COCCIDIOSIS

INTRODUCTION
 Sub phylum
 Sporozoa

 Class

 Coccidia

 Family

 Eimeridae Sarcosystidae
 Eimeridae
 Organisms commonly called coccidia are typically
intracellular parasites of epithelial cells of intestine of
vertebrates with few exceptions.
 All forms have a single host in which they undergo
asexual (Schizogony or merogony) and sexual
(Gametogony) cycle of reproduction.
 Sporulation of fertilized zygote usually takes place
outside the host.
 Coccidiosis is caused by Eimeria spp and Isospora spp.
s.no species location pathogenicity

1 E. tenella Caeca Most pathogenic - Caecal

Coccidiosis
CHIKEN
2 E. brunetti Lower small intestine, Caeca, Most pathogenic- Rectal
rectum, Cloaca Coccidiosis

3 E. necatrix Jejunum, mid-gut and other parts Most pathogenic- Intestinal

of large intestine coccidiosis

4 E. maxima Mid-gut Medium/ highly

pathogenic intestinal
Coccidiosis
5 E. acervulina Duodenum Mildly pathogenic

6 E. mivati Duodenum and Rectum More pathogenic

7 E. mitis Duodenum and jejunum Mild pathogenic

8 E. praecox Duodenum Mild/ Non- pathogenic

TURKEYS
1. E. adenoides small intestine and Most pathogenic
large intestine

2. E. gallopavonis Lower S.I, caecum, Moderately

colon pathogenic/ Non-
pathogenic
3. E. meleagridis Small intestine, Caecum Mildly pathogenic
and Rectum

4. E. meleagrimitis Small intestine Markedly

pathogenic

5. E. dispersa Small intestine Mildly pathogenic

GEESE

1. E. truncata Kidney Highly pathogenic

2. E. anseris Small intestine Low pathogenic

3. E. nocens Posterior small intestine Moderately pathogenic

CATTLE
1. E. zuernii Small intestine and Highly pathogenic
large intestine
2. E. bovis Ileum, caecum and colon Common pathogenic -
clinical coccidiosis
3. E. alabamensis Small intestine, caecum Non- pathogenic
and upper colon
SHEEP

1. E. ovinoidalis Caecum and colon Highly pathogenic

2. E. crandallis Caecum and colon Mildly pathogenic

Goat

1. E. arloingi Caecum and colon pathogenic

RABBIT

1. E. steidae Liver Pathogenic

2. E. intestinalis Intestine Pathogenic

3. E.flavescens Intestine pathogenic

 Horse

1. E. leukarti Small intestine Pathogenic in

heavy
infections

Pigs

1. I. suis Jejunum and small Pathogenic,

intestine not frequent
2. E. debliecki Jejunum and S.I Pathogenic,
not frequent
DOG
1. I. canis Small intestine and large Mildly Pathogenic
intestine

Cat

1. I. rivolta Small intestine Pathogenic

and large
intestine
2. I. felis Small intestine Mildly
and caecum Pathogenic
MORPHOLOGY
 Oocysts
 Most common shapes are spherical, ovoid/ ellipsoidal.

 It have refractile shell and some species with a small

pore at one end called micropyle covered with a
prominent polarcap.
 An outer wall enclosing 4 sporocysts each containing 2
sporozoites in the sporulated oocyst which is the
infective stage.
LIFE CYCLE 
 Prepatent period: In poultry- 5 days.
 Three phases
 Sporulation
 Infection and
schizogony
 Gametogony and Oocyst formation
EPIDEMIOLOGY
 Agent
 Production of oocysts

Immediately after prepatent period, oocysts

are passed in very large number in the faeces,
eg: E. tenella.
Occasionally small number of oocysts are
found in the faeces several months after a
single infection.
 Reproduction potential of a species of coccidium after
ingestion by a susceptible host influences the number of
oocysts. Eg. high biotic potential of E. tenella.
 Number of viable sporulated oocysts ingested by a host
influences the oocyst production.
 Increased resistance of host influences depressed oocysts
production.
 Caecal plugs in caecal coccidiosis retard the passage of
oocysts in the faeces.
 Causation of disease
 It depends on,
 Virulence of coccidium, eg: E. tenella and E.

necatrix
 Number of oocysts ingested.

 Oocysts introduced in empty crop causes a more

severe infection.
 Feeding calcium carbonate in excess of 3% in feed.

 Age of the host.

