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Coccidiosis
Farooq Sarwar
Talha Hussain
Amanat Ali
Definition
 Coccidiosis is a parasitic disease of the intestinal tract of animals
caused by coccidian protozoa.
 The disease spreads from one animal to another by contact with
infected feces or ingestion of infected tissue.
 Diarrhea, which may become bloody in severe cases, is the primary
symptom.
 Most animals infected with coccidia are asymptomatic, but young
or immunocompromised animals may suffer severe symptoms and
death.
Etiology
 Coccidia are almost universally present in poultry-raising operations, but clinical
disease occurs only after ingestion of relatively large numbers of sporulated
oocysts by susceptible birds.
 Both clinically infected and recovered birds shed oocysts in their droppings,
which contaminate feed, dust, water, litter, and soil.
 Oocysts may be transmitted by mechanical carriers (eg, equipment, clothing,
insects, farm workers, and other animals).
 Fresh oocysts are not infective until they sporulate; under optimal conditions
(70°–90°F [21°–32°C] with adequate moisture and oxygen), this requires 1–2
days.
Etiology
 Coccidia are host-specific, and there is no cross-immunity between
species of coccidia.
 The prepatent period is 4–7 days. Sporulated oocysts may survive
for long periods, depending on environmental factors.
 Oocysts are resistant to some disinfectants commonly used around
livestock but are killed by freezing or high environmental
temperatures.
Pathogenicity
 Pathogenicity is influenced by
 host genetics
 nutritional factors
 concurrent diseases
 age of the host
 and species of the coccidium
Pathogenicity
 Eimeria necatrix and Eimeria tenella are the most pathogenic in
chickens,
 E kofoidi and E legionensis are the most pathogenic in chukars
 E lettyae is most pathogenic in bobwhite quail.
 E phasiani and E colchici are pathogenic in pheasants.
Factors contributing to outbreaks
 litter moisture content exceeding 30% due to ingress of rain or
leaking waterers.
 immunosuppression (Marek’s disease, IBD, mycotoxins)
 suboptimal inclusion of anticoccidials or incomplete distribution
(poor mixing) in feed.
 environmental and managemental stress such as overstocking,
 inoperative feeding systems, inadequate ventilation.
Epidemiology
 Coccidiosis is seen universally, most commonly in young animals
housed or confined in small areas contaminated with oocytes.
 Coccidian are opportunistic pathogens; if pathogenic, their
virulence may be influenced by various stressors.
 Therefore, clinical coccidiosis is most prevalent under conditions of
poor nutrition, poor sanitation, or overcrowding, or after the
stresses of weaning, shipping, sudden changes of feed, or severe
weather.
 In general, for most species of farm animals, the infection rate is
high and rate of clinical disease is low (5–10%), although up to 80%
of animals in a high-risk group may show clinical signs.
 Older animals usually are resistant to clinical disease but may have
sporadic inapparent infections. Clinically healthy, mature animals
can be sources of infection to young, susceptible animals.
Clinical signs
 Signs of coccidiosis range from decreased growth rate to a high
percentage of visibly sick birds,
 severe diarrhea,
 high mortality
 Feed and water consumption are depressed
 Weight loss
 decreased egg production
Clinical signs
 increased mortality may accompany outbreaks.
 Mild infections of intestinal species, which would otherwise be
classed as subclinical, may cause depigmentation and potentially
lead to secondary infection, particularly Clostridium spp infection.
 Survivors of severe infections recover in 10–14 days but may never
recover lost performance.
1. E tenella
 E tenella infections are found only in the ceca and can be
recognized by
 accumulation of blood in the ceca
 and by bloody droppings.
 Cecal cores, which are accumulations of clotted blood, tissue
debris, and oocysts, may be found in birds surviving the acute stage.
Coccidiosis site parasitized
by E tenella in poultry.
2. E necatrix
 E necatrix produces major lesions in the anterior and middle
portions of the small intestine.
 Small white spots, usually intermingled with rounded, bright- or
dull-red spots of various sizes, can be seen on the serosal surface.
This appearance is sometimes described as “salt and pepper.”. In
severe cases, the intestinal wall is thickened, and the infected area
dilated to 2–2.5 times the normal diameter. The lumen may be filled
with blood, mucus, and fluid. Fluid loss may result in marked
dehydration. Although the damage is in the small intestine, the
sexual phase of the life cycle is completed in the ceca. Oocysts of E
necatrix are found only in the ceca. Because of concurrent
infections, oocysts of other species may be found in the area of
major lesions, misleading the diagnostician.
Developmental stages of E
necatrix from scraping of midgut
(poultry), Feulgen stain, 40X.
Gross lesions of E necatrix with
frank hemorrhaging into the
midgut in a chicken.
Coccidiosis site parasitized by E necatrix in
poultry.
