaphragm
and pericardium.
 Mixture, or "garbage can" of bacteria isolated.
Neoplasm of Cardiovascular System:
 Rhabdomyoma.
 Rhabdomyomsarcoma.
 Chemodectoma/Heart base tumor.
 Haemangiosarcoma.
 Neurofibroma.
 Schwannoma.
 Granular cell myoblastoma.
 Fibrosarcoma.
 Chondrosarcoma from mitral valve
 Malignant lymphoma.
Credit hour: 3
Lectures: 14~19
Respiratory System
Respiratory system: Respiratory system includes- lung and systems of tubes.

Different parts of Respiratory system are:
1. Nose and Nasal cavity
2. Pharynx
3. Larynx Air conducting portion
4. Trachea
5. Bronchus: Primary and Secondary
6. Bronchiole: Terminal and
Respiratory bronchiole
(Transitional portion)
Respiratory (gaseous
7. Alveolar duct
exchange) portion
8. Alveolar sac
9. Alveoli
Major Function:
1. Gaseous exchange.
2. In some species helps in body cooling.
3. Noxious gases are neutralized and dust are cleared by this system.
4. Maintenance of acid base function.
Terminologies:
 Rhinitis: Inflammation of the nasal mucosa.
 Pharyngitis: Inflammation of the pharynx.
 Laryngitis: Inflammation of the larynx.
 Tracheitis: Inflammation of the trachea.
 Bronchitis: Inflammation of the bronchus.
 Sinusitis: Inflammation of the lining membrane (mucous) of sinus.
 Pneumonia: Acute inflammation of the lung.
 Pneumonitis: Chronic inflammation of the lung.
 Eustachitis: Inflammation of the Eustachian tube.
Rhinitis
(Acute Rhinitis/Coryza/Acute Nasal Catarrh/Common Cold in Human)
Rhinitis is the inflammation of nasal mucosa.

Causes:
1. Irritant substances:
a. Physical agents: Dust, foreign body like chaff, pollen etc.
b. Chemical agents: Ammonia, chlorine, war gas, formalin etc.
2. Parasites:
e.g. Linguatula serrata in dog and the larvae of Oestrus ovis in sheep.
3. Fungi: Aspergillus fumigatus
4. Bacteria: e.g. Pasteurella multocida, Sphaerophorus necrophorus, Bordetella
Department of Pathology, FASVM, SAU, Dhaka 1

bronchiseptica (canine), Pseudomonas aeruginosa, Streptococcus equi (strangles in horse),
Staphylococcus sp. Mycobacterium tuberculosis, Cryptococcus neoformans etc.
5. Viruses: Canine distemper virus, Equine herpes virus 1, Infectious bovine
rhinotracheitis virus, Feline viral rhinotracheitis virus, Bovine malignant catarrhal fever
virus, Inclusion body rhinitis.
Gross lesions:
1. The mucous membrane is swollen and congested.
2. At first, a dry mucous discharge occurs subsequently which turned into mucopurulent
later.
1. Hyperemia, inflammatory cells and hydropic degeneration of the epithelial (goblet)
cells are seen.
2. Extension to sinuses results in sinusitis.
Sinusitis
 In cattle: Frontal sinusitis are common, and infection occurs through the wound at the
time of dehorning. Infection can spread up to the cranial cavity.
 In horses: Maxillary sinusitis are common, and infection occurs when there is diseases
in the molar teeth and walls of the dental alveoli.
 In human: Frontal sinusitis are common.
NB: The seven opening of pharynx is important in the context of sinusitis:

1. Two opening for the auditory tube
2. Isthmus faucium/oral opening
3. Laryngeal opening/aditus laryngeus
4. Oesophageal opening/aditus oesophageus
5. Two opening for caudal nares/choanae.
Eustachitis: Inflammation of the Eustachian tube. Pharyngeal infection can extend up to

Eustachian tube. Swelling occurs close to the Eustachian tube causing interference of hearing.
Otitis media: Inflammation of the middle ear. Infection can extend up to middle ear.
Catarrh of guttural pouch: Catarrhal Inflammation of the guttural pouch. Exudate cannot be
drained out due to swelling of the tubes and its positions. Exudates become dry and may form
caseous or solid materials.
Tympanites of guttural pouch: Excess gas accumulation in the guttural pouch (entrapped air
within the guttural pouch).
Cause:
1. Due to valve like action of the Eustachian tube- Head downward > air enter > valve
like action > air cannot expelled out > tympanites.
2. Gas derived from putrefaction of the exudates.

Nasal polyps (polyp/ polypus)
Definition: Inflammatory new growth within the nose or sinuses, which resembles to true
neoplasm.
Etiology: Unknown
Characteristics:
1. Pedunculated or elongated and may fill the nasal passage.
2. Smoothly covered with mucous membrane.
3. Inner tissue is fibrous and myxomatous that are infiltrated with neutrophils and
lymphocytes.
4. Numerous capillaries proliferation occurs.
Effects: Difficult respiration and hemorrhage occurs from nostrils.
Differential diagnosis: with followings-
1. Nasal granuloma in bovine.
2. Rhinosporidiosis.
3. Schistosomiasis.
4. Actinobacillosis.
5. Atopic allergy/chronic granular rhinitis.
6. Habronemiasis.
7. True neoplasm.
Nasal Congestion: is the blockage of the nasal passages usually due to membranes lining
the nose becoming swollen from inflamed blood vessels.
 Occurs whenever animals are exposed to cold air. The blood vessels in the nasal
passage are dilated, so that air breathed in may be sufficiently warmed. Secondary
bacterial infection may result in inflammation and edema.
Epistaxis: Hemorrhage (acute) / bleeding from the nostril/nasal cavity or nasopharynx.

Causes:
1. Trauma by heavy blow or during passing stomach tube.
2. Ulcerative infection: porcine atopic rhinitis
3. Convulsive expiration.
4. Parasites: Oestrus ovis.
5. Erosion of the vessels by pathological/mechanical processes in the nasal cavity-
neoplasms and fractured bone.
6. Compression of jugular veins by too tight collars in the working horse.
7. During certain infectious disease: Glanders (in horse), anthrax, purpura, infectious
bovine rhinotracheitis, malignant catarrhal fever etc.
8. Idiopathic: familial in certain race horses.
9. Uremia.
10. Poisoning: nitrates, bracken fern, sweet clover or mercurial.
Laryngeal hemiplegia/Roaring
Hemiplegia: means paralysis of one side of the body.

 Common in horse
 Characterized by abnormal sound, roaring
 Things: have to be remembered in roaring-
1. Arytenoid cartilage (left)
2. Cricoarytenoideus muscle (dorsalis)
3. Recurrent laryngeal nerves

Pathogenesis:
 In normal health, the arytenoid cartilages are drawn outwards during inspiration to
allow ingress of air. The important muscle that operates this is the Cricoarytenoideus.
If for any reason there is injury to and degeneration of the nerve supplying this muscle,
then the cartilage cannot open and so will stand in the way of air passing freely into
the wind pipe.
 In horses, a condition is noticed, in which there is hyaline degeneration and fibrosis of
the left Cricoarytenoideus muscle together with demyelinization and Wallerian
degeneration of the left recurrent laryngeal nerve that supplies the muscle. When the
nerve is paralyzed, and the muscle is degenerated and replaced by fibrous tissue, the
arytenoid cartilage does not open out during inspiration and so air cannot enter the
trachea freely and this condition is accentuated when the animal is exercised, and a
noise is heard by brushing of air with the arytenoid cartilage, This is therefore known
as Roaring.
Cause: The cause for the paralysis of the nerve is obscured. But-
 One theory:
 it is subjected to repeated trauma by the pulsation in the aorta as the nerve
circles around aortic arch where the nerve is situated during its course.
 Other causes:
 Lead poisoning and pressure on the nerve by aneurysms, enlarged lymphnodes,
abscesses, tumors, esophageal diverticula and other traumatic conditions.
Microscopic Lesions:
1. Atrophy and ultimately disappearance of the muscle fibers with replacement by fibrous
connective tissue in cricoarytenoideus muscle.
2. Demyelination and WALLERIAN degeneration of the left recurrent laryngeal nerve.
Effects:
1. Horse cannot used for raced purpose
2. May cause pneumonia.

Porcine atopic rhinitis
Background:
 It is an infectious disease of swine.
 Characterized by stunted development or deformation of the nasal turbinate
(conchal bone) and septum.
Host: Young pig.
Etiology:
1. Bordetella bronchoseptica
2. Pasteurella mutocida.
Gross lesions:
1. Mucosa of the turbinate bones shows a small depressed and congested foci.
2. Erosion of disappearance of mucous membrane.
3. Turbinate bones began to soften.
4. Snout growth is retarded.
1. Rarefaction and disappearance of turbinate bones.
2. Fibroblasts and osteoblasts are found in periosteal region.
3. Infiltration of lymphocytes and monocytes.
Bronchostenosis
Definition: It is a narrowing of the bronchial lumen due to obstruction or peripheral

pressure.
Cause:
1. Aspiration/breathing of foreign bodies/objects. e.g. sucking food into airway.
2. Accumulation of exudates.
3. Parasites within the lumen.
4. Inflammation of the wall of the bronchus producing alteration in it (the exudate
infiltrating the wall reduces the diameter of the bronchi).
5. Pressure from outside the bronchial wall. e.g. abscesses, tumors, enlarged lymph nodes
and exudates of the pleural cavities.
6. Spasm of the muscles of bronchi. e.g. in case of allergy (Asthma).
 A partial closure of the bronchi or bronchioles results in ballooning of the lung

involved, since air that enters during inspiration is not expelled during expiration and
so is trapped. Repeated inspirations will therefore result in ballooning of the alveoli.
 Complete obstruction of a bronchus results in collapse of the lung.
Bronchiectasis
Definition: This is dilatation of the bronchus.

Causes: This usually follows
 A chronic inflammation of the bronchi, in which the elastic tissue; the musculature
and even the cartilages may be destroyed. Due to toss of the elastic tissue, contractile
power of the bronchus is lost and so the bronchus dilates. At the place of dilatation,
exudate accumulates thereby still further dilating the bronchus.
 In chronic pneumonia, the contraction of the fibrous tissue exerts a pull thereby
widening the walls. The dilatation is facilitated by a weakening of the wall in bronchitis,
which, may also he found.
 In bronchostenosis, air accumulates during inspirations and so causes dilatations of

the bronchi below the level of obstruction. When the bronchi are completely closed
resulting in atelectasis, there is an elastic pull on the bronchial wall due to negative
pressure in the pleural cavity.
Gross lesions: two forms are recognized:

 The saccular, which is less common, is an out-pouching of the bronchial wall; usually
results due to localized necrotizing foci in bronchitis, found in cattle and sheep in
lungworm infection.
 The cylindrical variety, which is more common, especially in cattle, is a uniform
dilatation of the bronchi. Mucosa of bronchi and bronchiole are thrown into folds looks
like star shaped appearance in cross section.
In both form, the affected lung is collapsed and is carnified. There may usually be pleural
adhesion.
Macroscopic lesions:
 The wall of the affected bronchi shows variable infiltration by chronic inflammatory
cells.
 The musculature, cartilage and the lining epithelium may disappear in varying degrees.
Bronchiectasis in feedlot cattle: A specific type of bronchiectasis has been described in early
feedlot cattle.
Pathogenesis: Unknown.
Cause:
1. Pasteurella multocida
2. Corynabacterium pyogenes
3. E. coli
4. Staphylococcus spp.
5. Mycoplasma spp.
Bronchitis
1. Acute Tracheo-Bronchitis:
 This condition is usually encountered along with upper respiratory diseases.
More often it is a condition seen in pneumonias.
 Though bronchitis means inflammation of the bronchial epithelium frequently,
the inflammation spreads to the wall of the bronchus and from there to the lung
tissue-expanding peribronchitis or
 The infection may spill into the alveoli from the terminal bronchioles thereby
resulting in bronchopneumonia.
Causes:
1. Inhalation of irritants- dust, feed, industrial fumes, medicaments, smoke etc.
2. Infections-
a. Bacterial– Pasteurellosis
b. Viral- Ranikhet disease, Infectious bronchitis of fowls, Infectious bovine
rhinotracheitis
c. Parasites- Lungworms.
Gross lesions:
 The mucosa is thickened, reddened and covered by an exudate which may be
catarrhal, fibrinous or purulent.
 In aspiration of foreign material, a gangrenous bronchitis is seen in which

there is extensive necrosis of the mucosa which sloughs.
 The wall of the bronchus way also be destroyed.
 There is congestion and infiltration by inflammatory cells in whicn neutrophils
predominate.
 There may be increased secret ion of mucus and in severe cases the epithelium
may be destroyed.
 The lumen contains mucus, leucocytes, dead epithelial cells, lung worms and
their ova.
Results/ Outcome:
 Recovery
 Bronchiectasis
 abscess formation
 bronchopneumonia
 chronic bronchitis.
a. Canine tracheo-bronchitis/Kennel cough: Acute tracheo-bronchitis of dog characterized

by intermittent coughing.
Etiology:
1. Infectious canine hepatitis virus
2. Herpes virus
1. Presence of inclusion bodies.
2. Inflammatory reaction found in the lumen as well as wall of bronchus.
Note: If found only in wall, then not treated as bronchitis.
2. Chronic Bronchitis
Causes:
1. Mild, continuous irritant substances- smoke and dust
2. Chronic venous congestion-as in heart disease
3. Chronic infection of upper respiratory tract - chronic sinusitis
4. Bronchiectasis
5. Most common cause in animals is lungworm infection, tuberculosis and lung
abscesses.
Gross lesions:
1. The bronchial mucosa is thickened and has a velvety feel. Sometimes it may be
congested but more often is pale and edematous.
2. The exudate is mucoid or mucopurulent and in cases of worm infection, it is mixed
with worms and their eggs.
3. The bronchi may also be dilated.
1. Mucus exudates in the lumen of the bronchus.
2. Increase in goblet cells.
3. Lamina propria is infiltrated with lymphocytes and plasma cells.
4. Epithelial cells may loss in severe cases and may sloughs up leaving ulcerated
zone.
5. Hyperplasia of the epithelial cells.
Results/ Outcome:
 Bronchopneumonia

 Atelectasis (is the collapse or closure of a lung resulting in reduced or absent gas
exchange)
 Bronchiectasis
 Emphysema-putting greater strain/force on the right side of heart-chronic venous
congestion will result ultimately.
Lungs
Functions of lung:
1. Gaseous exchange
2. Cleansing mechanism
3. Release of surfactant
Cells in lung alveoli:

1. Type-I pneumocytes: Cover most of the surface of the alveoli, fried egg appearance,
form part of the barrier across when gas exchange occurs.
2. Type-II pneumocytes/Giant alveolar cell: Cuboidal epithelial cells that are scattered
in alveolar walls. They produce surfactant.
Surfactant: Phospholipid secreted by type-II pneumocytes/giant alveolar cell. It has
several fractions:
i. Phosphatidylcholine- lower the surface tension.
ii. Phosphatidylglycerol- increase the motility of molecule
iii. Surfactant associated apoprotein- binds the lipid.
Significance of surfactant:
i. Without it, the walls would stick together during exhalation.
ii. So, Premature babies – problem in breathing is largely because of lack
surfactant
3. Type-III pneumocytes:
a. Alveolar brush cell: Unknown function
b. Dust cells: Alveolar macrophages- Phagocytosis
c. Mast cells: Release of histamine, heparin etc.
Pneumonia
Definition: Acute infectious inflammation of the lung with copious exudate filling the alveoli
and clinically the patient have high fever with respiratory distress.
 Pneumonia is a very common disease found in animals except probably the cat, in
which it is rarely met with.
In human:
 Lobar or croupous pneumonia:
 Caused by Diplococcus pneumoniae, in which whole lobes may be affected
and characterized by a fibrinous or croupous exudate in the alveoli.
 Catarrhal or lobular or bronchopneumonia: which is
 Patchy, and in which only parts of a lobule or only a lobule are affected,
characterized by a catarrhal exudate of the alveolus.
In animals:
 Lobular pneumonia that is frequently seen.
 Most varieties in animal- may start as a lobular pneumonia but end up as a lobar variety.
 So all gradations may be met with in the same animal, and what more, the same
etiological factors may give rise to these different grades of pneumonia.

Genesis and development of pneumonia or steps / stages of pneumonia:
 We know that in animals, there is no condition similar to the lobar pneumonia of
human.
 But a description of the stages of human lobar pneumonia helps in the understanding
of the genesis and development of pneumonia the same is given below-
1. The stage of congestion: this is the early stage in which there is active hyperemia and
edema of the alveoli.
Gross lesions:
 The lungs are congested (due to hyperemia) and swollen (due to inflammatory
edema).
 The lungs still float in water.
 On section, blood tinged-fluid escapes.
 The capillaries on the alveolar walls are dilated and filled with blood.
 Alveoli contain a little serous exudates which recognized as pink stained
homogenous precipitates, and often a few red blood cells.
 Depending on the irritants, this may develop within a few minutes (chemicals) to
a few hours (infectious agents).
2. Stage of red hepatization: The affected area of lungs is consolidated or hepatized and
the consistency of the lungs will be resembling liver. So, it’s called hepatization.
Gross lesions:
 The affected portion of the lung is quite conspicuous being readily discernible
from the healthy.
 A distinct line of demarcation is found.
 Portions of the affected parts sink in water, since all air is replaced.
 Over this area, the pleura is inflamed and dull red in color.
 The redness is due to persistence of capillary hyperemia or the hemorrhagic
nature of the exudate.
 A membrane may form.
 Lymphatics are obstructed by fibrinous plugs.
 The pleural fluid is increased.
 The peribronchial and perivascular lymphatics are dilated with protein-rich fluid.
 The alveoli reveal a fibrinous exudate containing erythrocytes,
polymorphonuclear leucocytes and desquamated epithelial cells.
 Dilatation of lymphatics and widening of septal cells are observed.
 This stage of pneumonia develops in two days.
3. Stage of grey hepatization: develops in 2-3 days after red hepatization.

Gross lesions:
 The lung is still consolidated and sinks in water.
 The color is less red than the previous stage and some parts are grey like grey
granite.
 The alveoli appears to be less filled than in the previous stage.
 Fibrin can clearly be seen and strands may be found to pass from one alveolus to
another through the pores of Kohn.

 Erythrocytes have almost disappeared from alveoli.
 The grayness of the affected tissue in this stage is attributed to
i. ischemia of the alveolar capillaries due to pressure of exudate on them,
ii. increased infiltration by leucocytes
iii. thrombosis in the alveolar capillaries and
iv. Lysis of red blood cells.
v. The liquefaction of the exudate commences and the nuclei of polymorphs
become blurred and less distinct.
4. Stage of Resolution/recovery: characterized by the "resorption and restoration of

the pulmonary architecture.
 At this stage, liquefaction and removal of the exudate takes place.
 The liquefied material may be absorbed via lymphatics or veins or may be
expectorated.
lesions:
 The exudate is disappearing, remains is granular, polymorphs are either absent or
the few that remain are degenerated.
 A number of macrophages derived from alveolar epithelial lining as well as from
the blood are in evidence.
 The epithelium, most of which has died and desquamated is regenerated within
few days &
 Then, the lung returns to the normal state of functional activity as previous.
Routes of infection (pneumonia):

1. Through the respiratory passages-Bronchogenous route:
 This is by far the most common route.
 Some infectious agents like Aspergillus fumigatus, Streptococci, Staphylococci, E
coli and Corynebacterium pyogenes and some viruses (e.g., viruses of Ranikhet
disease and viral pneumonia of pigs), avian influenza, PPR may invade the lung
through this route.
2. Through the blood vascular system-Hematogenous route:
 Blood stream may carry bacteria (Pasteurellosis)
 Parasitic larvae to the lungs.
3. Through penetrating wounds:
 Wounds by bullets, knives, pitch forks etc., may penetrate the lungs from the
exterior, usually carrying bacteria and producing pneumonia.
 Similarly, foreign bodies penetrating through rumen, reticulum and diaphragm
may set up pneumonia.
Causes of pneumonia:
A. Bacteria:
Cattle Sheep
1. Mycoplasma mycoides 1. C. Pyogenes
2. Pasteurella multocida 2. Pasteurella multocida
3. Corynebacterium pyogenes 3. Staphylccocci
4. Actinobacillus lignieresii 4. Streptococci
5. Staphylococci 5. E. coli.
6. Streptococci
7. Mycobacterium tuberculosis

Horses Dog
1. Corynebacterium equi 1. Streptococci
2. Streptococcus equi 2. E. coli.
3. Pseudomonas mallei 3. Bordetella bronchiseptica
Swine 4. Staphylococci
1. Streptococci 5. Klebsiella
2. C. pyogenes Cat
3. Haemophilus suis 1. Pasteurella multocida
4. Pasteurella multocida 2. Coliforms
B. Viruses:
1. Equine infectious pleuropneumonia virus 8. Bovine respiratory

2. Equine influenza virus syncytial virus
3. Equine arteritis virus 9. Feline herpes virus
4. Calf pneumonia virus 10. NDV
5. Canine distemper virus 11. PPR
6. Canine herpes virus 12. Sheep pox.
7. Infectious bovine rhinotracheitis virus
c. Fungi: d. Parasites
1. Blastomyces 1. Metastrongylus apri in swine
2. Coccidioides immitis 2. Dictyocaulus viviparus in cattle
3. Histoplasma 3. Protostrongylus rufescens and
4. Actinomyces Dictyocaulus filaria in sheep and goats
5. Aspergillus fumigatus 4. Ascaris lumbricoides var suum in pigs.
6. Cryptococcus neoformans
7. Mucormycosis.
e. Mycoplasma f. Chlamydia
Mycoplasma mycoides Chlamydia psittaci
g. Irritants: Inhalation of dust, pollen, foreign bodies, smoke, hot and cold air, anesthetics,
war gases, medicinal agents etc.
h. Predisposing causes: Conditions, called predisposing factors make the animals more susceptible
to diseases of respiratory system. These are-
1. Fatigue 5. Parasitism
2. Exposure to cold air 6. Exposure after dipping in winter
3. Long travel by train or ship months
4. Severe hunger, malnutrition and 7. Cardiac weakness and recumbency for
chronic undernutrition a considerable time.
Gross lesions (general):

1. One or several lobules may be affected which are congested, edematous, dark red in

color, firm in consistency and sink in water
2. Foamy exudation occurs in cut surface
3. Areas adjacent to the affected show compensatory emphysema
4. The lymphatics are swollen and become easily visible
5. The lymph nodes are hemorrhagic and swollen
6. The bronchi contain hemorrhagic exudate.
Microscopic lesion:
1. Alveoli are filled up with exudate and serum, fibrin and different types of reactive cells
(neutrophils, macrophages, plasma cells, lymphocytes).
Complications/sequelae of pneumonia:
A. If fatal, death due to- toxemia, hypoxia and cardiac failure
B. If not fatal, then-
1. Delayed recovery.
2. Fetalization of lung/pulmonary adenomatosis/epithelialization.
3. Bronchiectasis and/or bronchiole is still obstructed, even after resolution of
alveolar exudate.
4. Atelectasis-when bronchiole is still obstructed, even after resolution of alveolar
exudates.
5. Suppuration and abscess formation- if organisms are pyogenic.
6. Gangrene- if organisms are non-pyogenic, saprophytic and putrefactive.
7. Septicemia- if organisms enter into blood and causing inflammation in other parts
of the body.
8. Incomplete resolution/carnification- fibrosis of the lungs and pleura may results
carnification (becoming flesh).
9. Severe necrosis replaced by scar tissue.
10. Chronic pleuropneumonia- adhesion in pleura and lung surface.
Special types of pneumonia:

 Lung alveoli filled with exudate and clinically there is fever and coughing.
 They have some peculiar characteristics.
1. Pneumonia due to Parainfluenza virus I
2. Embolic Pneumonia
3. Verminous Pneumonia
4. Gangrenous pneumonia
5. Hyaline membrane disease (lung)
6. Pneumonia of shipping fever
7. Hypostatic Pneumonia
8. Granulomatous Pneumonia
9. Interstitial pneumonia
10. Pneumoconiosis
11. Mycotic pneumonia:
1. Pneumonia due to parainfluenza virus I:

 The virus is also called Sendai virus in japan.
 This virus has the affinity to clear cells of bronchi. It has 3 phase:
a. Acute phase:
Gross lesions: Lung and spleen is edematous and congested.
 Bronchous and bronchiole epithelium produce syncytia formation

 Cytoplasmic inclusion body in affected cells
 Neutrophils, macrophages and lymphocytes in the alveoli
b. Ending of acute phase: Lesions subside and affected epithelium is sloughed off.
Regeneration of epithelium will start.
c. Resolution phase: Organizing alveolitis and obliterating bronchiolitis found.
2. Embolic pneumonia/metastatic suppurative pneumonia:

Generally caused by pyogenic bacterial emboli and occurred in hematogenous route.
Lesions:
Scattered pneumonic foci in sub-pleural surface (more blood supply in sub-pleura)
Abscess formation rather than hepatization.
3. Verminous pneumonia: Pneumonia in animals is caused by many species of parasites (lung

worms).
Lesions:
The exudate in the bronchi contains the adult worms with their embryonated eggs along
with neutrophils, macrophages, lymphocytes and desquamated epithelial cells.
The alveoli may contain worm ova/ larvae besides the inflammatory cells.
Host Parasites Habitat

Cattle Dictyocaulus viviparus Bronchi
Paragonimus westermanii Bronchi and cyst in the lung
Sheep Dictyocaulus filaria Bronchi

Protostrongylus rufescens Bronchi
Protostrongylus rushi Bronchi
Protostrongylus stilesi Bronchi
Mullerius capillaries Alveoli and blood vessels
Swine Metastrongylus apri Bronchi
Ascaris larvae Migration
Horse/Donkey Dictyocaulus arnifieldi Bronchi
Cat Filaroides abstrasus Bronchi
Dog Angiostrongylus vasorum Pulmonary arteries
Filaroides osleri Trachea and bronchi

4. Gangrenous pneumonia (foreign body/necrotic/Aspiration /medication /lipid/veterinarian
induced pneumonia):
Causes:
Faulty drenching in cattle and careless passage of stomach tube (horses)
Inhalation of irritant drugs, oils, anesthetics or feed (lambs and pigs)
Aspiration of
i) Milk or gruel (lipid food)
ii) Ingesta-in paralysis of throat in parturient paresis of cattle.
Hematogenous- from gangrenous lesions elsewhere in the body. e.g. gangrenous
metritis or mastitis.
Penetration of sharp foreign bodies through rumen and reticulum
Direct infection by Sphaerophorus necrophorus
Embolism
Tongue holding during administration of drug.
Gangrenous pneumonia may be a sequel of choke.
Pathogenesis:
 The irritants produce severe inflammation and extensive thrombosis of the blood
vessels resulting in necrosis.
 The leucocytes and bacteria produce liquefaction of the necrotic material, resulting in
cavitation.
 Putrefactive organisms produce gangrene.
Lesions:
There is extensive consolidation of the anterior and ventral portions of the lung with
foul smelling exudates.
The affected parts are greenish or black in color and sometimes large cavities are seen.
The area around these lesions shows congestion and intense reaction.
Sequelae: Death in all cases.
5. Hyaline membrane disease (lung): A fatal respiratory distress of premature baby or infants,
in which a membrane composed of proteins and dead cells lines the alveoli (the tiny air sacs
in the lung), making gas exchange difficult or impossible.
Lesions:
a. Presence of hyaline membrane in alveoli formed by fibrin and debris
b. Atelectasis is found.
Causes:
a. Due to asphyxia
b. Deficiency in surfactant
c. Disturbances in fibrinolytic system.
6. Pneumonia of shipping fever: Occur in young cattle at the time of transportation.

Characterized by respiratory distress. Sometimes it may cause fatal pneumonia or bronchitis,
intravascular clots and ultimately huge fibrinous inflammation.
Causes:
a. Pasteurella multocida
b. Mycoplasma spp.
c. Infectious bovine rhinotracheitis

Hypothetical pathogenesis:
7. Hypostatic pneumonia:
 In a recumbent patient, hypostatic congestion, edema occur in lower portion of the
lung due to gravitational force and porous nature of the lung.
 Inhaled pathogens can cause pneumonia easily than the healthy lung.
 This type of pneumonia is called hypostatic pneumonia.
8. Granulomatous pneumonia: If there is any granulomatous diseases in lung, lung become

susceptible to pneumonia and it is called granulomatous pneumonia. Granulomatous diseases
are-
 Tuberculosis
 Aspergillosis
 Histoplasmosis
 Actinobacillosis (lumpy jaw)
 Actinomycosis (wooden tongue)
 Coccidioidomycosis
Lesions:
1. Proliferation of macrophages and RE cells
2. Formation of giant cell
3. Presence of lymphocyte and plasma cell
4. Proliferation of Fibrous CT and presence of caseous mass, dystrophic calcification and
causal agent.
9. Interstitial pneumonia:
 Interstitial pneumonia is a disease in which the mesh-like walls of the alveoli become
inflamed.
 The pleura (a thin covering that protects and cushions the lungs and the individual lobes
of the lungs) might become inflamed as well.

10. Pneumoconiosis: a disease of the lungs due to inhalation of dust, characterized by inflammation,
coughing, and fibrosis.
Lesions:
1. Firm or hard tubercles usually white, gray or yellow color is present.
2. Dry and solid caseous necrotic center is found on cut surface.
3. Gritty sound while cutting the lung.
11. Mycotic Pneumonia:

 Inflammation of the lung caused by a variety of fungi is called mycotic pneumonia.
 Various fungi that may invade the lung and cause pneumonia are-
Aspergillus spp.- Aspergillus fumigatus is most common
Blastomyces spp.
Mucor spp.
Coccidioides spp.
Cryptococcus spp.
 Fowl is the most frequently affected by Aspergillus fumigatus.
 The spores of the fungus are found in the poultry litter and mouldy grain.
 Infection is by way of the respiratory tract.
 Spores may be inhaled with the infected dust or may be aspirated from the mouldy grain.
 Since this infection is very common in brooder houses, so called “Brooder
pneumonia”.
Gross lesions:
The lesion is nodular
Evacuation of the central caseous material into the bronchus results in a central cavity.
In lesions that are not progressive, increasing number of macrophages and epithelioid
cells may be present with a fibrous capsule.
Septate hyphae of the fungus with the inflammatory cells may be found around a central
caseous material.
In some cases, foreign body giant cells may be found at the periphery.
In lesions that are not progressive and are being obliterated, the hyphae are very short
and the lesion resembles that caused by actinomyces-the "asteroid body".
Pneumonitis
The literal meaning of pneumonitis is inflammation of the lung, chronic or interstitial
inflammation.
Special types of pneumonitis:
1. Hypersensitivity pneumonitis/Allergic alveolitis/ Farmer’s lung
2. Equine pulmonary emphysema/Chronic diffuse alveolar emphysema/Heaves/Brocken wind
3. Bovine allergic alveolitis/Bovine hypersensitivity pneumonitis/Bovine farmer’s lung
4. Equine allergic pneumonitis/ Equine farmer’s lung
5. Bronchial Asthma
Bronchial Asthma: Characterized by difficult wheezing having during the time of expiration
lasting from one to many hours. It is mainly a disease of human but has been reported in cattle,
cats and dogs.
Cause:
a. Allergic reaction against organic substances
b. Secondary bacterial infections
c. Appeared to be inherited.

Pathogenesis:
 this allergen can cause a spasmodic construction of smooth muscles of bronchioles and
bronchi resulting wheezing respiration.
 in dog, pollen inhalation can cause skin lesions as well as bronchial asthma.
Lesions:
a. Lymphocytes, monocytes and large number of eosinophils are found in bronchial and
bronchiolar wall
b. Accumulation of dense mucus exudate in the lumen
c. Astonishing hyaline thickening of bronchial basement membrane
d. Sometimes mucus condensed into a peculiar spiral strings (Curschmann’s B) called
Curschmann’S spiral.
e. Emphysema in the lung.
Pleuritis
It is the inflammation of the pleura. It is also known as pleurisy. Mostly pleuritis is secondary
to pneumonia, through primary infection of the pleura may occur.
Route of infection:
1. by direct extension from the underlying lungs or mediastinal glands or esophagus
2. by blood stream in septicemic diseases
3. Introduction through the thoracic wall- trauma by knives, bullets etc.
4. Introduction from the rumen via reticulum and diaphragm
5. through the esophagus-when sharp bones or pins may penetrate the pleura and convey
bacteria or in the horses when choke occurs.
Points to be remember:
1. Pleurisy may also be a condition noticed in specific diseases like swine erysipelas and
contagious bovine pleuropneumonia.
2. When pleura is involved in pneumonia, the condition is known as pleuropneumonia.
But it is not necessary that pleura should be affected whenever lungs are.
3. It is also possible to have pleuritis when the underlying lungs are healthy as in Black
Quarter.
4. In swine, due to generalized serositis (by Haemophilus suis) pleuritis may occur.
5. It is called Glasser’s disease.
6. In cattle, tuberculous nodule (3-10mm) found in pleural surface looks like dense white
and shiny. That’s why called Pearly disease.

Types of pleuritis:
Significance: If there is chronic pleuritis, there is adhesion of pleural surface by fibrous

connective tissue. So, pain during respiration.
Terminologies:
 Empyema: Accumulation of pus in pleural/thoracic cavity.
 Ossification of lung: Bone formation in alveolar wall found in old dog and cow.
 Hydrothorax: Accumulation of water or non-inflammatory fluid (transudate) in
pleural cavity.
Cause:
 Cardiac insufficiency
 Renal glomerular disease (hypoproteinemia in kidney)
 Mesothelioma.
 Chylothorax: Accumulation of lymph in the thoracic cavity.

Cause: Due to rupture of thoracic duct.
 Pneumothorax: It is the presence of air in the pleural cavity. This may be due to entry
of air into the pleura by the following ways:
 From the lungs- when some bullae rupture
 Through the chest wall-by piercing sharp objects.
Significance: Pneumothorax causes atelectasis of the lungs and this is of great
importance in the horse in which the right and left cavities communicate.
Atelectasis
The failure of the alveoli to open and contain air is called atelectasis. So the alveoli become
collapsed. This condition in may be congenital or acquired.
1. Congenital atelectasis: Also called atelectasis neonatarum. Animal is born dead and
has not breathed.
Causes:
a. Obstruction of the bronchi by mucus or inhaled liquor amnii.
b. Damage to the respiratory center that may occur in injury to the brain.
Lesions:
a. The lungs are dark and reddish-blue (red hepatized) in color due to dilatation of the
alveolar capillaries.
b. The lungs are firm to the touch and sink in water since there was no aeration.
c. The alveoli are collapsed and the epithelium lining the alveoli is cuboidal.
Sometimes the alveoli may contain fluid.
2. Acquired atelectasis (Pulmonary collapse):

Cause:
a. Obstruction; The lumen of the bronchus is obstructed and the air in the alveoli is resorbed.
The cause of the obstruction may be-
 In the lumen: foreign bodies, pus, mucus, masses of parasites
 On the wall: tumors, abscesses, enlarged lymph nodes, cysts
b. Compression; Extrapulmenary: Hydrothocax, pneumothorax, hydropericardium;
abdominal distension as in tympany of rumen and ascites.
Gross lesion:
a. There is never a total collapse but only focal.
b. The affected lung tissue is dark or reddish-blue in color and is depressed from the level of
the surrounding healthy lung
c. The affected part sinks in water and is leathery in consistency.
d. The pleura is thickened and wrinkled.
a. The alveoli are devoid of air and may appear as small or elongated clefts or the walls may
lie in apposition with each other with no lumen visible.
b. Due to the absence of pressure or alveolar air, the capillaries become dilated and with blood.
c. In later stages the alveolar epithelium may be desquamated while the tissue or the interlobular
septa may proliferate.
Pulmonary adenomatosis:
This is a disease of domestic animals, characterized by hyperplasia and hypertrophy of the
alveolar epithelium, giving it a glandular or adenomatous appearance. The disease has been
described in sheep (in various parts of the world and in India), cattle, pigs, horses and man.
Pulmonary Emphysema It is increased air in the lung. This is divisible into:

1. Acute alveolar emphysema: The alveoli are greatly distended and sometimes may rupture,
forming "Vesicles".
Causes:
a. Compensatory - In pneumonia or atelectasis when affected portions of lungs cannot dilate
other healthy parts dilate to a greater extent to fill the space created by the expansion of the
chest cavity.
b. Over exertion-in coughing and struggling over-ventilation occurs.
c. Feeding on lush pastures.
d. Allergic or toxic agents-feeding mouldy forage or mouldy sweet potatoes.
e. Parathion poisoning causes acute emphysema.
Gross lesions: Areas are projected or elevated and pale.
a. Many alveoli are too large and wide opening
b. Some alveoli have thick and some are thin walled.
2. Acute Interstitial emphysema: often accompanies the acute alveolar emphysema. In this
condition air collects in the interlobular space beneath the pleura and other interstitial tissue of

the lung. This is seen more often in cattle and sheep.
Causes:
a) Condition that produces dyspnea-pneumonia.
b) Bellowing- in estrus or when separated from calf; common in kosher-killed animals.
c) Perforation of lung by mechanical means- foreign body through the rumen and reticulum,
d) Forced breathing as in old hunting dogs.
e) Pulmonary strongylosis. .
Pathogenesis:
In these cases, alveolar emphysema, when it occurs, is so severe that the alveoli rupture and air
escapes into the interstitial tissue of the lung, especially in the inter-lobular septa. In severe
conditions air may escape via the thoracic inlet into the subcutis of the neck and may
accumulate there along the spine, from the pole to the base of the tail.
4. Chronic alveolar emphysema: Commonly called 'broken wind' or 'Heaves' in horses, in

which animal it is more often seen. Previously discussed.
Another type of pulmonary emphysema is in Great Britain named Bovine acute pulmonary
emphysema/Acute pulmonary edema/Fog fever/Typical interstitial pneumonia characterized
clinically by severe dyspnea, frothing at mouth and mouth breathing.
In Great Britain, this disease occurs when adult cattle are moved to lush nutritious pasture in
fall months (August-November). As this pasture grass has redrawn from earlier cut hay named
foggage or aftermath, so this is also called fog fever.
Gross lesion:
a. Lung is dark and congested
b. Emphysema found in interlobular fascia.
Microscopic lesion: Lung tissue become edematous and emphysematous.
Non-inflammatory diseases of lung

 Congestion
 Edema
 Infarction
 Thrombosis
 Embolism
 Hemorrhage
Tumors of the respiratory system:

Tumors in the nasal-cavity: Nasal polyps are soft moist masses. The following tumors are
encountered-
1. Adenocarcinoma
2. Neuro-epithelial/olfactory epithelial carcinoma
3. Virus induced adeno papilloma
5. Clear cell carcinoma
6. Chondrosarcoma
7. Mucoepidermoid carcinoma
8. Others:
a. Fibrosarcoma
b. Lymphosarcoma
c. Hemangioma
d. Osteosarcoma

Tumors of the lungs:
 In the lungs primary tumors are rare.
 Those reported are classified as having the following cell types: squamous cell,
columnar cells, mixed cells and undifferentiated cells.
 The exact sites of origin are still under dispute, whether from the bronchial epithelium
(though most of the tumors are believed to arise from this site) or the alveolar
epithelium or from the epithelium of the mucous glands.
 Both benign and malignant tumors occur.
 A few connective tissue tumors have also been described.
 Lymphocytoma is the commonest.
Tumors of the pleura: are rare. They may be-

(a) Primary-mesothelioma, a malignant tumor or
(b) Secondary-metastasis of melanoma.

Credit hour: 3
Diseases of Musculo-Skeletal System
Introduction/Background:
 Bone is the hardest organ of the body, which gives structural support to the body
as well as they are major hematopoietic organs.
 Various cell types may be seen when a section of bone is viewed under the light
microscope. These include-
1. Chondrocytes
2. Osteoblasts (contain alkaline phosphatase and produce non-collagenous bone
matrix proteins and possess receptors for parathyroid hormones)
3. Osteocytes
4. Osteoclasts (multinucleated cell) and endothelial cells,
In addition, bone has organic and inorganic components. The later includes calcium,
phosphorus, carbonate, magnesium, sodium, manganese, zinc, copper and fluoride.
Primary spongiosa: is the name given to the mineralized cartilage with its covering of
bone. Modeling of the primary spongiosa is carried out by osteoclasts.
Bone modeling: is a process by which bones maintain its gross contour, spatial
orientation and size.
Bone remodeling: is the process by which osteoclasts remove old bone without altering
the bone’s gross structure.
Abnormalities of growth and Development:

1. Chondrodysplasias
2. Osteopetrosis
3. Congenital cortical hyperostosis
4. Osteogenesis imperfecta
5. Angular limb deformities
6. Craniomandibular osteopathy
Terminologies used to describe skeletal abnormalities –

 Dystrophy - a disorder arising from faulty or defective nutrition.
 Dysplasia - abnormality of development.
 Amelia - absence of limbs.
 Phocomelia - hypoplasia of limbs, hands and feet.
 Synostosis - osseous union of bones that normally distinct.
 Syndactyly – fusion/unite of adjacent digits. '
 Lordosis- abnormal ventral curvature of the spines.
 Chondrodysplasia:
Dr. Amina Khatun, Assist. Prof., Dept. of Pathology, FASVM, SAU, Dhaka 1
 Skeletal dysplasias that develop on the basis of defective cartilage
development.
 Various forms of chondrodysplasias have been recognized in animals-
i. Hypochondrodysplasia
ii. Dyschondroplasia (cartilaginous dystrophy)
iii. Multiple cartilaginous exostoses
iv. Fibrous dysplasia
v. Affected animals have short legged disproportionate dwarfism that
is variable in degree.
Osteopetrosis
 Osteopetrosis occurs in dogs, sheep, Horses, Cattle and in various laboratory animals.
 It is the failure of osteoclasts to resorp (remodel) the primary spongiosa.
 As a result- spicules of bones with central cores of calcified cartilage fill the medullary
cavity.
 Affected bones are very dense (have no medullary cavity) but are susceptible to
fracture.
 Microscopically, growth plate remains normal, osteoclasts are sparse, and there is
persistence of primary spongiosa covered by thin layer of bone.
Metabolic bone diseases: These are diseases in which there is failure of -

1. Production of bone matrix
2. Its mineralization 'and
3. Its maintenance
The classical metabolic bone diseases are-

1. Rickets and osteomalacia
2. Osteoporosis
3. Fibrous osteodystrophy
Rickets and osteomalacia
Rickets is the disease of immature skeleton and is characterized by failure of

mineralization of bone and cartilaginous matrix. The disease in adult is called
osteomalacia.
Causes and Pathogenesis:
 Low serum calcium (Ca) levels stimulate the parathyroid glands and produce
secondary hyperparathyroidism.
 Increased parathyroid activity interferes with bone mineralization. The
causes of low serum Ca level include:
i. Vitamin D deficiency- Vit-D helps absorption of Ca from the intestine.
Its deficiency results decreased Ca absorption from the intestine that
results hypocalcemia.
ii. Dietary lack of Ca
iii. Continuous escape of Ca from the intestinal tract in combination with
fatty acid from unassimilated fat (celiac rickets).
iv. Formation of insoluble complexes between Ca and oxalates or phytate
can prevent Ca absorption. .
v. Deficiency of phosphorus (P) –
 Phosphorus deficiency may occur when soil deficient with P
or
 P deficiency may arise from steatorrhea, formation of
insoluble complexes and changes in the pH of the intestinal
content.
 Low phosphorus level interferes with Ca-P homeostasis.
vi. Unbalanced Ca-P (2:1) ratio in diets.
vii. Chronic kidney diseases-
 Interferes with the conversion of 25-hydroxycholecalciferol to
1, 25-hydroxycholecalciferol, which is an active form of
vitamin D and help intestinal Ca absorption.
viii. Drugs or diseases may interfere with liver vitamin D metabolism.
Liver convert vitamin D to 25-hydroxycholercalciferol which is a
major form of vitamin D in circulation.
ix. Certain drugs, such as bisphosphonates, can interfere with cartilage
matrix mineralization.
x. Rickets may be an inherited disease.
e.g. inherited deficiency of the enzyme 1-α hydroxylase in renal tubules.
This enzyme needs for hydroxylation of vitamin D.
Gross appearance:
 The ends of the long bones are enlarged.
 In severe cases, the bone of the limbs becomes permanently bent under the
weight of the animal's body.
 The abdomen becomes pendulous due to weakening of the muscles and tendons.
 When a long bone is sawed longitudinally,
- The growth cartilage is seen to be abnormally thick.
- The bones are abnormally soft and can often be cut with a knife.
- In birds, a crooked sternum with deviation to one side frequently occurs.
Microscopic appearance:
1. An increase in thickness of the zone of hypertrophic cartilage cells adjacent to
the primary spongiosa of the metaphysis
2. Disorderly arrangement of physeal chondrocytes. Normally chondrocytes
form regular rows running length wise of the bone.
3. Disorderly penetration of the cartilage by blood vessels
4. Defective calcification and failure of normal degeneration of the cartilage
5. Great excess of uncalcified osteoid in the metaphysis
6. Marrow tends to be fibrosed with a corresponding reduction of myeloid cells.
Significance and effects:
 Poorly calcified bone is painful and results in lameness or disinclination to
move.
 When the cause is corrected, the normal ossification promptly begins. The
strength and hardness of the bones normal.
Fibrous Osteodystrophy
 Generalized skeletal lesions that occur due to continuous and excessive action of
parathyroid hormone on bone.
 It is characterized by increased osteoclastic resorption of bone and fibrous
replacement.
Cause and pathogenesis: this disorder results from hyperparathyroidism which arise from
several different reasons. These include-
A. Primary hyperparathyroidism: primary parathyroid adenomas have been reported
in animals. In this case continuous increased parathormone activity resorped bone
with subsequent fibrous replacement.
B. Secondary hyperparathyroidism: this occurs due to hypocalcemia, regardless of
causes is the stimulus for the increased activity of the parathyroid glands. In animals,
secondary hyperparathyroidism occurs in–
a. Chronic renal diseases (renal secondary hyperparathyroidism)
b. Nutritional deficiencies (nutritional secondary hyperparathyroidism
a. Renal secondary hyperparathyroidism - is most common in dogs in which the
disorders termed renal rickets or rubber jaw.
 In chronic renal disease, loss of glomerular function results inability to
excrete phosphorus and thus accumulate in the blood and leads to
lowering serum calcium concentration.
 The damaged kidney and the inhibitory effects of increased phosphorus
decrease the production of active metabolite of vitamin D, the intestinal
absorption of calcium subsequently decreases.
 Hyperparathyroidism in response to hypocalcemia causes marked
resorption of bone, and hypocalcemia contributes to defective
mineralization of osteoblast (osteomalacia).
Grossly, in dogs, the bones of head enlarged and undergo pronounced

softening. The jaw becomes rubbery.
Microscopically,
 Increased resorption of cancellous and cortical bone together
proliferation of fibrous connective tissue results.
 Osteoclasts are found numerous on mineralized bony surfaces and
unmineralized bones tend to accumulate in medullary cavity.
 Affected bones may fracture and there may be articular collapse.
b. Nutritional secondary hyperparathyroidism: is caused by factors that tend

to
 Lowers the level of serum ionized Ca and to increase the output of
parathyroid hormone (PTH).
 The usual nutritional imbalances associated with the development
of fibrous osteodystrophy are deficiency of Ca or vitamin D or
excess of phosphorus.
 unsupplemented cereal rations fed to swine, all meat diets fed to
dogs and cats and bran fed to hoses (bran disease) are examples of
low Ca and high phosphorus diets that are likely to cause secondary
hyperparathyroidism.
 Increased level of PTH cause resorption of cancellous and cortical
bones together with fibrous replacement.
Classical gross lesions of fibrous osteodystrophy are most obvious in facial

bones and mandibles.
 The sharp features of head, especially in the region of zygomatic arch
and upper and lower jaws become rounded and indefinite, giving the
appearance of more swelling than really exists.
 Therefore this disorder is also called big head disease.
 In horse, this disease is called bran disease when result from
unsupplemented bran diets.
Microscopic lesions are similar to renal secondary fibrous osteodystrophy.