 Host
 Age

1 to 2 weeks- less susceptible

3 to 6 weeks – most susceptible
More than 6 weeks – resistant
Susceptibility increases with age in E.tenella.
 Breed
 White Leghorn, Rhode Island and Newhampsire are
resistant; Barred Plymouth Rock, Gersey White Giant
and Light Sussex are susceptible; Breeder and Layer
pullets are at greatest risk.
 Transmission

 Depends on the type of housing and management and by

ingestion of oocysts.
 Vitamin A defeciency increases the susceptibility to
coccidiosis.
 Transmission is mainly by faecal oral route.
 Risk factors
 In intensive management system, incidence is more
common.
 Reduced incidence in birds kept on wire floors and solid
floor houses.
 Dirt condition, overcrowding of stock results in greater
accumulation of oocysts and spread of infection.
 In broiler production, overcrowding with high
temperature.
 Carriers
 Mechanical carriers- sparkling beetles, migratory birds
and birds recovered from infection.
 Immunity

 Previous exposure results in species - specific resistance.

Some species induces a solid immunity, other species
need several infections and is self – limiting in nature.
Both CMI and humoral immunity are elicited.
 Immunity is due to 2nd generation schizogony;
 Trickle infection: Continuous level of ingestion of
oocysts induces very strong immunity but cause damage
the intestine.
 Severity of disease increases with concurrent infections;
Marek’s disease increases the severity of coccidiosis.
 Environment
 Favourable conditions
 Optimum temperature and : Temperature: 25- 32◦C.
 Survival of oocysts in the soil is about a year and
during winter.
 Unfavorable conditions
 Both unsporulated oocysts and sporulated oocysts are
extremely sensitive to desiccation (greater than 56◦C is
lethal) Direct sunlight is lethal to the parasite.
 Below 10◦C, cool and dry conditions, freezing kill the
oocysts.
 Bacterial or fungal growth kills / lethal to parasite.

 Chemical disinfectant: 10 % ammonia or methyl

bromide kills the oocysts.
PATHOGENESIS
 Caecal Coccidiosis
 Pathogenesis
 E. tenella is primarily responsible for caecal
coccidiosis but gametogenous stage of E. necatrix and
occasionally some stage of E. brunetti can cause;
Morbidity-100%; Mortality- 80 %.
sporulated oocysts are ingested by the birds and
mechanical and chemical factors in the gut cause the
release of sporocysts and then sporozoites in the
intestinal lumen.
 The sporozoites invade the intestinal mucosa and
transform in to round bodies called trophozoites.

 trophozoites grow and form in to 1st generation

schizonts.


 Nuclei of 1st generation schizonts develop in to sickle

shaped bodies called merozoites.
 Merozoites break the schizont as well as epithelial lining
and come in to the lumen, then each merozoite invade
other epithelial cells of alimentary tract.

 these merozoites grow in to trophozoites and then in

to 2nd generation schizoint in the epithelial cells.
 These merozoites again invade other epithelial cells and
sexual phase of life cycle starts.

 There is development of gametocyte intracellularly

which differentiate in to micro and macrogametocytes.
 Microgametocyte releases many microgamete which is
motile.
 Macrogametocytes transform in to macrogamete
 Fertilization takesplace and formation of oval shaped,
thickwalled oocyst.

 Oocysts are liberated by rupture of epithelium and

passed through faeces.
 The harm done to the host by the parasite is due to the
destruction of the epithelial cells.
 There is denudation of mucosa tissue damage, including
rupture of capillaries, results in loss of blood.
 The shock and the drastic interference with digestion
causes weight loss, poor feed conversion, haemorrage
anaemia and often the bird dies.
 Measurment of an aminoacid marker of muscle
catabolism in muscle and plasma of chickens infected
with caecal parasite Eimeria tenella demonstrated an
increase catabolism indicative of breast muscle
breakdown.
 These results indicated muscle breakdown is correlated
with intensity and duration of infection and also shows
that, muscle catabolism is a general feature of poultry
coccidiosis.
CLINICAL SIGNS
 Clinical form: Occurs due to the ingestion of large
number of oocysts over a short period and is
characterized by the presence of soft faeces with blood,
dullness, listlessness, drooping feathers, anaemias,
paralysis and death.
 Sub clinical form: Poor weight gain and poor conversion
rate.
 Lesions: Presence of dilated caeca with mixture of
clotted and unclotted blood, caseous caecal contents
adherent to mucosa, caseous plugs detached from
mucosa and shed in the faeces; White spots and
petechiae in caeca.
 Intestinal Coccidiosis
 Pathogenesis
Both acute and chronic coccidia can occur by
E. necatrix but sub clinical form is more
common. Death can occur within 5-7 days.
 Clinical signs
 Similar to caecal coccidiosis.Chronic watery
diarrhoea with blood (mucous droppings in E.
maxima infection); stunted growth, reduced egg
production, listlessness, anorexia, soiling of vent
and feathers; recovered birds are unthrifty and
emaciated for a long time.
 Lesions in the midgut
 Second generation schizonts accumulation in deep
mucosa as minute grayish white spots.
 Balooning of intestine filled with clots of blood/ fresh
blood and severe haemorrhage at 5-6 days after
infection.
 Intestine greatly thickened, dull red with fragile lining
and friable with gangrene.
 E.maxima - Salmon pink exudates and haemorrhage.
 Rectal Coccidiosis
 Occur by E.brunetti in small intestine to cloaca.
 White fluid droppings mixed with blood and mucosa.
 Coagulative necrosis and slight haemorrhage.
 Loss of body weight and reduced feed intake and in
appetence.
COCCIDIOSIS IN TURKEYS AND GEESE
 Pathogenesis
 Turkeys