3. E acervulina
 E acervulina is the most common cause of infection.
 Lesions include numerous whitish, oval or transverse patches in the
upper half of the small intestine, which may be easily distinguished
on gross examination.
 The clinical course in a flock is usually protracted and results in poor
growth, an increase in culls, and slightly increased mortality.
Developmental stages of E acervulina from mucosal
scraping of duodenal loop in poultry, new methylene
blue, 40X.
Gross lesions of E acervulina with white longitudinal
plaques in the duodenal loop of a broiler chicken.
Coccidiosis site parasitized by E acervulina in poultry.
4. E brunetti
 E brunetti is found in the lower small intestine, rectum, ceca, and
cloaca.
 In moderate infections, the mucosa is pale and disrupted but
lacking in discrete foci, and may be thickened.
 In severe infections, coagulative necrosis and sloughing of the
mucosa occurs throughout most of the small intestine.
Oocysts of E brunetti from mucosal scraping of small
intestine, new methylene blue, 100X.
Gross lesions of E brunetti in small intestine of
a broiler chicken.
Coccidiosis site parasitized by E
brunetti in poultry.
5. E maxima
 E maxima develops in the small intestine, where it causes dilatation
and thickening of the wall; petechial hemorrhage; and a reddish,
orange, or pink viscous mucous exudate and fluid. The exterior
of the midgut often has numerous whitish pinpoint foci, and the
area may appear engorged. The oocysts and gametocytes
(particularly macrogametocytes), which are present in the lesions,
are distinctly large.
Oocysts of E maxima, 100X. Coccidiosis site parasitized by E maxima in poult
Diagnostic table of coccidia
Differential diagnose
 Coccidioses should be differentiated from NE, UE and histomonosis
(typhlohepatitis).
Control
 Poultry that are maintained at all times on wire floors to separate
birds from droppings have fewer infections; clinical coccidiosis is
seen only rarely under such circumstances.
 Other methods of control are vaccination or prevention with
anticoccidial drugs.
Treatment
 sulfonamides are widely used:
 sulfadimethoxine, sulfaquinoxaline, I sulfamethazine, but they
should not I be used in layer hens.
 The supplementation I of vitamins A and K promotes the recovery.
References
 http://www.thepoultrysite.com/
 http://www.merckmanuals.com/
 Diseases of Poultry Y M saif
 A Color Atlas Of Poultry Diseases

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Coccidiosis in poultry

  • 2. Definition  Coccidiosis is a parasitic disease of the intestinal tract of animals caused by coccidian protozoa.  The disease spreads from one animal to another by contact with infected feces or ingestion of infected tissue.  Diarrhea, which may become bloody in severe cases, is the primary symptom.  Most animals infected with coccidia are asymptomatic, but young or immunocompromised animals may suffer severe symptoms and death.
  • 3. Etiology  Coccidia are almost universally present in poultry-raising operations, but clinical disease occurs only after ingestion of relatively large numbers of sporulated oocysts by susceptible birds.  Both clinically infected and recovered birds shed oocysts in their droppings, which contaminate feed, dust, water, litter, and soil.  Oocysts may be transmitted by mechanical carriers (eg, equipment, clothing, insects, farm workers, and other animals).  Fresh oocysts are not infective until they sporulate; under optimal conditions (70°–90°F [21°–32°C] with adequate moisture and oxygen), this requires 1–2 days.
  • 4. Etiology  Coccidia are host-specific, and there is no cross-immunity between species of coccidia.  The prepatent period is 4–7 days. Sporulated oocysts may survive for long periods, depending on environmental factors.  Oocysts are resistant to some disinfectants commonly used around livestock but are killed by freezing or high environmental temperatures.
  • 5. Pathogenicity  Pathogenicity is influenced by  host genetics  nutritional factors  concurrent diseases  age of the host  and species of the coccidium
  • 6. Pathogenicity  Eimeria necatrix and Eimeria tenella are the most pathogenic in chickens,  E kofoidi and E legionensis are the most pathogenic in chukars  E lettyae is most pathogenic in bobwhite quail.  E phasiani and E colchici are pathogenic in pheasants.
  • 7. Factors contributing to outbreaks  litter moisture content exceeding 30% due to ingress of rain or leaking waterers.  immunosuppression (Marek’s disease, IBD, mycotoxins)  suboptimal inclusion of anticoccidials or incomplete distribution (poor mixing) in feed.  environmental and managemental stress such as overstocking,  inoperative feeding systems, inadequate ventilation.