 Very often this disease occurs simultaneously with osteomalacia and
osteoporosis.
 Besides the nutritional and renal fibrous osteodystrophy.
 Toxic and osteodystrophy secondary to hepatic malfunctions or
chronic diseases have been reported in animals.
Osteoporosis
 Osteoporosis is a group of skeletal disorders that are characterized by

reduction in bone mass (osteopenia), with the remaining bone appearing
normal.
 The bone is therefore thin, brittle and subjected to fractures.
Causes and Pathogenesis

 Osteoporosis may be local or may involve the entire skeleton.
 It involves through an imbalance between bone formation and bone
resorption, with a net loss in bone mass being the end results.
Some of the causes include-
1. Calcium deficiency may lead to hypocalcemia, which is corrected by
increased parathormone output and increased bone resorption
2. Starvation leads to arrest bone growth due to dietary lack of Calcium.
3. Disuse osteoporosis is caused by lack of physical exercise. Reduced
physical activity leads to an increase in bone resorption and a decrease in
bone formation.
4. Postmenopausal osteoporosis is a common and important disease in
women. Declining levels of estrogens, physical inactivity and inadequate
Calcium intake are factors that may be important in this disease.
5. Prolonged use of corticosteroids results osteoporosis
Gross and microscopic lesions

 The cortical bone is reduced in thickness and the porosity is increased.
 The medullary cavity becomes enlarged due to endosteal resorption and
removal of metaphyseal cancellous bone.
 The bony spicules become thin, less numerous and more widely separated.
 The end result is light bone that lacks the normal density and is easily
fractured.
 Osteoporosis may be followed by osteodystrophy fibrosa.
Tumors of the bone and cartilage:

1. Osteoma/ osteosarcoma
2. Chondroma/ chondrosarcoma
3. Osteochondroma
4. Enchondroma
5. Fibroma/ fibrosarcoma
6. Hemangiosarcoma
7. Giant cell tumors of the bone
8. Synovial sarcoma
9. Fibrous histiocytoma.
Joint diseases:
Arthritis
 The term arthritis mostly implies inflammation of intra-articular structures.

 It is usually characterized by inflammatory cells in the synovial membrane
and often with changes in the volume and character of the joint fluid.
Arthritis
Degenerative Inflammatory
Infectious Non-infectious
Bacteria Immune based

Gonococcal arthritis SLE
Lyme disease Canine rheumatoid
TB arthritis
Scarlet fever (Rheumatic fever) Osteoarthritis (?)
Syphilis Polyarthritis
Actinomycosis
Steptococcus
Virus
Mumps
Dengue
Non-immune based crystal induced
Poliomyelitis Gout
Rubella Pseudoqout
Viral hepatitis Hydroxy apatite
Fungus
Aspergillus
Hisplasmosis
Coccidioidomycosis
Mycoplasma
Chlamydia
Degenerative Joint Disease

 It is a destructive disease of articular cartilage that is characterized by focal
erosion and fibrillation of articular cartilage.
 Affected animals have variable degrees of joint enlargement and deformities,
pain and articular malfunction.
 The etiopathogenesis of the disease is incompletely understood but it is
thought that initial change in articular cartilage is increased water content
and, focal loss of proteoglycan aggregates, which lead to softening.
 This may lead progressive loss of articular cartilage and eventually
fibrillation.
Osteochondrosis: is a degenerative growing cartilage that is characterized by focal
lesion of multi focal failure of endochondral ossification.
Systemic Lupus erythematosus (SLE)
 This is a complex autoimmune disease of humans and dogs. Antibodies are

formed. against variety of tissue components, including DNA, RNA and
other nucleoproteins.
 Affected dogs often manifest some form of shifting leg lameness caused by
polyarthritis.
Rheumatoid arthritis
 It is a chronic erosive polyarthritis.

 The cause is unknown, although it is clear that the cause is immune mediated.
 Antibodies of the IgG or IgM class are produced in response to an unknown
stimulus.
 Immune complexes are engulfed by neutrophils that release lysosomal
enzymes, which sustain the inflammatory reaction and injure intra-articular
structures.
 Additionally, IL-1 from synovial type A cells and from macrophages
stimulate chondrocytes to release substances to degrade cartilaginous matrix
and also stimulate synovial fibroblast to produce PGE2.
 This substance (PGE2) reduces chondrocyte proteoglycan synthesis and
contributes to the production of pain, fever and intra-articular inflammation.
 Antibodies against normal and altered collagen from articular cartilage may
be important mediators of the ongoing joint inflammation and injury that
occur in the disease:
Microscopically,
 There is hyperplasia of synovial lining cells as well as infiltration of large
number of plasma cells and lymphocytes into the subsurface-synovium.
 Foci of necrosis, exudation, fibrin and infiltration of neutrophils indicate
that the process is chronic but active.
 Large number neutrophils are present in the joint fluid.
Pathogenesis of rheumatoid arthritis:
Diseases of skeletal muscle

Function of muscle:
 Skeletal muscles primarily function to allow support and movement of the body.
It accounts for 40-45% of body weight.
 Skeletal muscle helps in respiration, parturition, defecation etc. Any disease in
the muscle disturbs in these functions.
 Skeletal muscles are striated muscle and nuclei are located at the periphery.
Skeletal muscle originates from mesodermal somite in the embryo during the first
trimester of gestation. Myoblast is the primitive mononuclear precursor cell of skeletal
muscle.
Developmental Disorders:
The most common developmental disorder is muscular dystrophy. The term muscular
dystrophy represents a group of hereditary muscle disorders with a yet unknown
biochemical or metabolic aberration of the muscle fibers. However, it may be also defined as
hereditary degenerative diseases of skeletal muscle.
The other disorders include

1. Muscular dysgenesis
2. Muscular dystonia - atrophy of muscle secondary to degeneration of nerve fibers, dorsal
root ganglia and gray matter of spinal cord.
3. Myotonia- Occurs in dog and cat. Muscles show continuous contraction.
4. Steatosis- occur in sheep, goat and swine. Replacement of muscle fibers by fat cells. It
is normally recognized at slaughter. Muscles of loin and back mostly affected.
5. Xanthosis - Lipofuscin accumulation in muscle fibers.
6. Myasthenia gravis - Muscular weakness, e.g. Megaesophagus.
The term steatitis differ from steatosis. Steatitis is inflammation of adipose tissue/fat.
Disturbances in growth
1. Atrophy
2. Degeneration atrophy
3. Disuse atrophy
4. Atrophy of cachexia and emaciation
5. Senile atrophy
6. Compression atrophy
Hypertrophy: Hypertrophy in muscle is mostly physiological and in most cases induced by

exercise or over functioning.
Degenerative condition of muscle:

 The most common type is so called hyaline or waxy degeneration. Microscopically,
affected fibers appear swollen and hypereosinophilic with loss of cross- striations.
 Another type is granular degeneration.
 Microscopically, it differs from hyaline degeneration in that small basophilic granule
in cytoplasm.
 The cause of the both of degeneration is similar, included are deficiencies, such as vit. -
E/ Se, various myotoxic drugs and plants and metabolic disorders such as azoturia and
capture myopathy.
Other less common types of degeneration are

1. Vacuolar or hydropic degeneration
2. Fatty degeneration
3. Lipofuscinosis
Diseases of skeletal muscles:

1. Infectious Diseases
A. Bacterial diseases or bacterial myositis
a. Malignant edema: Clostridium septicum. Clostridium sordelliii and Clostridium
perfringens
b. Black leg: Clostridium chauvoei
c. Abscess: Streptococcus equi, Corynebacterium pyogenes, Corynebacterium
pseudotuberculosis.
d. Woody tongue (pyogranulomatous glossitis): Actinobacillus lignieresii
B. Viral Diseases or viral myositis

a. Bluetongue virus (ovine)
b. Ibaraki virus (cattle)
c. Enzootic hemorrhagic disease (deer)
d. Marek’s disease (poultry)
e. Foot and mouth disease (Ruminants)
C. Parasitic diseases or myositis
a. Protozoal disease
 Toxoplasmosis
 Neosporosis
 Sarcocystosis
 Trypanosomiasis
 Hepatozoon canis infection
b. Helminths infestations
 Trichinosis
 Cysticercosis
 Taenia solium
 Taenia saginata,
 Cysticercus bovis
 C. cellulosae
 Larvae of Neoascaris vitulorum
2. Immune mediated myositis

3. Different types of myopathies
A. Steroid myopathy
B. Toxic myopathies
 Toxic plants
 Coffee senna
 Coyotillo
C. Nutritional myopathy (White muscle disease)
D. Equine rhabdomyolysis / Azoturia
E. Capture myopathy in wild animals
F. Herztod
Malignant Edema
 Malignant edema is a wound infection described in several species, principally in cattle

and sheep.
 This infection is associated with several Clostridial species (C. septicum, C. sordellii and
C. perfrinngens).
 It is more often a cellulitis than myositis, but it may have extensive necrosis and lysis of
muscle fibers. Necrotic fibers are intensely eosinophilic and undergo lysis. Little or no
cellular reaction is present.
Nutritional Myopathy/White muscle disease
(White muscle disease/Nutritional muscular dystrophy)
 It affects mainly sheep, cattle and pigs.

 The disease is due to deficiency of vitamin E (Vit. E) and selenium (Se).
Pathogenesis
 Vitamin E and Se are both involved with the protection of cellular
membranes from free radicles that cause peroxidation of membrane lipids.
 Se is an essential components of the enzyme glutathione peroxidase, an
intracellular enzymes involved in neutralizing free radicals.
 Vit. E, an anti-oxidant can be either extracellular or intracellular and also
reacts with free radicals to neutralize.
 However, if these mechanisms are defective or inadequate, then the cell
membranes become physiologically defective, allowing influx of Calcium
ion into the cytoplasm; this results in the accumulation of Ca ion in the
mitochondria which damages the mitochondria.
 The damaged mitochondria are unable to supply energy to the cell for
maintaining homeostasis, which results in cell death.
Gross lesions:
 Back, neck and respiratory muscles mostly affected.
 Early lesions appear as pale area and steaks.
 Later become opaque and white.
 Segmental myonecrosis possibly with calcification, regeneration by
budding and diffuse fibrosis.
Diagnosis
 The lesions of segmental myonecrosis are characteristics of this disease.
 Confirmation requires analysis of tissues for Se and Vit. E.
Black Leg/ Black Quarter (BQ)
Etiology: Clostridium chauvoei
Pathogenesis:
 Clostridium chauvoei spores are present in the soil and seldom in the
intestine of herbivores.
 Once they are in the intestine, they apparently able to cross the intestinal
mucosa and be disseminated by the blood throughout the body, to a wide
variety of tissues including muscle.
 If local environment becomes suitable, if muscle is devitalized and becomes
anaerobic spores can germinate, bacilli proliferate and produces powerful
toxins that can damage capillaries, produce a serohemorrhagic exudates,
and cause necrosis of muscle.
 The bacteria produce gas in the muscle.
 The gas together with iron of liberated hemoglobin gives the black
discoloration of the muscle.
 The edema fluid and gas increase the pressure within the muscle fibers and
fibers become separated.
Gross lesions:
1. The gross appearance of the muscle varies with the age of the lesions. In early
stages, the muscle is dark red and markedly distended by serous or sero-
hemorrhagic exudates that separate the fibers.
2. Later, the center of the lesions become dries, reddish black and porous because
of gas bubbles.
1. The muscle fibers are separated by serous or serohemorrhaqic exudates.
2. The serous fluids is usually low in protein content and stains faintly or notably
with eosin.
3. Muscle undergoes coagulation necrosis with minimal inflammatory cell
infiltration Gm positive bacilli can be seen in the lesions.
Diagnosis:
Characteristic lesions and isolation of bacteria.
Azoturia
(Equine Rhabdomyolysis/Monday morning sickness/disease/Palalytic myoglobinuria)
Background:
 Equine rhabdomyolysis is found to occur suddenly in horse, going to work after
complete rest for a few days, but maintained on full work rations.
 The disease usually occurs in Monday morning, i.e. after the weekend.
Causes and pathogenesis:
 This disease occurs in working horses following a few days of rest while on full
ration.
 During the resting period with full rations, large amounts of glycogen
accumulate in the muscle.
 After the resting period, when the horse gets start the exercise, the glycogen
breaks down into pyruvic acid.
 In presence of oxygen, Pyruvic acid enters into TCA cycle and produce energy.
 But when the large numbers of pyruvic acid are produced, the some of the
pyruvic acid converted to lactic acid due to shortage of oxygen.
 These lactic acids accumulate in the muscles and cause hardening and necrosis of
the muscle.
 The lumber, gluteal and femoral muscles mostly affected and become hard,
swollen and myoglobinuria soon follows due to lysis of muscle fiber.
Clinical signs:
 The animal suddenly stop, sweating, shiver and show great sufferings from pain in
the lumber region.
 Gluteal, lumber and femoral muscles become swollen.
 Coffee color/dark brown urine, because the urine contain large quantity of
myoglobin.
 The animal lies down and may die.
 The affected muscles become atrophied.
At necropsy, the muscles are dark, moist and swollen. Sometimes there are pale
streaks. The kidney may be swollen and congested and the urinary bladder may
contain blood in urine.
Microscopically, degeneration and necrosis of myofibres which is characterized by
swollen, eosinophilic, hyaline fragmented myofibres with loss of striations.
Phagocytosis and regeneration of muscle possible in surviving animals.
Credit hour: 3
Diseases of Genital System
Female genital system

Female genital system consists of following organs in consecutive order-
1. Two ovaries
2. Fallopian tube or uterine tube or oviduct (in case of birds)
3. Uterus
i. Horn of uterus
ii. Body of uterus
4. Cervix
5. Vagina
6. Vulva
7. Accessory sexual Organs &
8. Placenta
Disease of Ovary
Developmental Anomalies:
1. Agenesis
2. Hypoplasia
3. Gonadal dysgenesis- Freemartinism
4. Supernumerary ovaries
Oophoritis: The inflammation of ovary is called Oophoritis. It is generally results from the two routes
of infections. Such as:
1. Direct extension
2. Hematogenous infection
It is more susceptible in cattle.
Causes of Oophoritis:
1. Bacterial infections-
e.g. (a) Mycobacterium tuberculosis var bovis.
(b) Brucella spp.
(c) Actinomyces bovis.
2. Viral infections-
e.g. (a) Herpes virus bovis.
(b) Herpes virus suis.
(c) Akabane virus (affects in Zebra)
3. Mycoplasmosis
e.g. (a) Mycoplasma bovis
Microscopic appearances:
1. Infiltration of inflammatory cells.
2. Proliferation of fibrous connective tissue in case of chronic infiltration of inflammatory cells.
Gross appearances:
1. Varying amount of fibrin tags (bundle), granulation tissues and fibrous adhesion on the
serosal surfaces of the uterus (especially horn of uterus) that may interferes ovulation and
formation of tubo-ovarian or bursal cysts.
Terminologies:
 Salpingitis: Inflammation of fallopian tubes.
 Pyosalpinx: When pus is accumulated in the fallopian tubes.
 Hydrosalpinx: When water is accumulated in the uterine or fallopian tubes.
 Ectopic pregnancy: When implantation occurs in the fallopian tube or uterine tube called
ectopic pregnancy. Normally implantation occurs in uterus (horn of the uterus). So, it is an
abnormal condition.
 Uterus unicornis: Uni = one, cornis = horn. When one horn of the uterus is absent is called
uterus unicornis.
 Metritis: Inflammation of the uterus as a whole is called metritis.
 Endometritis: Inflammation of endometrium of the uterus.
 Perimetritis: Inflammation of the serosa layers of the uterine cavity or uterus.
 Pyometra: Excessive accumulation of pus in uterine cavity.
 Hydrometra: Excessive accumulation of water in uterine cavity.
 Endometriosis: Endometriosis is the presence of endometrium outside of uterine cavity (i.e.
in ectopic sites).
 Cervicitis: Inflammation of cervix.
 Vulvitis: Inflammation of vulva.
 Vaginitis: Inflammation of vagina.
 Hermaphrodite: Animals having abnormal sexual organ or organs of both sexes (have
complete or partial reproductive organs and produces gametes normally associated with both
male and female sexes). The genital tracts of both sexes develops primarily from the same
embryonic primordium.
 Free-Martin: When twin calves of different sexes are barned, the bull calf is generally
sexually normal but the heifer calf is generally sterile and external genital organs are
abnormal in structure. This heifer calf is called or known as free-martin or ovarian dysgenesis.
How animals show heat (Physiology):
Hypothalamus
FSH releasing factor (H)

GnRH
LH releasing factor (H)
Anterior pituitary gland
Secretes
FSH LH
Acts on
Ovary
Graafian follicle developed Ovulation

Stimulate
Secretes
Estrogen Corpus luteum

Secretes
Animals show heat Progesterone (P4), which

maintains pregnancy
Different types of cysts of the ovary (Cysts in and around ovary): The ovaries and surrounding
supporting ligaments are the common site for the development of cyst of various kinds. These are-
1. Follicular cyst
2. Luteinized cyst/ luteinized follicles
3. Cystic corpora lutea
4. Epithelial inclusion cyst
5. Cysts of sub-surface epithelial structures
6. Cystic rete ovarii
7. Tubo-ovarian-cysts
8. Cysts of mesonephric ducts and tubules
9. Cysts of paramesonephric ducts
.
Follicular cysts:
It is common in cattle and swine, less often in dogs and cats, rarely in sheep and goat, and
almost never in mares.
It arises from the secondary follicles (antral) that fail to ovulate, regress/involute or luteinize.
Failure of LH release during estrus (prior to ovulation) is thought to be the cause.
Increases estrogen level in non-cyclic pattern and there is signs of nymphomania.
There is cystic endometrial hyperplasia, hydrometra or mucometra.
Grossly: Follicular cysts protrude from the surface found in one or both ovary (affected).
Microscopically:
 Thickening of the theca-interna.
 Follicular cysts are lined by single or multiple layers of granulosa cells that may appear normal,
degenerated or partially luteinized.
 Follicular cysts do not contain any ovum.
Luteinized Follicles (Cysts):

Cause: An insufficient LH surge/ release to cause ovulation but sufficient amount of
circulatory LH to induce luteinization of the anovulatory follicle or possibly immaturity of
follicle at LH surge leading to failure of ovulation.
Grossly, luteinized follicles, unlike cystic corpora lutea, lack the ovulatory papilla that occurs
ovulation.
Microscopically: these cysts lined by one or more layers of luteinized cells containing lipid
droplets in cytoplasm.
These luteinized cysts contain ovum.
Clinical Signs: sign of anestrus.
Differences between Follicular cyst and luteal cyst:

SL Features Follicular Cyst Luteal Cyst
No.
1. Origin From secondary From Graafian follicle.
follicle.
2. Cause Lack of Luteinizing Insufficient amount of
Hormone (LH) LH surge but sufficient
amount of circulatory
LH.
3. Histology Lined by granulosa Lined by lutein cells.
cells.
4. Clinical Nymphomania. Anestrous.
manifestation
5. Blood Increased estrogen Increased progesterone
chemistry level in blood. level in blood.
6. Uterine Hydrometra, Cystic endometrial
changes mucometra etc. hyperplasia.
Ovarian Tumors:
 Granulosa cell tumor
 Papilloma cyst adenoma
 Papilloma cyst adenocarcinoma
 Theca cell tumor
 Interstitial cell tumor
 Teratoma (not tumor)
Diseases of Fallopian Tube
Developmental Anomalies
1. Agenesis
2. Segmental aplasia
3. Diverticulum
4. Duplication
Sulpingitis: Inflammation of the fallopian tube.

Causes: normally infectious and the most likely causes are-
 Brucella
 Chlamydia spp
 Tritrichomonas spp
 Campylobacter spp
 Mycobacterium tuberculosis
 Actinomyces bovis
Gross and Microscopic changes:
1. Hyperemia and swelling of the fallopian tube mucosa
2. Presence of small amount of exudates in the lumen
3. In severe cases obstruction
4. Microscopically infiltration of leukocytes which may be acute or chronic
Effect: Interferes varying degree with fertility.
Diseases of the Uterus
Developmental Anomalies:
 Aplasia-Congenital absence of uterus.
 Uterus unicornis-Only one horn is developed.
 Segmental aplasia
 Uterus bicorpor bicollis-Double body, double cervix but horn absent.
 Duplication of the uterine body
 Agenesis of the uterine glands.
Diseases of the Non-gravid Uterus:
1. Acquired changes in position

 Torsion
 Prolapse
 Rupture
2. Disturbances in Endometrial growth:
a) Uterine atrophy-After menopause in human and after anestrus in animals.

Causes: Age (Physiological) and hypopituitarism (disuse atrophy)
b) Uterine hyperplasia-Increase number of uterine lands.