 E. adenoids is the primary cause of turkey coccidiosis.

 Age: Young birds are highly susceptible especially at 4-5

weeks.
 Risk Factors
 Intensive breeding (result in heavy loss)
 Over crowding.
 Poor sanitation- dampness of house.
 Sporulation period- 1 day; P.P- 5 days.
 Pathogenicity by gametogony and schizogony.

 Clinical cases: Intestines with catarrhal

inflammation with or without haemorrhage;
Swollen and oedematous intestine with petechial
haemmorhage on the mucosa of caeca; Intestinal
contents are pasty and orange coloured, then
become compact, caseous, mucoid with blood;
tucked head under wings in affected cases.
 Geese
 Haemorrhagic enteritis by E. anseris.
 E. truncata- Mortality- 100 %, marked
emaciation, muscular in coordination,
enlargement of kidney with light colour,
numerous white nodules, streaks and lines and
destruction of kidney tubular cells; acute
nephritis may be seen.
 Diagnosis
 Correct and early diagnosis depends on 2 factors
 History of the flock
 Finding various types of lesions and their locations by
P.M. examination.
 Others
 Faecal examination for the presence of oocysts is of
little significance in severe out breaks and clinical
cases, as the mortality starts before the discharge of
oocysts.
 Examination of gut scrapings for the presence of
schizonts and unsporulated oocysts.
 Study of sporulated oocysts by allowing sporulation
of oocysts after mixing faeces with several volumes
of 2.5 % Potassium dichromate solution for 1 day to 2
weeks.
 TREATMENT
 Aim of the treatment is to allow sufficient schizogony
develop in unaffected birds to stimulate their resistance.
 Eg: Sulphonamides have the great effect on II stage
schizont without inhibiting I stage schizogony and
increases the resistance.
 Fully recommended dose should be given and withdrawn
gradually by reducing half of the dose, otherwise it is
lethal.
COCCIDIOSTAT
s Drug Dose Coccidia Stage of
. coccidia
n
o

1 Amprolium 125 ppm in feed / E. tenella, E. I and II

. water for 6 days necatrix and Schizonts
also E. maxima

2 Amprolium + 125 ppm + 8 ppm in Extended I and II

. Ethopabate feed/ water for 6 days spectrum Schizonts

3 Sulphaquinoxaline 0.5 % in feed, 0.043 % E. tenella, E. II Schizonts

. in drinking water for 2 necatrix and E.
days with 3-5 days acervulina
interval.
4 Sulphaquinoxaline Synergistic; 14 E. tenella, E. I and II
+ Pyrimethamine ppm + 45ppm in necatrix and Schizonts
feed/ water E. acervulina

5 Nitrofurazone + 55 mg/kg + 55 mg/ E. tenella and II Schizonts

Furazolidone kg E. necatrix

6 Ionophore
compounds

a Monensin 0.121 % in feed Superior to

amprolium

b Lasolacid 0.005 - 0.0075% in High degree

feed of activity

c Salinomycin 0.01% in feed Significant

activity
COCCIDIOCIDALS
1. Robenidine 0.0066% I Schizonts
CONTROL
 Primary prophylaxis in vaccination Coccivac - vaccine
with live attenuated oocysts of E. tenella, E. maxima, E.
acervulina, E.mivati and chicken isolates
 Route - Eye spray/cabinet spray/ in feed

 Age -  day old healthy chicken

 Precaution - vaccine sensitive to anticoccidials

 Other vaccines are Livacox - Q ( attenuated quadrivalent

vaccine), Immunocox
 Coccivac-D (8 species) for breeders and layers
 Initial infection of 100 -700 oocysts/ each species
followed by repeated daily doses of 1-5 oocysts for 20
days produces immunity by trickle infection which is
reinforced by reinfection of oocysts in the litter.
 Selective breeding of domestic fowl is effective control
method to increase the genetic resistance of the host.
 Nutritional supplement/ antagonism- Vitamin- A for
recovery of the host; Vitamin-k to reduce the mortality
due to haemorrhage and a high protein diet.
 Isolation of sick birds.