  • 8. Epidemiology  Coccidiosis is seen universally, most commonly in young animals housed or confined in small areas contaminated with oocytes.  Coccidian are opportunistic pathogens; if pathogenic, their virulence may be influenced by various stressors.  Therefore, clinical coccidiosis is most prevalent under conditions of poor nutrition, poor sanitation, or overcrowding, or after the stresses of weaning, shipping, sudden changes of feed, or severe weather.  In general, for most species of farm animals, the infection rate is high and rate of clinical disease is low (5–10%), although up to 80% of animals in a high-risk group may show clinical signs.  Older animals usually are resistant to clinical disease but may have sporadic inapparent infections. Clinically healthy, mature animals can be sources of infection to young, susceptible animals.
  • 9. Clinical signs  Signs of coccidiosis range from decreased growth rate to a high percentage of visibly sick birds,  severe diarrhea,  high mortality  Feed and water consumption are depressed  Weight loss  decreased egg production
  • 10. Clinical signs  increased mortality may accompany outbreaks.  Mild infections of intestinal species, which would otherwise be classed as subclinical, may cause depigmentation and potentially lead to secondary infection, particularly Clostridium spp infection.  Survivors of severe infections recover in 10–14 days but may never recover lost performance.
  • 11. 1. E tenella  E tenella infections are found only in the ceca and can be recognized by  accumulation of blood in the ceca  and by bloody droppings.  Cecal cores, which are accumulations of clotted blood, tissue debris, and oocysts, may be found in birds surviving the acute stage.
  • 12. Coccidiosis site parasitized by E tenella in poultry.
  • 13. 2. E necatrix  E necatrix produces major lesions in the anterior and middle portions of the small intestine.  Small white spots, usually intermingled with rounded, bright- or dull-red spots of various sizes, can be seen on the serosal surface. This appearance is sometimes described as “salt and pepper.”. In severe cases, the intestinal wall is thickened, and the infected area dilated to 2–2.5 times the normal diameter. The lumen may be filled with blood, mucus, and fluid. Fluid loss may result in marked dehydration. Although the damage is in the small intestine, the sexual phase of the life cycle is completed in the ceca. Oocysts of E necatrix are found only in the ceca. Because of concurrent infections, oocysts of other species may be found in the area of major lesions, misleading the diagnostician.
  • 14. Developmental stages of E necatrix from scraping of midgut (poultry), Feulgen stain, 40X. Gross lesions of E necatrix with frank hemorrhaging into the midgut in a chicken.
  • 15. Coccidiosis site parasitized by E necatrix in poultry.
  • 16. 3. E acervulina  E acervulina is the most common cause of infection.  Lesions include numerous whitish, oval or transverse patches in the upper half of the small intestine, which may be easily distinguished on gross examination.  The clinical course in a flock is usually protracted and results in poor growth, an increase in culls, and slightly increased mortality.
  • 17. Developmental stages of E acervulina from mucosal scraping of duodenal loop in poultry, new methylene blue, 40X. Gross lesions of E acervulina with white longitudinal plaques in the duodenal loop of a broiler chicken.
  • 18. Coccidiosis site parasitized by E acervulina in poultry.
  • 19. 4. E brunetti  E brunetti is found in the lower small intestine, rectum, ceca, and cloaca.  In moderate infections, the mucosa is pale and disrupted but lacking in discrete foci, and may be thickened.  In severe infections, coagulative necrosis and sloughing of the mucosa occurs throughout most of the small intestine.
  • 20. Oocysts of E brunetti from mucosal scraping of small intestine, new methylene blue, 100X. Gross lesions of E brunetti in small intestine of a broiler chicken.
  • 21. Coccidiosis site parasitized by E brunetti in poultry.
  • 22. 5. E maxima  E maxima develops in the small intestine, where it causes dilatation and thickening of the wall; petechial hemorrhage; and a reddish, orange, or pink viscous mucous exudate and fluid. The exterior of the midgut often has numerous whitish pinpoint foci, and the area may appear engorged. The oocysts and gametocytes (particularly macrogametocytes), which are present in the lesions, are distinctly large.
  • 23. Oocysts of E maxima, 100X. Coccidiosis site parasitized by E maxima in poult
  • 25. Differential diagnose  Coccidioses should be differentiated from NE, UE and histomonosis (typhlohepatitis).
  • 26. Control  Poultry that are maintained at all times on wire floors to separate birds from droppings have fewer infections; clinical coccidiosis is seen only rarely under such circumstances.  Other methods of control are vaccination or prevention with anticoccidial drugs.
  • 27. Treatment  sulfonamides are widely used:  sulfadimethoxine, sulfaquinoxaline, I sulfamethazine, but they should not I be used in layer hens.  The supplementation I of vitamins A and K promotes the recovery.
  • 28. References  http://www.thepoultrysite.com/  http://www.merckmanuals.com/  Diseases of Poultry Y M saif  A Color Atlas Of Poultry Diseases

Editor's Notes

  1. http://en.wikipedia.org/wiki/Coccidiosis
  2. http://www.merckmanuals.com/vet/poultry/coccidiosis/overview_of_coccidiosis_in_poultry.html