Cause: Pregnancy-Physiologically and Pyometra-Disease condition.
c) Adenomyosis: Presence of nests of endometrial tissue with glands within the myometrium.
Cause: can be prolonged estrogen stimulation.
d) Endometriosis:
 Presence of endometrial tissue outside the uterine cavity.
 It occurs in the animals that menstruate (human and nonhuman primates)
 Pathogenesis is not clear but may involve reflux of menstrual fluid from the uterine tube with
subsequent implantation of viable fragments of endometrial
tissue on the visceral organs.
 Grossly ectopic endometrium appears as soft, red brown or white polypoid masses or tissue
adherent to the serosa of pelvic organs.
 Normal appearing uterine tissue/glands on the surfaces of the pelvic organs.
e) Endometrial Polyp: are tissue growths inside the uterus that can cause abnormal uterine bleeding
or infertility
Effects: are pelvic inflammatory diseases
3. Hydrometra and Mucometra: Accumulation of thin or viscid fluids in the uterus is called
hydrometra or mucometra.
Cause may be cystic ovaries or endometrial hyperplasia.
4. Endometritis/Metritis: Inflammation of the endometrium/myometrium of uterus.

i. Acute endometritis:
Grossly, Mucosa is swollen and has rough surfaces often with necrotic debris.
Histologically, in acute endometritis, there may be neutrophilic infiltration in the stroma and
sloughing of epithelial cells.
Chronic endometritis: Acute endometritis often becomes chronic. Necrotic endometrium
replaced with fibrous tissue.
Outcomes:
 Acute endometritis can cause synthesis of PGF2α which cause premature regression of CL
and thereby shortening of estrus cycle.
 In chronic endometritis fibrous tissue replaces the endometrial gland and since decrease
production of PGF2α. This results persistent CL which causes anestrus.
Diseases of gravid/pregnant uterus:
 Early embryonic death- Death within 40 days of gestation.
 Fetal Death- Death after 40 days of gestation.
 Abortion: is the expulsion of the fetus or embryo from the uterus prior to an age/period
when the fetus or embryo could survive with a maximum supportive care in an extra-uterine
environment (based on WHO, it’s the termination of pregnancy prior to 20th week of
gestation).
 Still Birth: is the expulsion (delivery) of dead fetus from the uterus at an age (usually after
20th week of pregnancy) when the fetus or embryo could survive outside of the uterus with a
minimal supportive care.
Causes of abortion (still birth):

A. Microorganisms (infectious organisms) cause abortion or still birth-
1. Bacterial infections
 Brucellosis: (causes at 7~8th months of pregnancy), the organisms -
e.g. Brucella abortus - in cattle
Brucella ovis – in sheep
Brucella melitensis – in sheep/goat
Brucella suis – in swine
Brucella canis – in dog
 Campylobacteriosis: (causes at 4~6th months of pregnancy). The organisms-
e.g. Campylobacter fetus var intestinalis – in sheep/ goat
Campylobacter fetus var venerealis – in cattle
 Listeriosis: (causes at last trimester of pregnancy), the organisms
e.g. Listeria moncytogenes in cattle, sheep and goat.
 Leptospirosis: Leptospira interrogans in dog, and also in cattle and sheep.
 Corynebacterium pyogenes
2. Viral infections
 Herpes virus, e.g. EHV 4
 Arterivirus, e.g. EAV, PRRSV
 BVDV etc.
3. Fungal infections
4. Protozoan infections
 Tritrichomonas fetus in cattle
 Toxoplasma gondii in sheep, goat, rarely in swine
 Neospora caninum in dog, cat and sheep
5. Chlamydial infections
 Chlamydia psittaci and Chlamydia trachomatis in sheep and goat.
6. Rickettsial infections
 Coxiella burnetii (in human Q-Fever) in sheep and goat.
7. Mycotic infections
 Aspergillus spp.
 Absidia sp
 Mucor sp
 Rhizopus sp.
B. Non-infectious causes abortion or still birth-

 Traumatic injury
 Hormonal imbalance
 Effect of ergots
 Severe deficiency of some essential substances required for life for fetus or mother
etc.
 Mummification of fetus: It occurs in the absence of any intrauterine infection but because
of prolonged retention of a dead fetus in which all of the fluids are reabsorbed and the fetal
membrane collapsed around a desiccated, brown-black, leathery mass of dried fetal bone
and skin. It’s most common in multiparous animals but also occurs in monotocous animals
when a fetus is retained for a longer period of time.
 Pyometra: Acute or chronic suppurative infection of the uterus with accumulation of pus in
the uterine lumen.
Cause: Early embryonic death following nonspecific infection is probably the main important
cause. Tritrichomonus fetus in Bangladesh is the most important cause of pyometra. Besides
this, there are many other organisms like Actinomyces pyogenes, E. coli, Pseudomonas
aeruginosa, Streptococcus spp. Staphylococcus spp. may be present.
Gross Lesions:
 Large amount of yellowish or grayish color (depends on the bacteria involved) pus in
the uterine cavity.
 Wall of uterus may be leathery and thickened or thinned (depends on the duration of
pyometra. Thick = in acute case/early stage; thin = due to fibrous tissue proliferation).
Microscopic Lesions:
 Cystic endometrial hyperplasia.
 Stroma and uterine glands infiltrated with large number of neutrophils.
 Proliferation of F.C.T in the stroma.
 Post-partum involution of uterus: the physiological changes that occurred in the uterus
during post-partum period. When uterus is returning to the normal, non-gravid functional and
anatomical state, referred as post-partum involution of uterus.
 Retained placenta: occurs as a complication of the post-partum period. In cow, the fetal
membrane is normally expelled out from the uterus within 12 hrs after delivery. Beyond that
period, they are known as retained.
Causes: usually infectious diseases of placenta, abnormal gestation period, hormonal
imbalance and/or other mechanical factors.
Tumors of uterus:
1. Leiomyoma
2. Carcinoma of the endometrium and cervix
3. Lymphosarcoma
4. Fibropapilloma
5. Metastatic tumors
Mastitis: is the inflammation of the udder or mammary gland (in case of human called mammitis).
Causes of bovine mastitis:
 Streptococcus agalactiae
 Streptococcus dysgalactiae
 Streptococcus uberis
Male genital System
 Orchitis: Inflammation of the testes is called orchitis. It is characterized by hemorrhages,
parenchymal necrosis which is followed by influx of neutrophils diffusely in the interstitium
and in the lumen of the seminiferous tubules. Sometimes it becomes granulomatous
depending upon the cause.
Causes of Orchitis:
1. Brucella spp.
2. Chlamydia spp.
 Periorchitis: Inflammation of the outer serous cavity of the testicles.


 Epididymitis: Inflammation of the epididymis.

 Prostatitis: Inflammation of the prostate gland.

 Balanitis: Inflammation of the glans penis or clitoris.

 Posthitis: Inflammation of the prepuce.

 Balanoposthitis: Inflammation of both of the glans penis and prepuce.

 Phimosis: is a condition in which inflammatory swelling prevent the extension of the penis
from the sheath.

 Periohimosis: is the similar condition of phimosis, in which the penis being already
protruded and not possible or impossible to withdraw.

 Cryptorchidism: is the process of the retention of single or both testes that fail to descend
from the abdomen to the scrotum.

 Cryptorchid: Incomplete descent of testes is known as cryptorchid.

 Monorchid: Incomplete descent of one testicle

 Di-orchid: Incomplete descend of two testes.
Tumors of Testes:
1. Seminoma
2. Interstitial cell (Leydig) cell tumor
3. Sertoli cell tumor
4. Teratoma.
Diseases/Pathological Conditions of the Nervous system
Parts of nervous system
1. Central nervous system (CNS)
a. Brain
b. Spinal Cord
2. Peripheral nervous system (PNS)
Both brain and spinal cord contain gray and white matter. White matter contain
nerve fibres, ganglion and supporting cells.
Cells of Central nervous system (CNS)

1. Neurons
2. Glial cells/Supporting cells
a. Astrocytes
b. Oligodendrocytes
c. Ependymal cells.
d. Microglial cells.
Neuron: It has large nucleus with distinct nucleolus. Cytoplasm contain
prominent endoplasmic reticulum which is called “Nissle substances”. Each cell
has multiple dendrites and single axon.
Astrocytes: Normally elliptical and size is smaller than monocytes. Cytoplasm
is undetectable. They are two types-
1. Fibrousastrocytes: With long and thin process.
2. Protolplasmicastrocytes: shorter and wider process.
Functions:
1. It gives structural support to the brain & spinal cord.
2. Normally it found around the blood vessels.
Oligodendrocytes: Oligo means few, dendro means branches. They are
lymphocytes like cells with small processes. A hollow is found around the
oligodendrocytes.
Functions:
1. The cells supply nutrients particularly glucose to the neurons.
2. They produce myelin which helps in condensation of the nerve impulse.
1
CNS/dr.sajeda/dop/fahvm/sau
Ependymal cells:
These are epithelial cells to lines the ventricles and central canal. These cells
further modified to from choroid plexus epithelium. They have secretory and
absorptive function. Normally have no response to injury.
Microglial cells:
They are very small cells. They appear as small rod, ovoid, more often coma
shaped. Their function is primarily protective and acts as phagocytes.
Reaction of Nervous Tissues to Injury/Some Pathological Conditions

Chromatolysis : Following an injury, Nisslsulastanceslossitosharpeness and
gradually disappear. This proces is called chromatolysis .
Neuronophagia : Usually anecrosed neuronis surrounde by microglial cells &
macrophages and finally phagocytized.This process is
called neuronophagia. Individual cell is called
neuronophage.
Glial nodule : Nodular aggregation of glial cells is called glial nodule.
Astrocytosis : Proliferation of astrocytes is called astrocytosis .
Gemistrocytes : Following injury-astrocyte increase in size. Cytoplasm
becomes pink and nucleus become often eccentric.These
cells are called gemistrocytes.
Satellitosis : Following injury of unfavourable condition such as hypoxia

, oligodendrocytes proliferale and accumule near the
neurons. This process is called satellitosis. Individual cells
are called satellite cells.
Gitter cells : When any damage occurs in the peripheral nerve & myelin,
the microglial cells engulf axonal fregments & myelin.
They convert myelin to neutral fat. As result cytoplasm
becomes foamy. This lipid containing microglial cells is
called gitter cells. Presence of gitter cells indicates myelin
damage. Gitter cells also called hortega cells.
Microgliosis and : In response to injury microglial cells proliferate which is

Microglial star called microgliosis . When they appear as small clusters,
then they called microgliostar .
2
Some Terminology
Encephalopathy : Any degenerative condition in brain &spinal cord is

called encephalopathy.
 If it is neuron it is called neuronopathy.
 If it is axon it is called axonopathy.
 If it is myelin it is called myelinopathy
Malacia : General term , any nrcrosis in brain & spinal cord it
is called malacia .
 If it is brain it is called encephalomalacia.
 If it is spinal cord it is called myelomalacia.
Poliomalacia : Any necrotic condition in gray matter it called
poliomalacia .
Leukomalacia : Any necrotic condition in white matter is called
leukomalacia .
Encephalitis : inflammation of brain .
Myelitis : Inflammation of spinal cord.
Meningitis : Inflammation of meninges.
Encephalomyelitis : Inflammation of brain &spinal cord.
Meningoencephalitis : Inflammation of brain & maninges.
Meningoencephalomyelitis : Inflammation of meninges, brain & spinal cord .
Wallerian degeneration : If axonal degeneration occur due to secondary to
brain lesion or neuronal degeneration or due to
separation of axon from neuron due to direct injury.
Common Patho-physiologic Complications
1. Concussion : Temporary loss of conciousness with recovery

following a head injury.
2. Contusion : Grossly detectable lesion on brain from a blunt cerebral
injury.
3. Haemorrhage
4. Brain swelling
5. Edema
6. Ischemia
3
7. Atherosclerosis
Disease or Disease condition of nervous system
A. Viral Diseases: G. Disease due to helminth &
1. Rabies. arthopods:
2. Pseudorabies . 1. Larvae of oestras ovis & Hypoderma
3. Herpes simplex . bovis
4. Herpes B . 2. Coenurus cerebralis
5. Poliomyelitis . 3. Cysticercus cellulosae
6. Avian encephalomyelitis. 4. Echinococcus granulosis
7. Newcasledisease . 5. Setaria digitalis
8. malignent catarrhal fever. 6. Micronema deletria
9. japanise B encephalitis. 7. Larvae of Strongylus spp.
10.Canine distemper.
H. Poisons:
11.Visna/ Maedi. a. Carbon disulfide
12.Equine encephalomyelitis. b. Lead
13.Marek’s disease c. Hg /Mercury
14.Bovine Spongioferm d. Chlorinated hydrocarbons
Encephalomyelitis (BSE) e. Organic phosphates
or Prion disease . f. Striknine
B. Bacterial diseases : g. Sodium chloride
1. Listeriosis
I. Toxins:
2. Tetanus 1. Bacterial toxins :
3. Botulism a. Clostridium enterotoxaemia
4. Tuberculosis
5. Pseudotuberculosis 2. Plant toxins :
a. Astropine
C. Fungal infection: b. Braken fern
1. Blastomycosis (B.dermatitides) c. Lathyrus
2. Cryptococcosis (C.neoformens) d. Hemlocks
3. Coccidioidomycosis 3. Mycotoxin :
4. Histoplasmosis a. Muldy corn poisoning.
D. Chlamydial Infection: J. Deficiency disease:
Sporadic bovine encephalomyelitis 1. Cu deficiency:
(C.psittaci) Cause enzootic atoxia or sway back in
E. Protozoaldiseases: sheep.
1. Toxoplasmosis 2. Thiaminedeficiency:
2. Neosporosis Polioencephalomalacia in sheep &
3. Equinprotozoal encephalitis cattle.
3. Vitamin E deficiency:
F. Meningitis:
1. Nesseria meningitis Encephalomalacia & axonopathy in
2. Streptococcus suis chicks & pigs.
3. Haemophilus somnus
4
Neoplasm of nervous system:
Neuron:
1. Neuroblastoma
2. Gangliocytoma
3. Medaloblastoma
Glial cells :
1. Astrocytoma
2. Oligodendroglioma
3. Mixed glioma
4. Ependyoma
5. Epithelioma .
Meninges :
1. Meningioma
2. Meningiosarcoma
Peripheral nervoussystem :
1. Schwanoma
2. Neurofibroma
3. Neurofibrosarcoma.
Prion Diseases
Prion protein is an infectious agent but it has no nucleus which cause disease in
different animal . This disease is called prion diseases.
This includes a group of nervous system disease which produces disease in
several species. Diseases are as follows -
Species Disease
Sheep &goat : Scrapie
Human : Kuru, Creutzfeldt-jekob disease (C . J . D )
Cattle : BSE , Mad Cow Disease
Mink : Transmissible mink encephalopathy
Dear : Transmissible spongiform encephalopathy.
Cat : Spongiform encephalopathy.
Transmission: Vertical transmission (Meat, milk etc) and Intrauterine.
5
Bovine Spongiform Encephalopathy (BSE)
In cattle, the disease is first recognized in 1986 in England. Probably bone &
meat meal from scrapie affected sheep induce the disease in cattle.
Transmission: Direct spread between cattle to cattle is not been documented.
Clinical signs:
1. Affected animals develop slowly progressive behavioral & locomotors
change.
2. The animals gradually become excitable.
3. Exhibit apprehension & aggression when approached, handled or
disturbed.
4. A hind leg ataxia progress to the point of animals falling.
5. These sings along with weakness & loss of good bodily condition
progress over 1- 4 months leading to death.
Histopathology:
1. Presence of vacuoles in cells of gray matter that give the tissue a spongy
appearance.
2. The vacuoles are actually distending plasma membranes of affected cells.
The vacuoles may coalesce to form large vacuoles.
3. Hypertrophy and proliferation of astrocytes.
Diagnosis:
 Based on clinical history& signs.
 Histopathology
 Detection of prion protein by immunohistochemistry.
Lysosomal Storage Disease

Accumulation of catabolic products in the cytoplasm of cells due to defect or
deficiency of lysosomal enzymes is called lysosomal storage disease.
Causs:
1. Inherited-unknown cause.
2. Acquired-some plant toxins .eg. Swainisonine loco weeds.
3. In Bangladesh-Probably by Dholkolmi.
Type: On the basis of storage material-
1. Gangliosidosis: Stored materials is gangliosides.
2. Mannosidosis: Stored materials is mannose.
3. Ceroid-lipofuscinosis: Stored materials is ceroid & lipofuscins .
6
Clinical symptoms: Confused with gid disease & listeriosis.
Histopathology:
1. Vacuole can be seen in the cytoplasm of neurons in H & E stain.
2. Storage materials can be seen in the cytoplasm of neuron in special stain.
DR. SAJEDA SULTANA, DVM, MS

Lecturer, Dept. of Pathology
FASVM, SAU
E-mail: [email protected]
7
1
DISEASES OF URINARY SYSTEM

Kidneys: Anatomy and Physiology
Nephron:
Essential anatomic and functional unit of the kidney
Human kidneys contain 1-2 million neprhons
Rat 10-30 million nephrons
Nephron is consisted of
1. Glomerulus
2. Renal tubule
3. Proximal convoluted tubule
4. The loop of Henle with descending and ascending limbs
5. Distal convoluted tubule which connects with a collecting duct which in
turn empties into a duct of Bellini and then to the renal pelvis and ureter.
Cortex
1. Glomerulas
2. P.C.T
3. D.C.T
Medulla
1. Loop of Henle
2. Collecting tubules
Must be remembered
1. Renal pelvis
2. Minor calyx
3. Major calyx
4. Duct of Bellini
5. Ureter
6. Juxta-glomerular cells
7. Macula densa
8. Podocyte
9. Bowman’s capsule/visceral layer (podocytes)
10. Parietal layer
11. Mesangial cell
Function
1. 1/3 of cardiac output through kidney
2. 1% excreated through urine and 99% resorbed through the epithelia of
tubules.
3. 70,000 molecular wt. substances can not be filtrated through glomeruli.
DoRS/Sajeda/Dop/FAHVM/SAU
2
Congenital and Hereditary Anomalies

1. Aplasia or agenesis
one or both kidneys
if one kidney aplastic other kidney undergoes compensatory hypertrophy
Both kidneys aplastic: life incompatible
2. Renal hypoplasia
Kidneys are smaller than normal with little or no function
3. Horseshoe kidney
Kidneys are fused and look like horseshoe shape
4. Vascular anomalies
If blood, vessels partially occludes ureter then hydronephrosis may develop.
5. Displacement
In cat, blood vessels are longer than usual
Kidneys are movable called “floating Kidney”.
6. Cysts in the kidney/congenital polycystic kidney. Many cysts are found in kidneys
Autosomal recessive (childhood/infantile) polycystic kidney disease
Autosomal dominant (adult) polycystic kidney disease
Medullary cystic disease complex
Diseases of Glomeruli
Glomerulonephritis
Primary inflammation of glomeruli
Tubular disease or pyelonephritis secondarily may lead to glomerulonephritis
Primary glomerular inflammation may cause lesions in renal tubules.
Types of Glomerulonephritis
1. Acute proliferative glomerulonephritis
2. Membranous glomerulonephritis
3. Membranoprolifeativeglomerulonephritis
(Mesangiocapillary glomerulonephritis,Measangioproliferative glomerulonephritis)
4. Chronic glomerulonephritis
5. Focal embolic glomerulonephritis
3
1) Acute proliferative glomerulonephritis

Classic poststreptococcal glomerulonenhritis (children, and spontaneous and
experimentally induced disease entity in animals)
Common in young children but adult are also affected.
Upper respiratory infection by streptococci for a duration of 2 weeks or mare.
Onset of renal disease

Sudden
Fever
Nausea
Weakness
S/C edema
Excretion of brown or bloody urine in scant amounts
Fever may abate in about a week
Urine abnormally persists
May contiunue as a chronic disease
Gross
a) Kidney: enlarged and pale
b) Petechiae outlining the glomeruli
Microscopic
a) Glomeruli: congested or edematous
b) Glomerular tufts increase in size with increased number of endothelial and
mesangial cells
c) In early stage, neutrophils, monocytes appear in the glomerulus
d) Influx and proliferation of cells result compression of capillaries and the
absence of red blood cells
e) Parietal epithelial cells proliferate and adhere to the inner surface of bowman’s
capsule. They may form epithelial crescents found in subacute and chronic
form
f) Thrombosis and necrosis of glomerular capillaries, and hemorrhage may occur
g) No obvious thickening of bm
h) No alteration of foot process of epithelial cells
i) Deposits or "humps" of immune complex on the epithelial side of the bm and
may project between podocytes.
j) Occasionally deposits may be found in lamina densa and subendothelial portion
of bm.
k) When stained with silver techniques or pas the bm is disrupted by these
deposits, giving it the characteristic of “lumpy-bumpy” appearance.
l) Leukocytic infiltration adjacent to glomeruli or in nearby interstitial tissues
m) In acute stage of disease, P.C.T. shows hyaline droplets and tubular lumen
shows proteinaceous casts and red blood cells.
4
2) Membranous glomerulonephritis
Cause of nephrotic syndrome
Prolonged course
Early studies in children
Lipid droplets in epithelial cells of P.C.T (previously called "lipoid nephrosis)
Morphologic changes
a) Thickening, splitting, and reduplication of the glomerular BM
b) Loss of the foot processes and spaces of the podocytes of glomerulus
c) Glomerular BM becomes irregularly thickened detected by silver techniques or
PAS staining with LM
d) BM gives “lumpy-bumpy” appearance resembling the "wire loop" in LM
e) Immune complex deposits are found in epithelial sidc of BM
f) Epithelial cells/podocytes are swollen and contain fat
g) Epithelia of P.C.T also contain fat droplets
h) Glomeruli are enlarged, hypercellular and contain no blood
i) Bowman's capsule is distended
j) Crescents and adhesion may be found
k) Chronic glomerulonephritis may also develop.
3) Membranoproliferative glomerulonephritis
Synonyms
Mesangiocapillary glomerulonephritis
Mesangioproliferative glomerulonephritis
Characteristic
a) Marked increased in mesangial cells:
b) Increased mesangial BM substance
c) Thickened BM
d) Splitting BM
e) Proliferative changes (mesangial cells and mesangial BM) in tuft of capillaries
f) Epithelial crescents formation
Types: on the basis of Ig deposition
Deposits in subendothelial BM and in mesangium .
Linear. dense deposits with little Ig but with significant amount of complement
within BM
Host: Human and Finnish Landrace sheep: both: are deficient of C3.
Glycoprotein/Ig also deposits in Choroid plexus associated with focal malacia and
edema of brain
5
4) Chronic Glomerulonephritis
Late stage of one or more of the various forms of glomerulonephritis
Microscopically-
a) Increased number of cells (endothelial, mesangial, and epithelial) in glomerulus
with disorganization
b) Proliferative and sclerotic changes within the glomeruli
c) Periglomeruli fibrosis
d) Tubules are atrophied and replaced by interstitial fibrosis
e) Occlusion of the lumen of glomerular capillaries
f) Epithelial crescent formation along the parietal layer of Bowman's capsule
g) Bowman's space is obliterated due to adhesion between glomerulus and
proliferated epithelia
Grossly-
a) Kidneys decrease in size
b) Smaller than normal
c) Rough or pitted on the surface
d) Tough to cut
5) Focal Embolic Glomerulonephritis

Infection from endocarditis, pneumonia and other localized area can be transported to
kidney producing focal embolic glomerulonephritis.
Microscopically-
a) Colonies of bacteria in glomerulus
b) Necrosis of glomerulus
c) Infiltration of ncutrophils in glomerulus
d) Hemorrhage
e) Patchily scattered glomeruli arc affected
f) "Crescents" formation may occur
Grossly-
a) Scattered petechiae
b) Multiple tiny abscesses.
6
Diseases of renal tubules and Interstitium

Primary degeneration and inflammatory diseases of renal tubules and
interstitium may occur in absence of glomerular disease
Tubular and interstitial disease may be secondary to glomerular disease
Primary tubulointerstitial disease or interstitial nephritis is characterized by - .
1. Degeneration and necrosis of tubular epithelium
2. Edema .
3. Cellular infiltration
4. Other component of inflammation In interstitium
5. Lesion may progress to chronic interstitial nephritis depending on-
Severity of the insult and
Its duration
Chronic interstitial nephritis is characterized by-
1. Marked interstitial fibrosis
2. Absence of tubules
3. Dilated tubules
4. Fibrotic kidney with relatively normal glomeruli
Diseases of renal tubules and interstitium
Acute interstitial Chronic interstitial Pyelonephritis Miscellaneous tubular

nephritis nephritis disorders
a) Toxic tubular nephritis/toxic tubular a) Acute Pyelonephritis a) Tubular transport

nephrosis b) Chronic disease
Pyelonephritis b) Cholemic nephrosis
b) Hypoxic (Hemoglobinuric, shock, lower
c) Uric acid precipitates
nephron) nephrosis d) Cloisonne Kidney
c) Immunologic tubulointerstitial nephritis e) Sulfonamides in the
d) Infectious Interstitial Nephritis kidney
f) Fat in the kidney
g) Dilated renal tubules
7
1) Acute Interstitial Nephritis

a) Toxic tubular nephritis/toxic tubular nephrosis
Causes: Various irritant toxic substances
Group 1: Direct effects upon the cells of renal tubules
Aminoglycoside antibiotics
Heavy metals: mercury, cadmium, lead
Group 2:
Xenobiotics (toxin from the environment)
Organohalides : chloroform and phosgene. Metabolites of chlorine affect
epithelia of renal tubules
Cephlosporins : metabolites affect epithelia of pet
Mycotoxins : ochratoxin /\ causes nephrotoxicity of human and swine
Halogenated alkenes : necrosis of epithelia of P.C.T
Group 3:
Phosphate
Iron
Zinc
Osmotic nephrosis : i/v injection of sucrose, glucose, mannitol, or dextran may
cause hydropic swelling of , ' phagolysosornes
Oxalate nephrosis: hydropic degeneration of epithelial cells of kidney and
lumen may contain crystals of oxalate
Alpha 2- microglobulin nephropathy:
Male rats (except 1\TBR strain) of most strains produce a low molecular
wt protein in liver (18.7 kDa) called alpha 2-microglobulin
Glomerular filtration into lumen of P.C.T.
Pinocytic and endocyic uptake by epithelial cells (Phagosome)
Fuse of phagosome and lysosome
Phagosome observed by LM called "hyaline droplets"
This protein is degraded by hydrolases into amino acids and is
discharged into circulation
Certain xenobiotics
d-Iimonene, jet fuels, gasoline, lindane, hexachloroethane are
collectively called
"chemicals inducing alpha 2-microglobulin accumulation" (CIGA)
ClGA can bind to alpha 2-nlicroglobuIin causing interference of
degradation of alpha 2-microglobulin
8
Protein-CIG/\. complex accumulation in phagosomes of epithelial cells

causing apoptosis and entire cells may form casts in narrowing part of
loop of Henle
After long time, regeneration of pet or adenoma and adenocarcinoma
may develop in this loop of Henle or renal papilla
Series of events occur in male rats are called "alpha 2-n11croglobulin
nephropathy syndrome'
But low molecular wt protein is found in mice (mouse urinary protein,
MUP) and in human Bence-Jones protein in myeloma but no lesions are
produced like male rats.
These toxic substances act directly and produce-