 Reduced drug rate to older birds allows limited

exposure to developing coccidia so that it leads to
acquired immunity.
 Good ventilation to reduce humidity in the
house to keep the litter dry. Heaping the litter for
24 hours to reach a temperature of 50◦C and
forking for destruction of oocysts.
 Avoidance of contamination of feeders and
waterers with droppings.
 Continuation of anticoccidials in water for 5
days.
 Burning the infected materials and sprinkling the
quick lime @2-3 kg / 10 sq.feet over the litter.
 Avoidance of overcrowding in poultry houses.
Isolation of young chicks from adults.
 Keepthe waterers and feeders at higher level.
Feeding chicks with coccidiostat in chick mash.
Thorough disinfection and fumigation
(Ammonia + Potassium permanganate) in the
premises before the entry of newly hatched
chicks.
 The oocysts are destroyed by ultraviolet light, heat,
bacterial action in the absence of oxygen.
 Coccidiostats may be fed untill the birds are 809 week
old, after which they have ordinarily become immune.
 Lavamisole by its enhancing effect on cell mediated
immune responses is of special value in the prevention
of coccidiosis and have observed 100% survivability in
birds medicated with 2mg of levamisole/chick on 19 th
day of age.
 “Shuttle and rotation programmes” is used to combat
development of drug restistance. This programme
consists of a start medication, incorporating one
particular anticoccidial in feed, usually for the first three
weeks, followed by a change to another anticocidial in
the growerer feed. For the finishes period anticoccidials
are usually withdrawn from the feed to allow excretion
of drug residues before slaughter.
 Waterer and feeders should be washed weekly with hot
water and detergent.
 Waterers should be placed on wire platforms over floor
drains and the feeders should be raised high enough to
prevent their being fouled.
 Flies, rats and mice around the poultry houses should be
eliminated as they carry coccidia mechanically.
 If an outbreak of coccidiosis occurs, all sick birds should
be removed and ample food and water is to be given in
separate pen and remaining apparently healthy birds
should be treated with coccidiostat.
 All dead birds should be burnt or put some place where
chickens will never have access to it.
 Special rubber shoes should put on before entering pens
and should be cleaned thoroughly after each use.
COCCIDIOSIS IN CATTLE
 Morphology
 Oval oocysts
 Presence of micropyle and absence of micropyle
cap and residual cysts
 Sporocysts are elongate and ovoid with banana
shaped sporozoites.
 Life cycle
 P.P.P- 15 to 21 days

 Schizonts are seen in the central lacteals of the

intestinal villi.
 Epidemiology
 Agent
 Delay in the lifecycle may occur due to the arrestment
of schizogony stage and resumption occurs several
months later with subsequent shedding of oocysts;
Pathogenesis is by gamont stage of oocysts.
 Age of the host
 Primarily in young calves of 21 days old to 6 months
age; adults are also affected.
 Risk factors
 Massive intake of oocysts

 Overcrowding in unhygienic yards.

 Pasture where congregation of livestock around the

water holes.
 Lack of sanitation.

 In calves, which are recently turned out to permanent

calf-paddocks.
PATHOGENESIS AND CLINICAL SIGNS
 E. bovis
 Diarrhoea, dysentery, tenesmus, increased body
temperature and death.
 Lesion -Thickened, edematous, congested mucosae with
haemorrhage of caecum, colon and terminal ileum with
large amounts of blood.
 E. zuernii
 Most pathogenic; causes catarrhal enteritis.

