Overview of Coccidiosis in Poultry 2Coccidiosis is caused by protozoa of the phylum Apicomplexa, family Eimeriidae. In poultry, most species belong to the genus Eimeria and infect various sites in the intestine. The infectious process is rapid (4–7 days) and is characterized by parasite replication in host cells with extensive damage to the intestinal mucosa. Poultry coccidia are strictly host-specific, and the different species parasitize specific parts of the intestine. Coccidia are distributed worldwide in poultry, game birds reared in captivity, and wild birds. (Also see Cryptosporidiosis.)


Overview of Coccidiosis in Poultry 1Coccidia 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. 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. (Also see Coccidiosis.)

Pathogenicity is influenced by host genetics, nutritional factors, concurrent diseases, and species of the coccidium. Eimeria necatrix and E tenella are the most pathogenic in chickens because schizogony occurs in the lamina propria and crypts of Lieberkühn of the small intestine and ceca, respectively, and causes extensive hemorrhage. Most species develop in epithelial cells lining the villi. Protective immunity usually develops in response to moderate and continuing infection. True age-immunity does not occur, but older birds are usually more resistant than young birds because of earlier exposure to infection.

Clinical Findings

Signs range from decreased growth rate to a high percentage of visibly sick birds, severe diarrhea, and high mortality. Feed and water consumption are depressed. Weight loss, development of culls, decreased egg production, and increased mortality may accompany outbreaks. Mild infections of intestinal species, which would otherwise be classed as subclinical, may cause depigmentation. Survivors of severe infections recover in 10–14 days but may never recover lost performance.

The lesions are almost entirely in the intestinal tract and often have a distinctive location and appearance that is useful in diagnosis.


Eimeria 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.