Fatty change of tubular epithelia
Necrosis of tubular epithelia
Hyperemia
Limited infiltration of lymphocytes, neutrophils and proliferation of fibrous
connective tissue
If insult produces early death of cells then less number of cells are found. It is called
"nephrosis" (acute toxic tubular nephrosis).
1. Epithelia of P.C.T. undergo necrosis
2. If degeneration and necrosis not extensive then regeneration of tubular
epithelia may occur
3. In fatal cases destruction of P.C.T.
4. F.C.T. proliferation at the place of lost tubules producing" small, white,
granular, contracted kidney"
5. Glomeruli may come closer due to loss of tubules
6. One segment of kidney may be affected but other segment is normal (some
nephrons function and some nephrons rest)
7. Some tubules may undergo compensatory hypertrophy
8. Fatty changes
9. Hyperemia
b) Hypoxic (Hemoglobinuric, shock, lower nephron) nephrosis

Epithelial damage is primarily in the lower nephron i.e. in the last part of loop
of Henle and distal convoluted tubules.
Casts (hemoglobin or myoglobin) are found in lower nephron
P.C.T. are dilated due to obstruction in lower nephron.
9
Symptoms
1. Oliguria
2. Anuria
3. Ureinia
4. Shock or shock-like condition
Causes
1. Burns (extensive)
2. Large crushing and brusing injuries
3. Azoturia
4. Extensive hemolysis
5. Acidity helps precipitation of Hb in human but in herbivore urine is alkaline
but how precipitation occurs is unknown
c) Immunologic tubulointerstitial nephritis

Can be produced in experimental animals
Causes
1. Foreign and autologous immune complex diseases
Granular fashion deposition of immune complexes in tubular basement
membrane
Mononuclear interstitial nephritis
Degeneration of tubular epithelial cells
2. Antitubular basement membrane diseases (BM)
Antibodies directed 'against tubular BM reported in experimental animal
(New Zealand Black/New Zealand White F 1(EIWF 1) mice and human.
In a dog with chronic interstitial nephritis
IgG, C3 deposition are found along tubular BM (Immunofl uorescent)
Degenerative changes in tubular epithelia include vacuolation, swelling,
cytoplasmic acidophilia and pyknosis of nucleus
Lymphocytes, macrophages, multinucleated Giant cells with peripheral
nuclei
In advanced stage,
Tubular necrosis and cellular infiltration become extensive
Fibrosis and
Destruction of overall renal structure
In human being
Drug-associated tubular damage may be due to immune
mechanism
Drug (haptens) plus TBM (tubular basement membrane
Production of anti-TBM antibodies
3. Cytotoxic antibodies
4. Cell-mediated mechanisms
10
d) Infectious Interstitial Nephritis

Cause:
1. Leptospira spp. can cause extensive interstitial nephritis
2. Other organisms
Pyogenic bacteria: Purulent interstitial nephritis
Canine herpes virus: Tubular damage and interstitial nephritis
Microscopic lesion
1. Organism found in renal tubular epithelia
2. Inflammatory lesions are found in interstitium
RBC
Plasma
Neutrophils
3. Later
Plasma cells
Lymphocytes
Epitheloid cells
Interstitial fibrosis
Thickening of Bowman's capsule
2) Chronic interstitial nephritis
Marked fibrosis in interstitium (end result of acute interstitial nephritis)
Loss of tubules, foci of mononuclear infiltration and glomeruli are relatively
unaffected
Causes
1. Bacterial infections
2. Poisons
3. Immunologic injury
4. Ischemia, obstruction and radiation
In dog, chronic glomerulonephritis may lead to chronic interstitial nephritis (may be
ended sclerosing nephritis)
3) Pyelonephritis
A form of interstitial and tubular disease. Inflammation of renal pelvis and
parenchyma of the kidney.
Route of infection
Ascending infection from urinary tract: most common route
Cystitis then vesicoureteral reflux that carries organisms from bladder to the
renal pelvis and even into the renal tubules (intrarenal reflux)
Dissermination through the vasculature (hematogenous route/descending route
of infection)
11
Causes
1. E. coli., Staphylococcus aureus : dog
2. Corynebacterium renale, Actinomyces pyogenes : bovine
3. C. suis: swine
4. Actinobacillus equuli: foal (endocarditis, glomerulonephritis and pyelonephritis
through hematogenous route)
5. E.coli., Enterobacter (Aerobacter) aerogenes, Proteus vulgaris, alpha
hemolytic Streptococcus, hemolytic Streptococcus, Pseudomonas aeruginosa,
Klebsiella pneumoniae in human.
a) Acute pyelonephritis
Microscopic
1. Purulent inflammation and necrosis are found in renal parenchyma, collecting
tubules, calyces and in renal pelvis
2. Glomeruli and nephrons are not affected but may be entrapped in widespread
inflammation
3. Lesion may be focal or diffuse in one or both kidneys or in a single lobule in
bovine
4. Abscess formation may occur
5. Neutrophils and leukocytic casts are found in collecting tubules.
Gross
1. Congestion
2. Hemorrhages
3. Abscess in renal cortex, pus in pelvis
4. Ureter, bladder and urethal mucosae may be affected
Clinical features
1. Fever
2. Malaise
3. Pyuria (pus in urine)
4. Bactcuria
5. Dysuria with frequent urination may occur
Microscoipic examination of urine

Neutrophils
Granular and leukocytic casts
RBC
Bacteria
12
b) Chronic pyelonephritis
Acute pyelonephritis may lead to chronic pyelonephritis
Gross
1. Kidneys arc scarred and contracted
2. Small, fibrous, and contracted in severe cases
Microscopic
1. Lymphocytes, plasma cells and neutrophils in interstitium
2. Tubules are atrophic or dilated and contain casts, Pus and bacteria
3. Periglomerular fibrosis
4. Severe fibrosis and infiltration of lymphocytes, and plasma cells are found in
interstitium
5. Patient may die due to uremia
4) Miscellaneous tubular diseases
a) Tubular Transport disease
Substance exceeds renal threshold (e.g. glycosuria in DM). Glomerular disease causes
passing of larger molecule in urine (e.g. proteinuria)
Cause
1. Tubular damage by poisons (e.g. Hg) causing passage of many constituents in
urine
2. Sex-linked hereditary disease in male dog.
In human (Faconi syndrome): a counterpart is reported in basenji’s dog
Aminiaciduria
Glycosuria
Polydipsia
Polyuria
In Dalmatian breed dog (uricase present but defect in tubular epithelium
resorption)
Uric acid secretion
Uric acid calculi
cystinuria
Cystine uroliths
Lysine, arginine and ornithine nletabolism are also affected
b) Cholemic nephrosis
Bile pigments (yellow color and irregular in size) may be deposited in epithelia of
P.C.T. or loop of Henle
Causes
1. Obstructive jaundice
2. Severe liver disease
3. Hepatic injury: increased cystine, arginine, histidine, tryptophan excretion
cause damage of renal tubular epithelia (proved experimentally)
13
Gross
1. Formalin-fixed kidney gives green color (as bilirubin changes to biliverdin)
2. Fresh kidney gives yellow color
Microscopic
1. Bile pigment in epithelia of P.C.T. or loop of Henle
2. Degeneration of tubular epithelia
c) Uric acid precipitates

Urate crystals are found in collecting tubules
Microscopically
1. Yellow crystals are found in collecting tubules
2. In birds urate crystals are found in interstitial stroma (uric nacid results from
destruction of cells particularly erythoblasts. This change also occurs gout)
d) Cloisonne Kidney
Pigmented thickening of tubular basement membrane in P.C.T. of goats
Nature of the pigment is not known: hemosiderin and 'melanin negative.
Iron-positive only in some part but not all parts
Gross
1. Dark brown or black in color of renal cortex
Pathogenesis:
Low level of erythrocytic glucose-6-phosphate dehydrogenase and glutathione
Elevated serum-iron-binding saturation
Fragility of RBC
Ferritin deposits in affected basement membrane
Hemosiderin in tubular epithelial cells
Further study is needed
e) Sulfonamides in kidney
Sulfonamide medication with limited intake of water and an acid condition of urine
may damage the kidneys
Lesions
1. Toxic tubular degeneration and necrosis
2. Marked inflammatory infiltrations around the tubules
3. Glomerulonephritis (due to hypersensitivity)
14
4. Periarteritis nodosa
5. Necrosis of peripelvic tissues
6. Crystals in collecting tubules (cattle, dog) may lead to anuria
f) Fat in the kidney

Lipids or lipoids can be demonstrated in kidneys of animals and humans
Renal tubules, glomerular tufts, wall of Bowman’s capsule, interstitial
tissues, wall of blood vessels, pelvic epithelia, tubular lumens contain fat
In cat with the increase of age, P.C.T. epithelia contain abundant amount of
fat.
Causes
Like toxic and anoxic change in liver
DM (Diabetes mellitus)
Ketosis
Ovine toxemia of pregnancy /Malnutrition
Microscopic
1. Empty, round and clear spaces in cytoplasm of cells
2. Fat stains can detect lipids/lipoids
3. Lipid-filled macrophages in pyelonephritis are called xanthogranulomatous
pyelonephritis
4. Lipid-filled macrophages in glomeruli are called glomerular xanthomatosis.
g) Dilated renal tubules

Cause
Atrophy or flattening of epithelia of tubules due to back pressure caused by
from external pressure or otherwise, of the nephron at some lower point in its
course
Compensatory hypertrophy of epithelia of tubules is seen near area of fibrosis
Hypertrophic cells are characterized by hyperchromatic nuclei
Nephrosclerosis
1. Secondary or primary chronic fibrosis of kidney is often called nephrosclerosis

2. Glomerulonenhritis may lead to chronic fibrosis of kidney
3. Interstitial nephritis may also lead to chronic fibrosis of kidney
4. In human cause is- Arteriolar sclerosis (sclerotic blood vessel) Characterized
by Constriction of arteries and arterioles (due to cholesterole deposition)
15
Effect
Ischemia
Tubular atrophy
Necrosis
fibrosis
As no preceding nephritis so this form of nephroclerosis is called “Primary
Contractred Kidney”. Effect of primary contracted kidney
Hindrance of blood supply
Release of renin from Juxta-glomerular apparatus
Cause hypertension aggravating vascular disease and renal ischemia
Cause malignant hypertension and malignant nephrosclerosis
“Secondary contracted kidney” develops due to chronic nephritis.
Urinary obstruction and hydronehrosis

1. Calculi in penal urethra (cattle, sheep and goat) cause distension of urinary
bladder
“Water belly” develops due to rupture of bladder
Blood urea nitrogen may reach 400 mg/100 ml of blood
Animal dies due to uremia.
2. Complete obstruction of one side of kidney
Rapid atrophy of kidney without hydronephrosis or without other clinical
disturbance (must be differentiated from hypoplasia)
3. Partial obstruction (unilateral or bilateral)

After few months back pressure develops in kidney(s), Condition is called
hydronephrosis
Gross
1. Renal pelvis is gradually enlarged
2. Obstructed kidneys become a mere hollow sac.
Microcopic
1. Some scattered atrophic glomeruli are present
2. Pyelonephritis
3. Pyonephrosis (pus in pelvis)
Causes
1. Calculi: at renal pelvis, ureter, urethral process, sigmoid process.
2. Pressure on ureter and urethra by neoplasia
3. Carcinoma of bladder
16
4. Carcinoma of canine prostate

5. Giant kidney worm Dioctophyma renale
6. Inherited in rats and inbred mice
Effect
Hydronephrosis of one kidney
Compensatory hypertrophy of other kidney
Urolithiasis
Formation of stony precipitates anywhere in urinary passage is called urolithiasis; the
stone is called urolith or urinary calculi. Calculi are found in
1. Renal pelvls
2. Distended terminal tubules (the ducts of Bellni) I,
3. Ureter: cause excruciating pain known as ureteral colic. If it is forced to
bladder then colic is releaved (if small calculus)
4. If blocks ureter, then disuse atrophy of kidney and hydronephrosis develops.
5. Bladder: called '''cystic 'calculi"
6. Sigmoid flexure of ruminants (male) (female escapes due to larger and wider
urethra).
Size of calculi
Variable that is sand-like particles to a single stone filling renal pelvis and
bladder.
Characteristics of calculi are

Hard or relatively soft
White or yellowish
Smooth or rough
Rounded or faceted
Fragile or collection of sandy materials (e.g. siliceous stones)
Composition of calculi: varies greatly

Herbivorous animals (alkaline pH helps precipitation of silica)
Silicates and is admixed with phosphates, carbonates, oxalates of calcium,
ammonium and magnesium plus some proteins
Feedlots: calcium phosphates, calcium carbonates, triple phosphates
Sheep: xanthine calculi (nuclein derivative)
Carnivorous and omnivorous animals: similar to human as acidic urine
17
Different types of stone

1. Oxalate stones (calcium_oxalate) : very hard and heavy, white or yellow,
covered with sharp and hard spines that damage epithelia and cause
hemorrhages.
2. Uric acid calculi: form in acid urine and common in Dalmatian dogs that
excrete large amount of uric acids-
Composed of ammonium and sodium urates; and uric acids
Small or medium size
Firm or moderately hard
Yellow to brown in colour
Spherical or irregular in shape
3. Phosphates calculi
Common in dog though acid urine
White or gray or chalky consistency
Soft and friable
May form sand-like granules
Bacterial infection causes break down of urea to ammonia that cause
increase of pH of urine favors precipitation of phosphates
Magnesium and ammonium phosphates are common in dog
4. Xanthine stones
Brownish red
Concentrically laminated.
Fragile and of irregular in shape
5. Cystine stones
Found in man, woman and male dog
Small, soft and variable shape
Shiny greasy appearance
Yellow to darker after exposure to air
Cystine, an amino acid and relatively insoluble and precipitate in bladder of
animals due to failure of tubular resorption
6. Siliceous calculi
Rare in carnivores but develops if diet contains a large amount of silicic
acid.
18
Causes
An organic matrix, nucleus, or nidus is necessary requirement for deposition of
inorganic crystals resultant stone formation. This nucleus is usually a
mucopolysaccharide or mucoprotein. The nucleus could consist of
Dead leukocytes
Fibrin
Cellular debris
Agglutinated bacteria
Supersaturated solution of crystalloid of urine
1. Castrated males are more affected than intact male and female: as early
castration interferes development of lumen of genitourinary tract due to
deficiency of testosterone.
2. Some specific conditions

Bacterial infection of urinary tract: nidus formation and alteration of urinary
pH (phosphate calculi in dog)
Aminoaciduria: cystine calculi in male dogs.
Metabolic defect in uric acid metabolism: urate calculi in Dalmatian dog
Vit. A deficiency: Squamous metaplasia of urinary epithelia causing
increased nidus formation
Implantution with diethylstilbestrol or grazing on estrogenic plants (urinary
calculi in sheep). Hormone causes squamous metaplasia of genitourinary
tractI epithelia that limit the growth in size of the genitourinary organs
Hyperparathyroidism: increased excretion of calcium causing urolithiais
and ncpnrocalcinosis
A picorona virus: calculi in male cats by experimentation
Dietary mineral Imbalance: diets With imbalance of calcium, phosphates,
and magnesium causing urolithiasis or nephrocalcinosis
Inadequate water intake: if diet is rich in silicates or other minerals or other
predisposing factors exist then dehydration favors calculus formation
High sodium chloride intake plus ample amount of water intake reduce
incidence of urolithiasis
Effects
1. Mechanical irritation then severe pain
2. Urethra may be obstructed
3. Obstruction of urine flow and then colic may develop
19
Neoplasms
1. Embryonal nephroma
2. Nephroblastorna
3. Wilm's tumor: s/m present
4. Adenoma
5. Adenocarcinoma
6. Transitional cell carcinoma.
7. Oncocytoma: rats (cells of collecting ducts)
8. Metastatic neoplasm
Ureter
1. Aplasia to complete duplication
2. Inflammation (e.g. TB)
3. Stricture
Congenital
Result of inflammation
4. Neoplasms
Papillomas
Carcinomas
Metastatic tumor
Bladder
1. Cystitis
Fibrinous
Purulent
Catarrhal
Hemorrhagic type
Emphysematous cystitis (gas produced by bacteria)
Mucinous, adenomatous, squamous metaplasia are found in chronic cystitis
especially in bovine enzootic hematuria
2. Other disorders
Hemorrhages
Hypertrophy
Obstruction by calculi
Enlarged canine prostate
3. Parasites of urinary bladder
Capillaria plica: cat
Trichosomoides crassicaudata: rat
Schistosoma haematobium: human
4. Neoplasms
Papillomas
Transitional cell carcinoma
Squamous cell carcinoma
Adenocarcinoma
Leiomyoma and leiomyosarcoma
Rhabdomyosarcoma
Metastatic tumor (e.g. malignant lymphoma)
20
Urethra
1. Calculi
2. Gonorrhea: human
3. Tritrtchomonus foetus: bull
Bovine enzootic hematuria

Bladder, ureter and renal pelvis of cattle and buffaloes are affected. Characterized by
Hyperplastic inflammation
Hemorrhage
Metaplasia (mucinous or stratified squamous or mixture)
Carcinoma develops and may metastasize to regional lymph nodes
Cause
Bracken fern poisoning
Difference between primary contracted kidney and secondary

contracted kidney
SL.
Feature(s) Primary Contracted Kidney Secondary Contracted Kidney
No.
Contraction of kidney due to its Contraction of kidney due to
1. Definition
own diseases diseases of other organs.
Arteriolar Sclerosis Diseases of other organs
Cholesterol in the blood vessels of Transported into the kidney by

kidney haematogenous route
Lumen become narrower Nephritis and fibrous connective

2. Pathogenesis
tissue proliferation
Less blood and nutrition supply
Degeneration, nephrosis and finally

fibrous connective tissue
proliferation
Organism
3. No organism is found. Organism is found.
involved
Reactive
4. No reactive cells Reactive cells present.
cells
Amount of
5. Less More
fibrous C.T

FASVM, SAU
Diseases of Haemic and Lymphatic System
Hematopoiesis (= Hemopoiesis): the process through which all blood cells are
made.
Development of Hematopoiesis
In the embryo, hematopoiesis begins as clusters of stem cells, called

blood islands, within the yolk sac.
In the fetus, hematopoietic activity is found in the liver, spleen, thymus,

lymph nodes and bone marrow.
In neonates, hematopoiesis is confined primarily to the bone marrow

involving both flat and long bones.
In growing age, hematopoietic activity in the central areas of long bones

regresses and is replaced by fat (ie change from red marrow to yellow
marrow in diaphyseal regions).
In adults, most active hematopoiesis occurs in the flat bones (vertebrae,

pelvis, skull, sternum, ribs) and in the extremities of the long bones (ie
epiphyseal / metaphyseal regions) in the spaces between the spicules of
cancellous bone; the medullary cavity in the diaphyseal region of the long
bones contains mostly fat.
In adults, when hematopoiesis occurs anywhere other than the marrow

(usually the spleen), it is referred to as extramedullary hematopoiesis.
1
H&LS/DR.Sajeda/DoP/FAHVM/SAU
Pathological condition of bone marrow
Hyperplasia
When there is an increase in the demand of the red blood corpuscles or the
leukocytes, the red bone marrow proliferates, and extends into the shaft of the
long bones. These changes are known as hyperplasia.
It is recognized grossly by increasing in the amount of active (red) bone marrow
and a decrease of fatty marrow as compared with the normal for a given age.
There are two varieties of myeloid hyperplasia-
Erythoblastic hyperplasia
Grossly, it is characterized by replacing the fat marrow by red marrow.
Microscopically, there is increase number of precursors of erythrocytes
(erythroblast).
Causes:
 Most of the anemia except toxic aplastic anemia (due to inability of the
bone marrow to function)
 Human pernicious anemia (due to deficiency of erythrocyte- maturating
factors)
 Human and dog fish tapeworm , Diphyllobothrium latum (the
megaloblastic hyperplasia)
Leukoblasitic hyperplasia
Grossly, it is characterized by replacing the yellow marrow by grayish marrow
Microscopically, there is increase number of the precursors of leukocytes.
Causes:It is associated with infections accompanied with leukocytosis and with
pyogenic infection.
Hypoplasia
Grossly, it is characterized by increase the proportion of fatty marrow. The
remaining hematopoietic tissue scattered in little islands through the fatty
marrow.
Microscopically, there are less erythropoietic cells, less cellularity of all types
of cells and more fat cells.
Cause
 Toxic aplastic anemia
 Certain deficiency diseases.
Effects
 Anemia
 Decrease number of all types of blood cells.
2
Agranulocytosis
Complete absence of granulocytes from the circulating blood due to complete
aplasia of the leukocytic cells of bone marrow.
Cause:
 Aplastic anemia
 Causes that suppress bone marrow
Effect: Fatal as body cannot protect infection
Osteomyelitis: Inflammation of the bone marrow due to infection.
Route of infection
 Local wound e.g.fracture
 Hematogenous metastasis
Macroscopic appearance: Accumulation of pus which cause softening and
necrosis of overlying bone.
Microscopic appearance: Accumulation of polymorph nuclear leukocytes and
fibrin are noticed.
Cause: Pyogenic infections-
 TB
 Brucellosis
 Coccidioidomycosis
Osteomyelitis was difficult to treat but recently antibiotic has reduced some
risks.
Fibrosis: Replacement of bone marrow by fibrous tissue.
Cause: Not known but
 As a sequelae of hypoplasia or aplasia of bone marrow.
 Accompanied with myxyomatous degeneration.
 Starvation/cachextic condition.
3
Anemia
Reduction bellows normal the number of erythrocytes and /or hemoglobin
concentration or both per unit volume of blood.
 In neonatal animals following ingestion of colostrums, erythrocytes
numbers decrease and gradually return to adult level over succeeding
weeks.
 Animal residing at high altitudes have higher erythrocytes counts.
 Anemia is not a disease but manifestoing of some other disease, e.g.
Malaria can cause anemia
Basic concept of Classification: Morphological basis depends on two features

1. Size of erythrocytes: MCV (Mean corpuscular volume). On the basis of
MCV the size of erythrocyte may be
 Macrocytic
 Normocytic
 Microcytic
2. Hemoglobin content of erythrocytes: MCHC (Mean corpuscular

hemoglobin concentration) and MCH (Mean corpuscular hemoglobin).On
the basis of MCHC the Hb content of the erythrocytes may be
 Normochromic
 Hypochromic
 Hyper chromic :
Terms used in describing anemias and diseases of blood