 Lesions: caecum and colon are filled with semi fluid

haemorrhage material or fresh blood with mucus.
 Clinical signs:

 Watery faeces with unpleasant odour, soiling of posterior

part of animals.
 Severe cases: animals succumb and die after 7 days of
clinical signs.
 Chronic cases: Bloody/ bloodless pasty mucus faeces,
anorexia, convulsions, tremor, weakness, emaciation,
death due to pneumonia (secondary bacterial infection).
 Winter Coccidiosis
 By E. zuernii in cattle during cold/ stormy weather
during winter where concentration of sporulated oocysts
increase.
 Mixed infections
 Abdominal pain, foul smelling diarrhoea, with blood or
with soiled strings, drooping ears, rough coat, soiled
hind quarters, tenesmus and anaemia.
 Inability to raise on legs, partial paralysis of anal
sphincter; recovery is rare at this stage and death occurs
in young calves.
 Secondary pneumonia, emaciation in severe cases.
 Neurological coccidiosis
 Caused by Eimeria sp.

 Mortality-70%;

 Clinical signs are encephalopathy, diarrhoea, tenesmus,

haematochezia, CNS dysfunction, twitching,
hyperesthesia followed by nystagmus, opisthotonus,
tremors, bellowing, snapping of eyelids, occasionally
blindness, death within 1 month.
DIAGNOSIS
 Characteristic signs - Bloody diarrhoea and tenesmus.
 Faecal examination for oocysts.

 Post mortem examination if no oocysts are found.

 Differential diagnosis

 Johne’s disease - chronic diarrhoea

 Necrotic enteritis - Sudden death

  Hypomagnesemia - Hyperaesthesia, prolapse of 3rd eyelid.
 Cobalt deficiency - Pica
 Salmonellosis - Septicaemia.

 Treatment
 Amprolium - 20 -25mg/ kg for 4 to 5 days.

 Sulphamezathine - 0.125 mg/ kg for 13 days.

 Neurological coccidiosis - Calcium boro gluconate and

amprolium @ 50mg/ kg
COCCIDIOSIS IN SHEEP AND GOATS
 Epidemiology
 Agent: P.P.P – 15 days; Pathogenicity is by gametogony
and schizogony
 Age of the host
 Upto 6 months of age in lambs and kids; usually 4-7 weeks of
age.
 Transmission: Newborn lambs / kids pick up the
infection by suckling their soiled dams through soiled
litter, drinking water and infected pastures.
 Carrier status: Adults are symptomless and transmit
infection to the young ones.
 Season: Flare-up during onset of rains and winter.
 Risk factors

 Unhygienic condition

 Intensive grazing

 Oocysts contamination around feeding troughs

 Confinement in feedlots

 Weaning
 Pathogenesis
 Diarrhoea with foul smelling and with or without streaks
of blood.
 Constipation, severe abdominal pain, tenesmus, anaemia,
inappetence, unthriftiness, loss of weight, slight rise of
body temperature, ailing kids lie down due to abdominal
pain, soiling of hind quarters with faeces attracting blow
flies.
 Diagnosis, Treatment and Control: Similar to cattle.
COCCIDIOSIS IN RABBITS
 Epidemiology
 Age: Commonest around weaning and young
rabbits are highly susceptible
 Risk Factors: Intensive breeding and rearing
under poor sanitation.
 Pathogenesis
 Hepatic Coccidiosis
P.P.P- 18 days; Appear 12 days after infection,
rabbits die without sign in heavy infections;
Clinical signs -Diarrhoea, distension of the
abdomen, meteorism, inappetence,
constipation, icterus and oedema of the body.
Lesions: Enlargement of bile ducts;
haemorrhage and enlargement of liver.
 Intestinal Coccidiosis
 P.P.P- 7 days; Occurs frequently.
 Clinical signs –Diarrhoea, indigestion, bloating,
inappetence, reduced weight gain, sudden death
without symptoms or convulsion and paralysis.
 Lesions: Acute/ sub acute, rarely chronic, thickened
wall with grayish white deposits, contents are pasty,
diarrhoeic and with blood streaks.
 Diagnosis
 Demonstration of oocysts in the faeces and postmortem
examination.
 Treatment

 Sulphonamides like sulphamezathine in drinking water

@ 0.2 % effective.
COCCIDIOSIS IN DOGS, HORSES AND
PIGS
 Coccidiosis in Dogs
 Young puppies and kittens are more prone.
 Risk factors - Overcrowding and poor sanitation.

 Infection by predator- prey relationship.

 Usually carry coccidiosis infections but rarely
severe disease occur; causes diarrhoeic
syndrome
 Treatment - rarely practiced.
 Coccidiosis in Horses
 Causes diarrhoea and death in heavy infections only.

 Coccidiosis in Pigs

 Clinical condition is not frequent.

 Enteritis in piglets ( 1-2 weeks age groups) and

diarrhoea.
 Older animals are carriers.