 Anisocytosis: Erythrocytes are not uniform in sizes.
 Poikilocytosis : Bizarre or abnormal shaped erythrocytes
 Nucleated erythrocytes : May be found in blood
 Rubriblasts : May be found in blood
 Basophilic stippling: dark specks are found in one cell.
 Polychromatophilia : Are not uniformly stained even in one cell or
among the others
 Heinz bodies : purplish granules (denatured Hb) are found near the
membrane of RBC
 Target cell : Stating is found in the center of the cell but the periphery is
empty
 Megaloblast: It is an immature cell in the erythrocyte series comparable
to prorubricyte stage seen in animals due to vitamin B12 or folic acid
deficiencies.
4
Classification of Anemia: Anemia may be classified on the basis of
morphology and etiology:
A. Morphological classification: Based on MCV and MCHC anemia can
classified to:
1. Macrocytic normochromic anemia: Vitamin B12 and folic acid
deficiency, liver diseases.
2. Macrocytic hypochromic anemia: Acute blood loss or acute hemolysis.
3. Normocytic normochromic anemia (Toxic aplastic anemia): Due to
depression of erythrogenesis, neoplastic diseases, irradiation and certain
toxicities
4. Microcytic hypochromic anemia: Iron and copper deficiency
B. Etiological classification: On the basis of etiology anemia is classified into
five groups-
1. Hemorrhagic anemia
2. Hemolytic anemia
3. Deficiency anemia
4. Toxic aplastic anemia
5. Myelopthisic anemia
1. Hemorrhagic anemia: Results from severe hemorrhages. Hemorrhagic
anemia is divided into two types
Acute hemorrhagic anemia: Morphologically acute hemorrhagic anemia may
be normocytic normochromic followed by normocytic hypocromic and
macrocytic hypocromic.
Chronic hemorrhagic anemia: Macrocytic hypocromic.
Causes:
Acute hemorrhagic anemia Chronic hemorrhagic anemia
 Trauma  Unhealed peptic ulcer in Human
 Thrombocytopenic perjure  Hook worm
 Poisoning: Sweet clover, warfarin  Bunostomum phlebotomum in
& bracken fern. cattle
 Trichloroethylene- extracted  Ancylostoma duodenale in man
soybean oil meal  A.caninum in dog
 Stomach worms
 Haemonchus contorus in cattle
 Strongylus vulgaris, S.equinus
and S. edentatus in horse
 Hemophilia A & B
 Vitamin C deficiency.
5
2. Hemolytic anemia:
 It results from excessive destruction of the circulating erythrocytes,
occurring within the blood stream.
 It usually accompanied by icterus, hemoglobinuria and hemoglobinuria in
acute form, and with stimulation of bone marrow in chronic form.
 Extravascular hemolytic anemia occur when erythrocytes phagocytized
by macrophages due change in its shape or when recognized as foreign.
In this form there is no hemoglobinemia or hemoglobinuria, but there is
hemolytic icterus.
Causes
Infectious Toxic
 Piroplasmosis  Snake venoms
 Anaplasmosis  K and Na chlorate poisoning
 Eperythrozoonosis in swine and cattle  Chronic lead poisining
 Hemobartonellosis in dog and cat  Chronic copper poisoning
 Malaria in human, monkey and birds  Ricin
 Equine infectious anemia  Phenylhydrazine
 Trypanosomiasis  Saponin
 Stretococcus hemolyticus  Poisoning by kale and rape
 Clostridium hemolyticum bovis
 Clostridium welchii Immunologic causes
 Leptospirosis  Erythroblastosis fetalis
 Autoimmune hemolytic anemia
3. Deficiency anemia: Deficiency of several compounds and vitamins which is
essential for haemoglobin synthesis.
Causes:
 Deficiency of Iron: Required for Hb  Deficiency of Cobalt and folic acid:
Synthesis. Lead to deficiency of Vit. B12 required
 Dietary deficiency of iron. for development and maturation of RBC.
 Defective assimilation  Dietary deficiency of Vit. B12 in
 Malabsorption of iron. monogstric animals & man (Cobalt).
 Chronic blood loss.  Killing of ruminal flora by oral
 It is microcytic hypochromic anemia antibiotics (Cobalt).
with prominent poikilocytosis.  It is macrocytic normochromic.
 Deficiency of Copper: Required for  Deficiency of Pyridoxine: It is
utilization of iron for Hb Synthesis microcytic hypochromic and
 Excessive molybdinum inhibit Cu sideroblastic anemia
absorption  Deficiency of Vit. E and Selenium:
 It is microcytic hypochromic anemia. Helps in stabilizing plasma membrane of
 Deficiency of Riboflavin and Vit. C RBC
6
Toxic aplastic anemia
 It occurs due to failure of bone marrow to produce erythrocytes.
 It is characterized by normal size, shape and color of erythrocytes beside
absence of signs of active erythropoiesis “absence of megaloblasts,
normoblasts and reticulocytes”. Moreover, the granulocytes formation is
depressed.
Grossly:
 Bone marrow is predominantly fatty
 Scattered islands of hematopoietic cells
 Sometimes sclerotic
Causes
 Toxic irradiation e.g, X-ray, radium,  Other causes
isotopes  Nephritis and uremia : a) toxic
 Benzol poisoning action of retained waste
 Trinitrotoluene product b) interference of
 Sulphonamides erythropoietin production.
 Chloramphenicol  Chronic infection : has effects
 Brecken fern upon Hb synthesis
 Trichloroethylene  Neoplasticdisease:selectivedep
(extracted from soybean meal) ressionoferythrogenesis.
Myelophthisicanemia : (Myelo=the marrow; phthisis=a wasting disease)
It is type of anemia associated with physical destruction of bone marrow
“erythropoietic tissue”. Examples: anemia associated with leukemia or with
leucosis of fowl.
Causes
 Various carcinomas
 Leukemia
 Malignant lymphoma
 Osteopetrosis
 Infection e. g TB, Brucellosis, Coccidioidomycosis
Significance and effect of anemia
 Anoxia of the tissues
 Anoxia may lead to fatty change in heart, liver and other susceptible
organs.
 Rapid and irreguler pulse and Dysepnea/shortness of breath
 Muscular weakeness
 Hemolytic anemia may lead to hemolytic jaundice
 Hemorrhage due to anoxic damage of endothelia
 Edema
7
Lesions of anemia
 The mucous membranes are pale.
 The blood may be pale and watery.
 The skin is pale and become thin and inelastic due to atrophy of
epidermis and dermis
 Hemolytic jaundice “yellow skin, mucous membrane and others” are seen
in case of extravascular and intravascular hemolytic anemia.
 Gray dots in liver may be hematopoietic centers or may be minute foci of
necrosis.
 Hemoglobinemia and hemoglobinurea seen in hemolytic anemia
characterized by intravascular hemolysis.
 Erythroblastic hyperplasia characterized by replacement of fat in long
bones by red marrow.
 In toxic a plastic anemia the bone marrow shows markedly hypocellular
with reduction of cell lines.
 Blood film shows anisocytosis (variable sizes), poikilocytosis (variable
shapes), nucleated erythrocytes. Also, basophilic stippling “minute dark
spots in erythrocytes” is seen. In polychromatophilia, the erythrocytes
don’t stain uniformly.
Heinz bodies are refractile bodies within erythrocytes which denaturated
hemoglobin formed due to oxidative injury. It seen in toxic hemolytic
anemia.
 Section of spleen or liver may show extramedullary hematopoietic
centers “hyperchromatic cells”
 Retrogressive changes and necrosis are noticed in cells of
parenchymatous organs and muscles of heart.
 Hemosiderosis is evident in case of hemolytic anemia.
NB: Removal of cause can cure anemia except toxic aplastic anemia.
8
Some other important anemias:
Pernicious anemia: It is an acquired autoimmune disorder characterized by
megaloblastic macrocytic anemia due to vitaminB12 deficiency and lack of
intrinsic factor resulting from immunological destruction of parietal cells of the
stomach.
Pathogenesis:
Auto immune disorder
↓
Production of antibodies & effector T-cells against intrinsic factor and parietal
cells respectively
↓
Neutralization of intrinsic factor and destruction of parietal cells
↓
Lack of intrinsic factors
↓
Failure of absorption of dietary vitamin B12
↓
Deficiency of vitamin B12
↓
Pernicious anemia
NB: Intrinsic factor (glycoprotein) and vitB12 form a complex called
erythrocyte maturation factor (EMF) which is absorbed through ileum and
stored in liver.
Autoimmune hemolytic anemia: In this disorders the RBC are prematurely
destroyed by anti-RBC antibodies against antigens on the membrane of RBC.
Type-II (cytotoxic) hypersensitivity cause damage of the RBC.
Causes:
 Idiopathic
 Secondary
 Infections: Mycoplasma pneumonae, infectious mononucleosis,
cytomegalo virus.
 Other autoimmune diseases: SLE, rheumatoid arthritis, autoimmune
hepatitis
 Chronic lymphocytic leukemia.
 Malignant lymphomas
 Drus: Methyldopa, mefanamic acid etc
 Carcinoma: rare
9
Some terminology
Polycythemia : Increase in number of erythrocytes in circulation . Three types-
1. Relative polycythemia : 2. Absolute polycythemia / Erythrocytosis :
Decreased plasma volume without Absolute increase in the total red cell.
increase in total cell Causes
Cause  Prolonged mild anoxemia
 Vomition  High altitude
 Diarrhoea  Sufficient anoxia
 Hemorrhage  Patent foramen ovale
 Pulmonary emphysema
 Pulmonary fibrosis
Polycythemia vera: It is a neoplastic myeloproliferative disorder that affects chiefly

the erythroid series. It is characterized by increased PCV without hypoxemia or
reduced plasma volume.
Retculoendotheliosis : Myeloproliferative disease of cat characterized by

proliferation of undifferentiated reticulum cells in bone marrow, spleen
(splenomegaly), liver (hepatomegaly), lymph nodes (enlarged) and these cells
can enter into circulation .
Purpura hemorrhagica : Common in horse but also occurs in swine. Denotes a

syndrome characterized by many petechial and ecchymotic hemorrhages in the
skin, external and internal mucous membrane. Latin word “purpura” means
purple colored hemorrhagic spots. It is thought that the injury of the capillaries
occurs due to hypersensitivity or immune complex deposition.
Thrombocytopenic purpura : A reduction in number of circulating platelets

purpura hemorrhagica owing to prolongation of bleeding time .
10
Diseases of leukocytes
Leukocytosis: Inflammatory increase in number of leukocytes.
Causes:
1.Neutrophile leukocytosis/Neutrophilia: 2.Eosinophile leukocytosis/Eosinophilia:
Physiological:  Allergic diseases: Asma, hay fever,
 New born animals serum sickness.
 In Pregnancy  Parasitic infections: Trichinosis,
 During exercise helminthiasis.
 High protein diet.  Skin affections: Eczema, scabies.
 Certains drugs & poisons: Sulfa
Pathological:
drugs, chlroropromazine, arsenic,
 Acute infections: By cocci,
copper, digitalis.
leptospira, E.coli, Actinomyces bovis,
 Diseases: Chronic myelocytic
psittacosis organism, poliomyelitis
leukemia, Hogdkin’s disease.
virus, small pox virus etc.
 Following recovery from acute
 Metabolic: Uremia, diabetic coma,
diseases
burns.
 Chronic eosinophilic myositis in dogs
 Poisoning: Lead, digitalis, mercury,
 Following splenectomy
epinephrine.
 Mild irradiation.
 Acute haemorrhages & haemolysis
 After surgical operations.
3. Lymphocytosis: 4. Monocytosis:
 Viral infections: Mumps, influenza.  Protozoal diseases:
 Bacterial infections: Brucellosis, Trypanosomiasis, malaria, kalaazar.
tuberculosis.  Bacterial diseases: Brucellosis,
 Thyrotoxicosis tuberculosis.
 Adrenocortical insufficiency  Rickettsial affections: typhus.
 Lymphatic leukemia  Monocytic leukemia
 Vaccination  During convalescence following
 In convalescence acute diseases
 Hodgkin’s disease
11
Leukopenia : Decrease in number of leukocytes in circulation.
Causes:
Diminished production of WBC: Increased destruction of WBC:
 Bracken fern poisoning  High doses of ionizing radiation
 Viral diseases: Rinderpest,  Bacterial toxins: Clostridium
distemper, infectious canine welchii, Pasteurell spp.
hepatitis, mucosal disease.  Protozoal diseases: Theileria parva
 Bacterial diseases: Brucellosis,  Hypersplenism
typhoid, tuberculosis. Altered distribution of WBC:
 Protozoal diseases: Kalaazar  Anaphylactic shock: Leukocytes
 Fungal disease: Histoplasmosis are trapped in liver, spleen & lung.
 Rickettsial disease: Tick borne  In stress condition: Cortisone
fever liberated from adrenal cortex.
 Cachectic condition and starvation
 Hypothyroidism & hypopituitarism
 Hypoplasia of bone marrow.
 Anemias: Aplastic & myelopthisic
Leukemia: Neoplastic increase in number of leukocytes in blood where

involvement of bone marrow is very common. Neoplastic cells increase in
blood called leukemic leukemia and increase in tissue called aleukemic
leukemia
Hemoglobinemia and hemoglobiuria : Hb releases after hemolysis of

erythrocytes producing hemoglobinemia and if exceed kidney threshold then
come out through urine called hemoglobinuria that must be differentiated from
hematuria. After sedimentation or centrifugation Erythrocytes settle down at the
bottom of the test tube.
Heinz bodies anemia: Heinz bodies are refractile inclusions found in the
erythrocytes of horses that undergo phenthiazine therapy. These are supposed to
be associated with denatured protein and are seen in haemolytic anemias. Their
presence indicates erythrocyte injury.
In man Heinz bodies are noticed following treatment with primaquine,
sulphanilamide, phenylhydrazine, paraaminosalicylic acid, nitrofurantine etc.
12
Four genetic diseases of leukocytes
1. Chediak-Higashi syndrome: Man, cattle, cat

2. Cyclic neutropenia (gray collie syndrom) : Disease is characterized by a
periodic neutropenia occurring at regular intervals of 8-12 days.
3. Pelger- Huet anomaly: Man, rabbit, and dog . Nuclei of maximum
neutrophils and eosinophils are nonsegmented.
4. Leukocyte adhesion deficiency: A hereditary disease recorded in Holstein –
Fresian calves, dog and human.
Splenomegaly: Enlargement of the spleen.

Causes:
Cattle: Horse:
 Anthrax  Equine infectious anemia
 Salmonellosis  Metastatic melanoma
 Babesiosis  Tuberculosis
 Anaplasmosis  Anthrax
 Theileriosis  Salmonellosis
 Acute congestion in bacterimic & 
toxemic conditions
Dogs: Pigs:
 Using barbiturates & chloroform  Erysipelas
 Histoplasmosis  Salmonellosis
 Haemangiomas& haemangiosarcomas  Eperythrozoonosis
 Lymphomatosis  Acute congestion
 Myelogenous leukemia  Torsion
Fowls:
 Spirochetosis, lymphoid leukosis
In some conditions for all species:
 Congestive heart failure
 Bone marrow destruction
 Histiocytes of liver saturated
 Hepatic fibrosis
13
Lymphadenitis
Lymph nodes are not glands but the inflammation of the lymph nodes is called
lymphadenitis which is a misnomer, however, a commonly used terminology.
Causes:
Specific:
 Anthrax : (Bacillus anthracis ; Hemorrhagic lymphadenitis)
 Strangles : (Steptococcus equi; abscess formation in horse, puppies)
 Mycotic infection: e.g Histoplasmosis
 Immunosuppression by HIV, SIV, FIV
 TB
 Pseudotuberculosis
 Ovine caseous lymphadenitis
 Tularemia
 Actinobacillosis
Nonspecific:
 Pneumonia affects bronchial lymph bodes (Hyperemia, edema)
 Rhinitis or an infected tooth affects manibular and pharyngeal lymph
nodes
 Mastitis affects supramammary lymph nodes (The nonspecific
lymphadenitis is called lymph nodes draining reaction)

FASVM, SAU
14
1
ORGANS OF SPECIAL SENSE
Eyes and
Different Parts of
Eye
External Middle Layer/Vascualr Layer Inner

Layer (tunic)/Uveal Tract Layer
Cilliary
Sclera Cornea Choroid Iris Retina
Body
Adnexa: Contain eyelids that have cutaneous and conjunctival surfaces. Have
tear and sebaceous glands (Meibomianglands)
Congenital Anomalies of the eyes

Microphthalimia : One or both eyes are small. Usually seen in swine (due to
hipovitaminosis A of dam) and fogs (hereditary).
Cyclops : Only one eye due to fusion of the two orbits. Usually seen in
monsters.
Ankyloblepharon : Both eyelids are fused together.
Strabismas : Squint ( ) in human beings. Also seen in Siamese cat, calves
of beef greed and Collie dogs.
Entropion : Inward turning of the eyelids. Usually hereditary in sheep, dog
and foals.
Ectropion : Outward turning of the eyelids. Usually lower eyelid is
affected and also is hereditary.
Congenital : Adhesion between anterior surface of the iris and posterior
anterior synechia surface of the cornea.
Aphakia : Absence of lens.
Microphakia : Small spherical lens.
Anophthalmia congenitus : Complete absence of one or both eyes. Usually
seen in foal, calves, pups and piglets.
Congenital anterior synechia : Adhesion between anterior surface of the iris and
posterior surface of the cornea.
Dermoids of cornea : Tumors in which cornea of one or both eyes is
partly covered by skin containing hair.
DoRS/Sajeda/DoP/FASVM/SAU
2
Some Important Terminology

Blepharitis : Inflammation of the eyelids.
Exopthalmos : Protrusion of the eyeball.
Enopthalmos : Sinking of the eyeball into the orbit.
Endopthalmitis : Inflammation of the internal portion of the eye.
Panophthalmitis : When inflammation spreads throughout the internal and
external structures.
Conjunctiva
Conjunctivitis: Inflammation of the conjunctiva.
Causes:
2. Chemicals
1. Bacteria
a. Lime
a. Brucella spp.
b. Irritant gases-
b. Listeria spp.
@formalin vapor
c. Pasteurella tularensis
@Sulphur
d. 2ndary infection by-
@Smoke
@Staphylococcus aureus
@Acids
@Pseufomonas aeruginosa
@Alkalies
@E. coli.
@Sheep fips
3. Foreign bodies 4. Parasites 5. Allergen
a. Awns Thelazia lachrymalis in horse a. Pollen
b. Oak husk T. rodesi in ox b. Horse serum
c. Mud T. caliipada in dog
d. Dust T. leesi in camel.
e. Sand
Symptoms:
1. Congestion of the conjunctiva
2. Increased production of tears which flow over the face.
3. The teares are clear at first but soon become turbid and thick due to
presence of leukocytes and mucoid materials.
4. Purulent conjunctivitis occur if invaded by pyogenic organisms.
5. Infection may spread to the cornea and keratitis may occur.
3
Cornea
Pannus: is a condition in which vascular granulation tissue is found between
the corneal epithelium and the Bowman’s membrane.
Keratitis: Inflammation of the cornea.

Cause: Same as conjunctivitis.
Symptoms:
1. Photophobia and blepharospasm (tightly closed eyelids)
2. Oedema of corneal epithelium followed by epithelium due to infiltration
of leukocytes.
3. Vascularization of cornea may be seen. (Ulceration of cornea due to
deficiency of dietary tryptophan and riboflavin).
4. Keratoconjuncivits Sicca: Defective production of tears leads to excessive
dryness of corneal surface.
Infectious Keratoconjunctivitis/Pink Eye: Epizootic in many parts of the
world. Common in summer and autumn. Flies transmit from animals to animals.
Cause: Moraxella bovis.

Symptoms:
1. Conjunctivitis, copious lachrymation, photophobia and blepharospasm.
2. Slight elevation of temperature and anorexia.
3. Within two days of onset of symptoms corneal opacity develops followed
by ulceration and finally vascularization may occur.
4. Purulent discharges may be seen.
5. In the later stage, opacity decreases and complete recovery occurs with 1
year immunity.
4
The Lens
Cataract: Opacity of the lens due to disruption of the lamellar structure of lens
fibres. Ultimately lead to blindness or impairment of vision. May be partial or
complete and also be congenital or acquired. Very common in dog.
Causes:
A. Congenital:
a. Failure of hyaloids artery
b. Abnormal arrangement of lens
c. Hereditary
d. Chicks from Vitamin E deficient Fowls
B. Acquired:
a. Luxation
b. Impaired nutrition
c. Degenerative ocular diseases
d. Trauma
e. Senility
f. Diabetes mellitus
g. Nutritional- deficiency of vitamin D, vitamin C and cystein.
h. Toxins
i. Poisons- ergot
j. Absorbed radiation.
The Uveal Tract

Anterior uveitis/Iridocyclitis: Inflammation of the iris and cilliary body.
Posterior uveitis: Inflammation of the cilliary body and choroid.
Anterior synechia: Adhesion between anterior surface of the iris and posterior
surface of the cornea.
Posterior synechia: Adhesion between Posterior surface of the iris and the
anterior surface of the lens capsule.
5
Glaucoma
Glaucoma is not a disease entity but a composite of clinical and pathological
manifestations that result from persistent increase in intraocular pressure.
Glaucoma may be unilateral or bilateral.
Classification:
1. Primary glaucoma / primary angle closure glaucoma /narrow angle
glaucoma: Due to defective development of the iridocorneal angle.
2. Secondary glaucoma: due to:
a. Occlusion of the pupil due to posterior synechia iridocyclitis/anterior
synechia, luxation of lens, intraocular haemorrhages and neoplasms,
detachment of retina and inflammation followed by trauma of the
eyeball.
b. Occlusion of the filtration angle due to
Gross lesions:
1. Globe is enlarged
2. Cornea , lens and vitreous may be opaque.
Microscopic lesions :
1. Cornea : Edema & bullae formation .
2. Iris : Thin & atrophic
3. Ciliary process : Thin , atrophic , compressed
4. Choroid : Compressed & atrophic .
5. Retina : Degenerative change.
6. Optic nerve : Depression of optic disc or cupping of optic disc .( In
elephant normally cupping of optic disc present)
6
Pathogenesis of Glucoma
Pathogenesis of Glucoma
Aqueous humor is secreted into the posterior chamber by colliery

epithelium
From the posterior chamber, this fluid moves through the pupil into the
anterior chamber.
This fluid drains from the anterior chamber at the filtration angle near
the limbus, where it passes through the spaces of Fontana and
eventually reaches the veins of the limbus through the canals of scheme.
If the filtration angle or pupil is occluded for any reason
Due to occlusion of filtration Due to occlusion of pupil, aqueous

angle, aqueous humor canot drain humor canot drain from the
from the anterior chamber to posterior chamber to anterior
veins og limbus. chamber .
Excess aqueous accumulates in

Excess aqueous accumulates in posterior chamber and thus
anterior chamber and thus give increases the pressure of posterior
pressure to the posterior chamber chamber
Development of glucoma
Neoplasm of Eye & Adnexa :

2. Melanoma
3. Papilloma
4. Retinoblastoma.
7
EAR
External ear :  Concha
 External auditory meatus
 Ceruminous Glands (Sebacious & apocrine)
Middle Ear :  Typanic cavity
 The Ossicles- Melleus, Incus & Stapes
 The Eustachian tubes / auditory tubes
Internal Ear :  Membronous labyrinth
 Osseous labyrinth
Pathological condition of external ear
Otitis Externa:
Causes:
1. Foreign Bodies
2. Ectoparasites
a. Psoroptes communis
b. Otodectes cynotis
c. Otobius megnini
d. Stephanofilaria zaheeri
3. Fungus: That produces dermatomycosis.
4. Specific Diseases: Actinomyces bovis
Symptoms:
1. Presence of thick pus in the external auditory meatus (otorrhoea) and
thickening of the lining of the meatus.
2. Shaking of head.
Pathological condition of middle ear

Otitis Media:
Inflammation of the middle ear . Normally there is no communication between
the external and middle ear as the tympanum seals the passage. Inflammation
may reach to middle ear by rupture tympanic membrane or the way of
eustachian tubes.
Causes:
1. Penetration of foreign bodies
2. Ear mites
8
Sequelae of otitis media:

1. Otitis interna
2. Deafness
3. Paralysis of 7th cranial nerve
4. Meningitis
5. Encephalitis
Pathological condition of inner ear

1. Otitis interna
2. Vestibular syndrom / Acute vestibular ataxia.
3. Congenital deafness

FASVM, SAU
Pathology Skin and Appendages
Introduction
 This consists of the skin and its associated structures like adnexa (sweat
and sebaceous glands), nails, scales, feathers and hair.
 The skin is the single largest organ in the body and represents a physical
barrier to the animal to protect them from environmental hazards.
 It is the visible and accessible organ in the body; however it is by far the
most overlooked both clinically and at PM examination.
Important Functions of the Skin

 Prevents fluid loss and heat loss against external physical and chemical
agents.
 It conserves critical substances particularly H2O
 It synthesis vitamin D
 It excretes excess water, urea etc.
 It stores carbohydrates and fats
 It also filter harmful ultraviolet rays from the sun
 It is an organ of immunocompetence like dendritic cells which present
antigens to the immune system.
Though the skin is flexible, soft in some areas and elastic, it is vulnerable to
damage by chemical or physical or biological insults. It is divided into 3 layers:
1. Subcutis or hypodermis
2. Dermis
3. Epidermis
skin/dr.sajeda/dop/fahvm/sau 1
Common terminologies used in skin pathology
Macroscopic Terms
Macule : A spotted area of <1.0cm in size characterized by its flatness and
usually distinguished from the normal surrounding skin by its
colouration which may be reddish. When it is >1cm it is called
patches.
Papule : This is an elevated solid area of 5mm or less in diameter.
Nodule : An elevated solid area greater than 5mm in diameter.
Plaque : This is an elevated flat topped area usually greater that 5mm in
diameter.
Vesicle : This is a fluid-filled area of 5mm or less in diameter.
Bullae : This is a fluid-filled raised area greater than 5mm in diameter. It is
also known as a large blister.
Blister A common term used to describe a vesicle and pustules

Pustule : This is a discrete pus-filled raised area.
Wheal : This is an itchy transient elevated area with variable blanching
which could be reddish or bluish or erythema formed as a result of
dermal edema especially in light skins or hairless areas.
Excoriation : This is a traumatic lesion characterized by the breakage of the
epidermis causing raw or linear or jagged area. It is caused either by
barbed wire or rough substances or from scalpel blade cut.
Scale : An accumulation of loose fragments (flakes / dandruff) of cornified
skin; can be primary (eg primary seborrhea) or secondary (eg
chronic inflammation).
Crust : Accumulation of dried material (eg exudate, blood /serum, scale,
medication) on skin surface; can be primary (eg primary seborrhea)
or secondary (eg self-trauma, pyoderma, etc).
Comedo : A hair follicle lumen plugged with cornified cells and sebaceous
material; can be primary (eg Schnauzer comedone syndrome) or
secondary (eg demodecosis).
Lichenification : A thickening and hardening of the skin with exaggeration of the
superficial markings.
Callus : A thickened, rough, alopecic, lichenified plaque that develops on the
skin.
Microscopic Term
Hyperkeratosis: This is an increase in the thickness of the stratum corneum. It
may be absolute, which is more common, or relative which occurs due to the
thinned underlying epidermis. This can be of 2 forms:
1. Orthokeratotic hyperkeratosis: this is an increase in the anucleated
stratum corneum layer.
2. Parakeratotic hyperkeratosis: increase in the nucleated S. corneum layer.
 Both are common findings in any chronic dermatosis. They simply imply
altered epidermopoiesis, whether inflammatory, hormonal, neoplastic or
developmental in origin.
 The presence of diffuse parakeratotic hyperkeratosis is most consistent with

ectoparasitism, Zinc responsive dermatoses, some vitamin A-responsive
dermatoses, thallotoxicosis, dermatophilosis and dermatophytosis.
 Diffuse orthokeratotic hyperkeratosis suggests endocrionopathies, nutritional
deficiencies, secondary seborrheas and developmental abnormalities (
Ichthyosis, hypotrichosis, colour mutant alopecia).
Hypokeratosis: This is a decrease in the thickness of the s. corneum.
 It is much less common that hyperkeratosis and reflects an exceptionally
rapid epidermal turnover time and/or decreased cohesion between cells of
the s.corneum.
 This may be found in seborrheic and other exfoliative skin disorders.
 It may also be produced by excessive surgical preparation of the biopsy site
or by friction and maceration in intertriginous areas.
Dyskeratosis: This is a premature and faulty keratinization of individual cells
of s.corneum.
 The cells are characterized by swollen and diffusely esonophilic cytoplasm
and condense dark staining nuclei.
 The condition is seen in pamphigus complex, lichenoid dermatoses,
papilloma, squamous cell carcinoma, keratoacanthoma and warty
dyskeratoma.
Hyperplasia: This is an increase thickness of the non-cornified epidermis due
to an increased number of epidermal cells.
 The term acanthosis is often used interchangeably with hyperplasia.
However, acanthosis specifically indicates an increased thickness of the
stratum spinosum and is usually due to hyperplasia and occasionally to
hypertrophy of cell of the c. spinosum.
 This condition is often accompanied by vete ridge formation in which “pegs”
of epidermis appear to project downward into the underlying dermis.
Hypoplasia: It is decreased thickness of the non-cornified epidermis due to a
decrease number of cells.
 Atrophy is decreased thickness of the non-cornified epidermis due to a
decreased size of cells.
 An early sign of epidermal hypoplasia or atrophy is the loss of the vete
ridges in areas of the skin where they are normally present.
Acantholysis: Loss of intracellular connections resulting in intraepidermal

clefts, vesicle and bullae.
 Acantholysis may be caused by severe spongiosis, ballooning degeneration,
proteolytic enzymes released by neutrophils or eosinophils in inflammatory
process, developmental defects as in bovine familial acantholysis and
neoplastic transformation as in squamous cell carcinoma, actinic keratosis
and warty dyskeratoma.
 Marked acantholysis is seen with the autoimmune pemphigus complex.
Exocytosis: It is the migration of inflammatory cells and /or erythrocytes
through the intercellular spaces of the epidermis. Exocytosis of inflammatory
cells is an indication of any inflammatory dermatoses.
Erosion: This is a discontinuation of the skin exhibited as an incomplete loss of
the epidermis with the basement membrane intact. This should be differentiated
from epitheliogenesis imperfecta which is a developmental defect.
Ulceration: Discontinuity of the epidermis with loss of basement membrane,
portions of the dermis and subcutaneous part. It may be seen as a raw, bleeding
surface often contaminated and may contain granulation tissue, pus or scab.
Hyperpigmentation (Hypermelanosis): This is the presence of excess melanin
deposited in the epidermis. It may be focal or diffuse or confines to the basal
layer. It is seen in chronic inflammatory and neoplastic dermatoses.
Hypomelanosis: Presence of decreased melanin in an area otherwise normally
high pigmented e.g. iris. It may be associated with congenital or idiopathic
defects in melanization.
Dermal Defects
Dermal collagen hyalinization: This is the degenerative change of dermal
collagen in which there is confluence, increased eosinophilia.
Dermal fibroplasias: Characterized by increase in the formation of and
development of fibrous tissue element in the dermis. It is often synchronously
found along with granulation tissue in which there is accentuation of the
vascular element within the tissue.
Fibrosis of the skin: This is the latter of fibroplasias and is characterized by
increased fibroblasts and collagen as well as decreased vasculature of the
dermis. Sclerosis or scar tissue formation is usually the end point of dermal
fibrosis.
Papillomatosis: This is the projection of the dermal papillae above the skin
surface. It is seen in chronic inflammation and neoplastic dermatoses. It is
associated with epidermal hyperplasia. There are 2 types:
1. Villus type- these are dermal papillae covered by one or two layers of
epidermal cells projecting into a vesicle or bullae.
2. Fistulous type- this is devoid of cellular covering and also projection into
a vesicle or bullae.
Degenerative conditions of the skin

These include
 Hydropic vacuolar or ballooning degeneration seen in viral diseases
especially and in conditions of irritation by exogenous substances.
 Vesiculation and bullae formation.
 Abnormal depositions e.g. mineral, amyloid, carbohydrates etc.
 Hydropic degeneration
Congenital Anomalies
Epitheliogenesis imperfecta: This is congenital inherited, discontinuation of
the squamous epithelium of the skin and oral mucosa membrane. It occurs
occasionally in calves and piglet and extremely rare in dogs.
Congenital Ichthyosis: This is the presence of cutaneous lesions resembling
fish scales. This skin is composed of large horny plates separated by deep
fissures. It is seen in calves and dogs.
Congenital alopecia: This is hairlessness of varying degrees at birth. It is often
related to iodine deficiency. It may be partial to complete absence of hair. Seen
in all domestic animals.
Vegetative dermatoses: This is an inherited disease of land race breed of pigs.
It is characterized by hairless, papillomatous plaques on the skin and giant cell
pneumonia with fetalization of alveolar wall.
Photosensitization dermatitis
It is recognized as an entity in farm animals especially in sheep and cattle and
the clinical signs appear a few hours after exposure to strong sunlight. These
include:
 Burning or itching sensation
 Erythema and inflammatory oedema
 In cattle it affects mainly hair and unpigmented teat of udder.
 In sheep if affects the head and ear
 The lesion may heal in a week but may eventually become infected or
gangrenous
Pathogenesis
Photosensitization results from action of sunlight upon certain fluorescent
pigments which have accumulated in tissue over time. Three distinct conditions
can give rise to this type of accumulation-
Congenital porphyria photosensitization: This is a metabolic defect in the

synthesis of haeme pigment protoporphyrin resulting in the release of free
Uroporphyrin III and Coproporphyrin III which accumulates in the tissue and
serum.
This condition occurs spontaneously in cattle and swine. When it accumulates
and the sun acts on it, it becomes fluorescent and inflamed.
Hepetotoxic photosensitization: This is caused by phyllocrythrin, a

degradation product of chlorophyll which is excreted in the bile. Obstruction to
bile secretion as in hepatitis can give rise to unusual level of phyllocrythrin and
when the excretion capacity of the liver is deranged, the phyllocrythrin
accumulates in the blood and sensitized the animal to light.
Ingestion of certain plants such as Lantana camara can also cause
photosensitization.
The primary photosensitization: This is due to ingestion of exogenous
photodynamic agents such as plants, lush green stage or rapidly growing plants
like Hypericum perforatum (St. John’s wort). Hypericin obtained from H.
perforatum is such a photosensitization agent which becomes inflamed when
exposed to sunlight
Autoimmune skin diseases or Pemphigus

This occurs in cats, dogs and man and is characterized by formation of blisters
or vesicles on the skin or mucus membrane as a result of auto antibodies
directed against intercellular cement in the skin.
These antibodies can be demonstrated by immunoflourescent stain. The binding
of the auto antibodies to intercellular cement leads to acantholysis i.e. separation
of epidermal cells from one another, cleft formation, vesicles and bullae.
Types of Pemphigus
1. Pemphigus vulgaris: this is the most severe form which occurs in the
mucocutaneous junction of the nose and lip. The prognosis is poor. The
acantholysis is in the suprabasal region.
2. Pemphigus vegetant: this is similar to vulgaris but is accompanied by
papillomatous proliferations on healing.
3. Pemphigus foliacious: this occurs in the supracorneal region. There is
acantholysis and vesicle formation. The prognosis is good.
4. Pemphigus erythematous: this is milder than pemphigus foliacious.
5. Bullus pemphigus: subepidermal vesicles occur because the auto antibodies
are directed against the basement membrane of the skin and mucus membranes.
Alopecia
This is lack of hair, wool or feathers. The old hair falls out and further growth
does not occur. This is a symptom of many skin diseases such as dermatitis,
eczema, mange etc.
In fowls congenital lack of feather is known as apennosis and may be found
throughout the body or in some parts.
Etiology
In most of species, hair loss occurs normally in the spring and autumn for the
coat to be changed. However, hair loss may be due to failure of follicle to
produce a fiber or it may due to damage hairs previously.
A. Failure of follicle to produce hair fibers
1. Inherited hypotrichosis, symmetrical Alopecia. The skin in the affected
area becomes completely bald.
2. Congenital hypothyroidism “goiter” due to deficiency of iodine in dam.
3. Congenital, after viral infection of dam as in Bovine Viral Diarrhea in
cattle and sheep.
4. Infection of follicles or neurogenic due to damage of peripheral nerve.
5. Sertoli cell tumors in Male dog.
B. Damage of produced fibers: It is mainly symptomatic Alopecia due to
other diseases.
1. Dermatomycosis as ringworm, (dermatophytosis).
2. Poisoning of thallium or molybdenum.
3. Deficiency of copper and zinc and vit. A, vit. E.
4. Excessive palm- whale or soybean in milk replaces of calves usually
result in weakness of hair fibers.
5. Traumatic as in sweat itch of horses.
In case of symptomatic alopecia it is a temporary case or condition that will be
improved by removal of the original causes.
Pathogenesis
 In many of metabolic alopecia there is weakness of fibers, which
degenerated rapidly.
 In congenital Alopecia, there is failure in follicles to form fibers.
 Damages of nerve ending and blood capillaries are impaired.
 Chemical depilation may occur by cytotoxic agents- cytoplasmic
degeneration in follicle of hair (chemotherapy).
Eczema
This is a dermatitis characterized by vesicle formation, infiltration by
inflammatory exudates, watery discharge and development of scales and crusts.
Casues:
This occurs when the skin is in contact with allergens either applied on skin and
so called exogenous or arise from blood stream and known as endogenous
allergen.
A. Predisposing Factors
1. Nutritional deficiency, trauma and chemicals.
2. Genetic causes.
3. Prolonged soiling, dampness and accumulation of debris.
4. Constant scratching due to external parasites.
B. Exogenous Allergens:
1. Using of chemicals as antiseptics and disinfectants.
2. Some Ectoparasites as flea-saliva in dog and cat, which cause
hypersensitivity of skin.
C. Endogenous Allergens:
These are substances, which are ingested and absorbed through the gut and
introduced to blood stream and affect on the skin indirectly ingestion proteins.
Pathogenesis
Primary lesion is erythema, Spongiosis due to in intra and intercellular edema
forming vesicles which is characteristic for eczema, this leads to rupture of
vesicles and causes weeping of skin with formation of scabs. This occurs in
acute stage of eczema and may disappear rapidly Chronic form may persist
accompanied with parakeratosis and pachydermia.
Dermatitis
The term dermatitis include those condition characterized by inflammation of
the deeper layer of the skin, including the lymphatic with secondary
involvement of epidermis.
Etiology
The causes and types of dermatitis in all animals classified into:
1. Bacterial dermatitis:
 Due to invasion of bacteria as in udder impetigo in cattle.
 Pyoderma due to Staph. aureus.
2. Mycotic dermatitis:
 Dermatophilus congolensis in sheep, cattle, and horses.
 Ringworm
 Strawberry foot Rot (Dermatophilus pedis).
3. Viral dermatitis
 Poxvirus infection.
 Contagious pustular dermatitis.
 Lumpy skin disease in cattle.
 Foot & Mouth disease, vesicular exanthema.
 Vesicular stomatitis – mucosal disease.
 Blue tongue – bovine malignant catarrh.
4. Parasitic dermatitis
 Mange and other mites.
 Myiasis of hypoderma and others.
5. Nutritional dermatitis: Deficiency of vit. B. complex, vitamin, A, zinc,
nicotinic acid, riboflavin, biotin, pantothenice acid.
6. Physical dermatitis
 Sunburn and photosensitization.
7. Chemical dermatitis
 Arsenical compound.
 Potassium- mercuric iodide.
8. Allergic dermatitis
Pathogenesis
 Involvement of deeper layers including blood vessels, lymphatic and
epidermis.
 Black necrosis at the site of inflammation.
 Erythema with other factors causes an increase in the thickness of skin
accompanied by edema.
 Pain or itching.
Neoplastic diseases of the skin

The skin is the most common site for neoplasia in dogs, horses, cattle and cats.
Neoplasm can arise from all structures in the skin. The tumour can be primary
or secondary.
In general, ectodermal neoplasms (from epidermis & adnexa) are benign and
many types of mesodermal tumours (from fibrous tissue, muscle, fat, blood
vessels) in contrast are histologically malignant and regularly exhibit locally
infiltrative growth and occasionally will metastasize.
Papillomatosis (Warts)
This is usually observed in cattle, horses, dogs and goats. The predilection sites
of this condition on the skin of cattle are the head, neck and shoulder. In horses
it is chiefly on the muzzle and lips. In dogs it is in the oral mucosa.
Gross
 The tumors are small, rounded, finely dimpled elevations or the
abnormally cauliflower-like appearance.
 Hair is absent from the lesion.
 The surface is grayish, rough and horny.
Histopathology
 The dermal papillae are drawn out into long, thin strands and they are
covered by thickened epidermis which matures in the regular sequence
from basal to superficial layers.
 The proliferation of epithelium is greatest over the top of the papillae and
here keratinization is incomplete.
 There is breakdown of intercellular bridges at the stratum granulosum
layer and their cytoplasm becomes vacuolated or homogenous and
acidophilic. There may be presence of inclusion bodies in these cells.
Others:
 Squamous Cell Carcinoma
 Melanosis
 Basal Cell and Adnexal Tumor
 Fibrosarcomas

FASVM, SAU
1
ENDOCRINE GLANDS
Endocrine glands are specialized organs that produce hormones for homeostasis.
Endocrine Glands are:
1. Pituitary
2. Thyroid
3. Parathyroid
4. Adrenal
5. Pancreatic islets
6. Pineal glands
7. Ovary and Testes
Pituitary Gland
The master glands of the body.
Mostly regulatory function on different endocrine glands. Therefore,
malfunction of pituitary glands disturb the functions of other glands. The
disturbances associated with hyper or hypopituitarism.
Hypopituitarism
Cause: Aplasia/Hypoplasia/inflammation/infections (Infection of brain sometimes
extended to pituitary).
Lesions
Dwarfism
Gonadal hypoplasia
Prolonged gestation
Diabetes insipidus (decrease production of ADH)
Hyperpituitarism
Cause: Adenomas/carcinomas.
Thyroid Gland
Hypothyroidism
Resulting from failure to synthesize adequate thyroid hormone with decreased level of
circulatory thyroxin.
Causes:
Aplasia
Hypoplasia
Inflammation (Thyroditis),
Various non-toxic goiters from iodine deficiency or goitrogen
Metastaic tumors that destroys thyroid glands
Biosynthetic defects in the thyroxin synthesis
DoES/Sajeda/DoP/FASVM/SAU
2
The essential features of hypothyroidism includes

Abnormally low basal metabolic rate
Affected animals become lethargic
Muscular weakness
Dilated Cardiomyopathy.
Hyperthyroidism
This disorder most common in cats but also seen in other species.
Causes
Hyperplasia
Adenomas/carcinomas
Hyperpituitarism
Lesions
Cervical swelling
Often coughing and dyspenia
Individual becomes active, alert but gradually depressed, weight loss,
polydipsia, polyuria.
GOITER
The term used for noninflammatory and non-neoplastic enlargement of the thyroid
gland. Associated with hypo or hyper thyroidism
Several forms exists

1. Simple goiter (hypolastic goiter/Colloid goiter)
2. Multinodular goiter (adenomatous goiter, nodular thyroid hyperplasia)
3. Exophthalimic goiter (goiter of hyperthyroidisrn, taxic goiter or Graves' disease)
1. Simple goiter (hypolastic goiter/Colloid goiter: have many causes and diverse
histopathologic features. Three general causes exists-
Iodine deficiency: Classical cause of simple goiter.
Goitrogen: Interferes with the biosynthesis of thyroid hormone. Many plants
especially with those of Brassica and Crucifera spp contain goitrogen.
Hereditary biosynthetic defects of thyroid hormone.
Grossly, thyroid glands are uniformly enlarged.
Microscopically, hyperplasia of the thyroid follicle. The follicles are lined by one or
more layers of tall columnar epithelial cells. New follicles often small and lacks
colloidal substance. At this stage it is called hyperplaslic goiter. Hyperplastic goiter
often progress to colloid goiter which is characterized by large follicles filled with
colloidal substances and lined by flattened epithelia.
3
Parathyroid Gland
Hypoparathyroidism: Decreased plasma calcium level (milk fever) and other titanic
convulsions.
Hyperparathyroidism (Primary or Secondary): Bone abnormalities/metastatic
calcification.
Pancreatic Islets
The common pathologic manifestation includes diabetes mellitus.
Diabetes mellitus
Diabetes means "siphon" or "o flow through" and mellitus refers to honey.
Causes: Occurs due to an absolute or relative deficiency of insulin which is
characterized by-
hyperglycemia, Dehydration,
Fasting Increased appetite and
Glycosuria, Ketosacidosis
Osmotic polyuria,
Polydipsia,
Pathogenesis: The pathogenesis of diabetes mellitus is complex and mostly lies on
the understanding of the function of insulin.
Insulin helps the glucose to enter into cells, as well as the transmembrane
transport of aminoacids, formation of glycogen, triglycerides etc.
In deficiency of insulin, glucose can not enter into cells and thus
hyperglycemia results.
When pass through the kidney and blood glucose level exceeds the renal
glucose threshold level, glumeruli filtrate large amount of glucose into
tubule (glycosuria).
The excess glucose in tubular

tubular cells rumen increasespolyuria.
which causing the osmotic pressure and
thus instead of re-absorption water reenters into kidney tubules from tubular
cells which causing polyuria.
4
ssClassification: Diabetes mellitus are divided into-

1. Primary or idiopathic diabetes mellitus: Primary diabetes mellitus are of two
types:
Type I: also termed insulin dependent diabetes mellitus, results from a reduction in
number of beta cells and absolute decrease insulin. Different virus infection is thought
to be the cause.
Type II: also termed as noninsulin dependent diabetes. This is most common type in
human; and has a much stronger genetic influence. Insulin levels are usually normal to
high, but are low with respect to the plasma glucose level.
2. Secondary diabetes mellitus: results from destruction of islets due to acute or

chronic pancreatitis or due to neoplasms. Common in humans and in animals, most
frequent in dogs and cats and occasionally in cattle and horses.
Lesions
Lesions include loss of beta cells, lymphocytic infiltration, fibrosis and amyloid
deposition.
Secondary effects are not well studied in animals

FASVM, SAU
Oncology
Oncology: The branch of pathology which deals with the study of tumor is
known as oncology.
Neoplasia
( New growth/Neoplasm/Tumor )
Definition: According to the eminent British oncologist Sir Willis: A neoplasm
is an abnormal mass of tissue, the growth of which exceeds and is
uncoordinated with that of normal tissue and persists in the same excessive
manner after cessation of the stimuli which evoked the change.
Exception: Carcinoma in situ is not a mass.
Tumor is virtually autonomous, functionless and preys on the host.
Solid tumor consists of
 Parenchyma- consisting of neoplastically transformed cells of epithelial
or mesenchymal origin.
 Stroma consisting of connective tissue & blood vessels.
Characteristic of a neoplasm: New growth of cells which-

 Proliferate continuously/ autonomously without control.
 Bear a considerable resemblance both morphologically and functionally
to the healthy cells from which they arise.
 Have no orderly pattern of growth.
 Serve no useful function for their hosts.
 Stems from a variety of causes that alter the molecular events involved in
the control of normal cell proliferation and differentiation.
Key elements- Uncontrolled proliferation and no useful function.
Gross appearance of neoplasm:

Gross appearances of neoplasm are not usually helpful in diagnosis of tumor
growth. But few points may be of some diagnostic value.
1. Enlargement- is the general concept of neoplasm, but there may be
exceptions, such as, most of the malignant carcinomas and melanomas
may never reach to the considerable size before they kill the patient.
2. In case of benign tumors there are found pedunculated growth with one
stalk at the base.
3. The malignant tumors grow by infiltration & invasion and the base is flat
& smooth.
4. In case of malignant neoplasm there may be found ulceration and
continuous bleeding.
1
Oncology/Dr.Sajeda/DoP/FAHVM/SAU
Classification & nomenclature of neoplasm
1. Classification on the basis of behavior
a. Benign tumor (Squamous cell papilloma)
b. Malignant tumor (Squamous cell carcinoma)
2. Classification on the basis of origin
a. Epithelial tumors ((Squamous cell papilloma))
b. Mesenchymal tumors (Leiomyoma)
c. Mixed tumor (Willm’s tumor- a malignant tumor of kidbey)
d. Tumors of totipotential cells (Teratoma)
e. Tumors of embryonic tissue (Retinoblastoma)
f. Tumors of embryonic vestiges (Chordoma)
3. Other classifications
a. Organ of origin
b. Naked eye appearance
c. Histology
d. Function
e. Etiology
Some important terminology:

Teratomas: Teratomas originates from totipotential cells which are normally
present in the ovary and testes.
Hamartomas: Hamartomas is a tumor like malformation formed by local tissue
or tissues which are haphazardly. It is a focal overgrowth of mature, normal
tissues in abnormal properties.
Neoplastic polyp: It is a pedunculated benign or malignant tumor that projects
above a mucoal surface and projects into the lumen. But the term polyp
preferably is restricted to benign tumor. Malignant polyps are better termed as
polypoid cancers.
Choristoma: It is a nonneoplastic mass formed in the ectopic (unusual) sites.
Carcinoma in situ/Preinvasive carcinoma: When dysplasia is marked and
involved the entire thickness of the epithelium, the lesion is known as
Carcinoma in situ/Preinvasive carcinoma. It is a epithelial neoplasm which has
all the features of malignancy but has not yet invaded through the basement
membrane. It is so termed as preinvasive stage of carcinoma. It may progress to
invasive carcinoma. If excise early, there is complete recovery.
2
Latent cancer: When the tumor is clinically silent but has the histological
features of carcinoma and does not metastasize. Prostate carcinoma in elderly
people.
Dormant cancer: After surgical removal and/or anticancer therapy there may
be no clinically detectable tumor remaining in a patient. In such a patient
malignant cells may remain occult/dormant at a distant site even for several
years and then grow causing signs and symptoms.
Nomenclature of Tumors:
NB: Some times the word malignant is used to indicate the malignant tumors, e.g.
malignant melanoma, malignant lymphoma.
3
A short histological classification and nomenclature of some selected neoplasms
are presented in the following table:-
Tissue of origin Benign Malignant
A. Epithelial tumors
1. Stratfies squamous epithelium Squamous cell papilloma
Squamous cell carcinoma
2. Transitional epithelium Transitional cell papilloma
Transitional cell carcinoma
3. Glandular/ductal epithelium Adenoma
Adenocarcinoma
4. Basal cell epithelium -
Basal cell carcinoma
5. Hepatocytes -
Hepatic cell carcinoma
6. Melanocyte Naevus
Malignant melanoma
7. Placental epithelium Hydatidiform mole
Choriocarcinoma
(Trophoblast)
B. Mesenchymal Tumors
1. Connective Tissue
a. Mature fibrous tissue Fibroma
Fibrosarcoma
b. Embryonic fibrous tissue Mast cell tumor
Myxosarcoma
c. Cartilage Chondroma
Chondrosarcoma
d. Bone Osteoma
Osteosarcoma
e. Adipose tissue Lipoma
Liposarcoma
f. Histiocytes Histiocytoma
Malignant histiocytoma
g. Mast cells Myxoma
Malignant mast cell tumor
2. Endothelium
a. Striated muscle Hemangioma
Hemangiosarcoma
b. Lymphatics Lymphangioma
Lymphangiosarcoma
3. Muscle
a. Smooth muscle Leiomyoma
Leiomyosarcoma
b. Blood vessels Rhabdomyoma
Rhabdomyosarcoma
4. Hematopoietic tissue
a. Erythroblasts -
Erythroid leukemia
b. Myeloblasts -
Myeloid leukemia
5. Lymphatic tissue
a. Lymph nodes, spleen, thymus -
Malignant lymphoma/ lymphosarcoma
b. Lymphoblasts -
Lymphocytic/lymphoblastic leukemia
6. Neural tissue
a. Glia Glioma
Glioblastoma
b. Neurons Ganglioneuroma
Neuroblastoma
c. Nerve sheath Melanocytoma
Neurofibrosarcoma
C. Mixed tumors
a. Kidney -
Wilm’s tumor/Embryonal nephroma
b. Mammary gland Benign mixed tumor of mammary
Malig mixed tumor of mammary
gland /Complex adenoma
gland/Complex adenocarcinoma
c. Salivary gland Benign mixed tumor of salivary
Malignant mixed tumor of salivary
gland/Complex adenoma
gland/Complex adenocarcinoma
d. Apocrine gland Benign mixed tumor of apocrine
Malignant mixed tumor of a.
gland/Complex adenoma
gland/Complex adenocarcinoma.
D. Tumors of totopotential cells Mature or benign teratoma
Immatute or malignant teratoma apocrine
4
Difference between Benign and Malignant Tumors
SL Characteristics Benign Tumors Malignant Tumors
1. Structures
a. Differentiation/Anaplasia Well differentiated. Well differentiated to anaplastic (undifferentiated)
b. Pleomorphism & Orientation of cells Absent & Not distribute. Present & Distributed.
c. Polarity Maintained. Lost.
 Not hyperchromatic;  Hyperchromatic;
 Not pleomorphic;  Pleomorphic;
d. Nucleus
 Nucleolus is little altered;  Nucleoli are usually large;
 Mitotic figures are few & normal.  Mitotic figures are numerous & abnormal.
e. Nucleus-Cytoplasm ratio Normal (1:4 to 1:6). Increased (maybe 1:1)
2. Growth
a. Rate of Growth Grow and expand slowly over years. Grow rapidly within few days or weeks.
By expansion. Do not penetrate basement By expansion & infiltration. Break through basement
b. Mode of Growth
membrane. membrane.
c. Continuance of Growth May stop growing or regress. Mostly progressive.
d. Size Usually small. Usually larger.
e. Stroma Well formed and abundant. Poorly formed and scanty.
3. Capsule, Invasion, Tissue destruction & Haemorrhage
Encapsulated-most tumors usually cohesive Not capsulated (rarely false capsule).
a. Capsule
& expansile mass.
Local invasion occurs and infiltrates surrounding
b. Local invasion No local invasion.
normal tissues.
c. Destruction of adjacent tissues Very little. Abundant.
d. Haemorrhage & Necrosis Little tendency. Common.
4. Metastasis Never occurs. Frequent.
 Moderate well formed blood  Numerous thin walled blood vessels seen.
vessels seen.  Blood supply not coordinated, so
5. Blood Supply
 Adequate blood supply, so no degeneration & necrosis of the tissues of the
degenerative changes. tumor.
Mostly due to mechanical pressure & Fatal almost invariably.
6. Clinical effects
obstruction. Usually not fatal.
7. Recurrence Do not usually recur. Recurrence is common.
5
Difference between Carcinoma and Sarcoma
SL Characteristics Carcinoma Sarcoma
Malignant tumors of epithelial Malignant tumors of
1. Definition
cells. mesenchymal cells.
Most common over the age of Most common in first & second
2. Age consideration
50. decades but occur at all ages.
3. Frequency A common malignant tumor. A much less common tumor.
4. Rate of growth Often slowly growing. Usually very rapidly growing.
5. Histological Structures
Epithelial cells of origin except Mesenchymal cells of origin
a. Resemblance of cells
in anplastic tumor. except in anplastic tumor.
Malignant cells are arranged in
Malignant cells are arranged in
b. Orientation of cells: groups or columns except in
diffuse sheets.
anplastic tumor.
Often well formed and
Stroma Mostly poorly formed and often
c. surrounds each group of
charcteristics separates the cells.
malignant cells.
d. Blood vessels Not numerous. Numerous.
Haemorrhage and Less extensive except in
e. Extensive.
Necrosis anplastic tumor.
f. In situ phase Occur Does not occur.
6. Metastasis
Occur early in regional
a. Lymphatic spread Uncommon.
lymphnode.
May occur but usually a little
b. Blood spread Occurs very early.
late.
c. Organs metastasize Liver and lung. Lung.
Many carcinomas are highly
7. Radiosensitivity Moe radioresistant.
radiosensitttive.
6
Normal cell division and Termination
When normal cells become detached from one another they undergo mitotic
division until contact with one another recurs. The signals that initiate and
terminate cell division emanate from the cell surface and are transmitted to the
nucleus by means of a series of primary and secondary chemical massages that
take place in the cell membrane and cytosol respectively.
The genes involved in normal cell division and differentiation are termed Proto-
oncogenes. These are now more than 30 known cellular Proto-oncogenes. The
protein products of Proto-oncogenes are divided into four major categories on
the basis of their functional activities. These categories are-
(a) Protein kinases,
(b) Proteins that bind with glutamyl transpeptidase(GTP),
(c) Growth factors, and
(d) Nuclear transcriptional proteins.
The activation and suppression of transcription of the Proto-oncogenes is
controlled by regulatory genes. The products of these regulatory genes either
initiate or terminate DNA synthesis and transcription of genes involved with
cell growth and differentiation. The phosphorylated proteins are generated by
the signal transduction pathways. They activate or inactivate the regulatory
genes , which “turn on” or “turn off” proto-oncogenic expression and cell
division.
Hence mutations responsible for neoplastic transformation may involve proto-
oncogenes directly or the genes that regulate their expression. Such mutation
lead to formation of abnormal gene product which fails to respond to the cell’s
normal feed back mechanisms. The effect of this is continuous and unregulated
cell division and neoplasia.
Regulatory genes
↓ regulate
Proto-oncogenes
↓ regulate
Cell division ------------------------------- Normal cell
7
Causes of Neoplasia
The causes of neoplasia are numerous and diverse. But all the causes induce
mutations in those portions of a cell’s genome that control mitotic division and
differentiation. The causes of these mutations include:
A. Spontaneous errors in DNA replication, including chromosomal
translocation.
B. Carcinogens: Environmental agents that causes tumor.
1. Various forms of radiations.
2. Chemical carcinogens.
3. Oncogenic viruses
4. Oncogenic parasites.
C. Predisposing/Risk factors
A. Neoplasms resulting from spontaneous genetic mutations:

Neoplasms arising from spontaneous genetic mutations may be difficult or
impossible to distinguish from those caused by known environmental
carcinogens (chemicals, radiation).
B. Carcinogens:
a. Various forms of radiations.
 Ultraviolet (UV) radiation: UV light from sunlight associated with
skin cancer in both humans and animals.
 Various forms of ionizing radiations: X-rays and gamma rays.
 Young growing organisms are more affected.
 In adults bone marrow, testis, intestinal mucosa are more affected
because there occur continuous mitosis.
b. Chemical carcinogens:
The possible rule of chemical for the growth of cancer has been described
in 1775 in England. The chemical carcinogens are of two types:
 Direct acting carcinogens- Do not require metabolic activity in the
body.
 Indirect acting carcinogens- require metabolic activity in the body.
8
Chemical carcinogens:
 Direct acting carcinogens:
 Alkylating agents  Acylating agents
 β-Propriolactone  1-Acetyl-imidazole
 Dimethyl sulfate  Dimethyl carboxylchloride
 Diepoxbutane and other epoxide
 Ethyl methane sulfonate
 Nitrogen mustard
 Indirect acting carcinogens
 Polycyclic and heterocyclic  Plant and microbial products
aromatic hydrocarbons  Afla toxin B1
 Benzanthracene  Betel nuts
 Benzopyrene  Cycasin
 Dibenzanthracene  Griseofulvin etc.
 Cigarette smoke, tars
 7-12-Dimethylbanzanthracene
 Aromatic amines, amides and azo
dyes  Other chemicals
 2-Nephthylamine  Nitrosamine and amides
 Benzidine  Insecticides and fungicides
 2-Acetylaminofluorene  Arsenic
 Dimethylaminobenzene  Vinyl chloride
 4-Aminophenol  Asbestos,
 3-Hydroxyzanthine  Chromium
 Nnickel etc.
c. Virus-induced neoplasms
The viruses causing neoplasm are called oncogenic viruses. In 1908 the rule of
virus in production of tumors has been established. The oncogenic viruses are
classified into 22 distinct taxonomic families. 7 DNA virus families and 15
RNA virus families.
Oncogenic viruses:
 In animals:
 Bovine papilloma virus-  Lymphosarcoma virus-
causes papilloma in cattle. causes lymphosarcoma in cattle.
 Avian leucosis virus-  Canine transmissible venereal tumor
causes avian leucosis in (CTVT) virus- Produce CTVT in
poultry. bitch.
 Marek’s disease virus-  Rous sarcoma virus-
causes Marek’s disease in Cause rous sarcoma in poultry.
poultry.
9
 In humans:
 Human papilloma virus  Hepatitis C virus
 Epstein-Barr virus  Kaposi sarcoma virus
 Hepatitis B virus  Human T-cell leukemia virus
d. Parasite induced neoplasms

Certain helminthic parasites have been associated with the occurrence of
specific types of neoplasms, but the mechanism is not well defined.
 Schistosoma hematobium- can produce carcinoma in the urinary bladder
of humans. In Egypt its incidence is high.
 Spirocarca lupi- cause fibrosarcoma in the esophagus of dog.
 Gongylonema neoplasticum- produce neoplasm in the stomach of rat.
 Heterakis isolonche- can produce fibrosarcoma in the cecal wall of the
pheasant.
 Cysticercus fasciolaris- the larval stage of Taenea taeniaeformis can
produce fibrosarcoma in the surrounding connective tissue.
 Eimeria stiedae- Papilliferous cystadenoma of bile duct epithelium in
rabbits.
D. Predisposing/Risk factor:
 Heredity/Genetic predispositions: Familial  Environmental factors:
or inherited.
 Age: Carcinoma occur over 50 years of  Diet
age and sarcoma mostly at young age.  Cigarette smoking
 Hormol influence: Breast and  Alcohol consumption
endometrial carcinoma (Oestrogen),  Air pollution
prostatic carcinoma etc.  Occupational hazards.
 Acquired premalignant or
precancerous disorders: Regeneration,
hyperplasia, dysplasia and metaplasia
provide fertile soil for spontaneous
mutations and malignant transformation.
10
Carcinigenesis (Pathogenesis)
 Carcinogenesis is the process of development of tumors. Mutation lies at
the heart of carcinogenesis.
 Mutation may be acquired in somatic cells by the action of carcinogens or
may be inherited. Spontaneous mutation may occur during DNA
replication, e.g. in regeneration and hyperplasia.
 Most tumors are monoclonal, i.e. a single mutant cell proliferates to form
the tumor mass.
 Malignant transformation results from mutation of protooncogenes,
cancer suppressor genes, apoptosis regulating genes and DNA repairing
genes. Genes.
 Carcinogenesis is a multistep process.
Molecular basis of Cancer
11
Note:
Radiation:
 UV radiation generates highly charged free radicals from water and oxygen
in the cytosol, which in turn damages DNA.
 UV light suppress cell-mediated immunity.
Chemicals:
 Initiations: All direct/indirect acting chemical carcinogen act as initiators and
react with nucleophilic (electron rich) sites of the cell, particulary DNA.
Initiators alone cannot form tumor. It causes rapid and irreversible changes.
 Promotions: Promoters (risk factors) are not mutagenic and cannot induce
tumor themselves. They lead to proliferation and clonal expansion of
initiated (mutated) cells. It causes reversible changes.
Virus:
 By interfering with the normal regulation and expression of proto-oncogenes
and anti-oncogenes in infected cells.
 By introducing viral encoded homologs of proto-oncogenes (viral-
oncogenes) in the host cell genome.
12
Metastasis/Spread of tumor
Malignant tumors spread by-
A. Invasion or local spread in the surrounding tissues
B. Metastasis or distant spread in the target organ.
A. Invasion or local spread in the surrounding tissues
 It is an active process. It occurs along the tissue planes e.g. surrounding
extracellular matrix, perineural spaces and vascular lumina as these are
less resistance to tumor growth.
 Cartilage and fibrocartilage of intervecertibral discs are extremely
resistant to neoplastic invasion. Muscles are less susceptible to invasion.
Step and Mechanism of Tumor Invasion:
ECM=Extra cellular Matrix
B. Metastasis or distant spread in the target organ

Metastasis: The process by which a primary malignant tumor spreads to form
secondary tumor at distant site discontinuous with the primary tumor.
Routes/Pathways of Metastasis:
 Tranccoelemic spread/Seedling of body cavities: By direct exfoliation of
tumor cells from a primary neoplasm into a body cavity with subsequent
implantation and growth of the cells on mesothelial surfaces, a process
referred to as seeding.
 Lymphatic spread: By invasion of lymphatics and transport of tumor cells
as emboli in the lymph
13
 Haematogenous or blood spread: By direct invasion of blood vessels
with dissemination of the neoplastic emboli via the blood stream.
 Implantation:
 By natural passage (hollow organs): Cells from the tumor of renal
pelvis, bronchi and bowel→washed/dropped down to the bladder,
bronchial tree and bowel respectively→ implantation→new growth.
 Inoculation: This is rare hazard in surgery. While operating on a
tumor, the sugeon may inadvertently implant some neoplastic cells
on the edges of the wound where a new tumor may develop or may
spread in different part of the body.
 Coitus: Cells of venereal tumor in dog may be implanted from the
glans penis to vagina or vice versa.
 Spread by nerves: Cells of tumor may penetrate along the perineural
lymphatics to a considerable distance.
Step and Mechanism of Metastasis (Lymphatic/Haematogenous route):
Image
14
Diagnosis of Cancer
Cytology Histopatholog Tumor Markers Immunohistochemistr Flow Cytometry Molecular Diagnosis

y y
Exfoliative Cytology: Exfoliateed Specimen: Tumor markers are biochemical

cells (stomach aspirates, sputum, Biopsy: A mass or a piece of indicators of the presence of tumor.
urine, vaginal/uterine discharge, tissue is removed for  Different types of antigens
fluid of body cavities). histopathology. e.g. Lymphnode  Different types of hormones
biopsy by excision, truecut needle  Serum enzymes
biopsy of liver & kidney.  Other markers
Fine Needle Aspiration Cytology Large Materials: Whole organ or
(FNAC): From the mass, part of organ. e.g. Breast.
lymphnode, liver etc.
Staining: Examinations:
 Papanicolaou Stain (PAP)  Sectioning: Paraffin & Frozen
 H & E Stain  Staining: H & E.
15
Clinical Effects of Tumor
Benign Tumor:
1. Local effects:
a. Discomfort and mechanical difficulties: During labour by leiomyoma
of the uterus.
b. Pressure in adjacent tissues: Benign meningeal tumor causing epilepsy.
c. Obstruction: Papilloma arising in bile duct may lead to jaundice.
d. Intussusceptions of gut: Leiomyoma or polyp of the gut.
e. Torsion of the tumor: Torsion of ovarian tumor leading to infarction and
acute lower abdominal pain.
f. Ulceration: Secondary bacterial infection and haemorrhage from surface
tumor.
2. Hormonal effects: Production of excess hormones. Benign thyroid tumor
causing thyrotoxicosis, pituitary adenoma causing gigantism, acromegali and
Cushing’s syndrome.
3. Malignant transformation: Villous adenoma of colon often transform into
adenocarcinoma.
Malignant Tumor: Almost always fatal if untreated.
1. Local effects:
a. Obstruction: Intestinal obstruction by carcinoma of colon.
b. Invasion & destruction of surrounding tissues including vital organs:
Carcinoma of cervix of uterus invades ureter.
c. Ulceration, haemorrhage & secondary bacterial infection: Melaena in
neoplasm of gut and haematuria in neoplasm of urinary tract.
d. Pain
2. Haematological changes:
a. Anaemia
b. Neutrophilic leucocytosis
c. Occasionally eosinophilia.
3. Starvation: If cancers in mouth, oesophagus and stomach.
4. Cancer cachecxia: Wasting condition with progressive loss of body fat due
to alteration in fat metabolism. The patient becomes lean with wekness,
anorexia and anaemia,
5. Excess hormone production: By tumor of endocrine gland.
16
6. Impairment of immune system: May occur in Hodgkin’s disease and
multiple myeloma.
7. Paraneoplastic syndrome: Endocrinopathies occur by tumor of
nonendocrine origin due to ectopic hormone production.
8. Death
Staging of cancers
It is the extent of spread. It determines the severity of the lesion and is of
clinical significance. Different staging systems are used. TNM staging system is
in generally used.
TNM staging system:
Grading of Cancer
The grade of a cancer is an assessment of its degree of malignancy or
aggressiveness. Grading is done on degree of differentiation, nuclear size and
pleomorphism and mitotic activity.
Grade I : More than 75% cell differentiation.
Grade II : 50-75% cell differentiation.
Grade III : 25-50% cell differentiation.
Grade IV : Less than 25% cell differentiation.
17

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Course Title: Systemic Pathology and Oncology (Theory)

Course code: PATH-261

How to do study systemic pathology? Approaches to good results…

Books Recommended of the course:

Systems of the body:

Diseases of Digestive System

Digestive system of chicken: has following parts-

Pathological lesions/disorders in the mouth/oral cavity:

Clinical signs of stomatitis:

Neoplasms of oral cavity:

Neoplasms of salivary glands:

A. Inflammatory degenerative lesions:

Esophagitis: Inflammation of esophagus resulting from foreign objects, wasting

2. In horse: it is due to gradual accumulation of ground or wholegrains or tough grasses

C. Motility disorders/ lesions: e.g. Reflux esophagitis.

Grossly: there is hyperemia, erosion and ulceration.

Megaesophagus: Segmental non-localized dilatation of the esophagus due to neuromuscular

Diseases/ Disorders of Rumen (fore stomach of ruminants)

Effect of bloat: it causes-

Ruminal Acidosis/Grain Overload/Acute Carbohydrate Engorgement

It is a sporadic disease of ruminants caused by ingestion of sharp foreign materials and

Piercing of reticulum by metallic or sharp objects during contraction

Can pierce and carry infection to the peritoneum, diaphragm, pericardium,

The most commonly associated bacteria are pyogenic bacteria:

Diseases in omasum: rare

Diseases of stomach and abomasum

Symptoms: Anorexia, vomiting and abdominal pain.

1. Acute Catarrhal gastritis: Characterized by the increased mucus secretion.

2. Acute hemorrhagic gastritis: characterized by presence of free blood (without inflammatory

4. Chronic hypertrophic gastritis (Giant rugal gastritis/ gastritis hypertrophia gigantica):

Microscopically: Loss of partial cells with compensatory hyperplasia of goblet cells,

Tumors stomach and abomasum:

Diseases of the Intestine:

Causes of inflammation of intestine:

Lesions: Depend on causes.

Peritonitis: Inflammation of the peritoneum usually due to secondary numerous diseases

Tissue reactions: As peritoneum is lined by secretory serous epithelium, it produces huge

Some special note:

Hydroperitoneum (inflammatory) /Ascites (noninflammatory)

Disease of Liver and Biliary System

B. Degeneration and Deposits in the liver:

Types of hepatitis: Based on severity, there are three types of hepatitis-

3. Toxic hepatitis or toxic liver disease:

Mechanism of Toxic Liver Disease:

Characteristics: Cirrhosis is characterized by-

5. Hemorrhage (As liver produce prothrombin).

Diseases of Bile Duct & Pancreas

Cholangitis: Inflammation of the bile duct.

Cholecystitis: Inflammation of the gall bladder.

Pancreatitis: Inflammation of the pancreas. It is very rare in domestic animals.

Intended Learning Outcomes/Objectives (ILOs): The students will be able to -

1. The Systemic Circulation:

Important points to be considered:

Short description on congenital cardiac anomalies:

ii. Atrial Septal Defect [patent foramen ovale (PFO)]:

iii. Ventricular Septal Defect (VSD):

iv. Atrioventricular septal defect (AVSD):

b. Right to left shunts: