Overview of Coccidiosis in Poultry

, DVM, PhD, Department of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee

Last full review/revision Jun 2014 | Content last modified Jun 2016

Coccidiosis 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 generally host-specific, and the different species parasitize specific parts of the intestine. However, in game birds, including quail, the coccidia may parasitize the entire intestinal tract. Coccidia are distributed worldwide in poultry, game birds reared in captivity, and wild birds. (Also see Cryptosporidiosis.)

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. 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, age of the host, and species of the coccidium. Eimeria necatrix and Eimeria 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. E kofoidi and E legionensis are the most pathogenic in chukars, and E lettyae is most pathogenic in bobwhite quail. Several Eimeria species are pathogenic in pheasants, particularly E phasiani and E colchici. 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:

Coccidiosis, poultry

Signs of coccidiosis 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 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.

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

Chickens:

Eimeria tenella, gross lesions, broiler chicken

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Coccidiosis (site parasitized by Eimeria tenella), poultry

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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.

Eimeria necatrix, developmental stages, poultry

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Eimeria necatrix, gross lesions, chicken

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Coccidiosis (site parasitized by Eimeria necatrix), poultry

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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.” The white spots are diagnostic for E necatrix if clumps of large schizonts can be demonstrated microscopically. 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.

Eimeria acervulina, developmental stages, poultry

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Eimeria acervulina, gross lesions, chicken

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Coccidiosis (site parasitized by Eimeria acervulina), poultry

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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.

Eimeria brunetti, oocysts

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Eimeria brunetti, gross lesions, chicken

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Coccidiosis (site parasitized by Eimeria brunetti), poultry

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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.

Eimeria maxima, oocysts

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Coccidiosis (site parasitized by Eimeria maxima), poultry

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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.

Coccidiosis (site parasitized by Eimeria mitis), poultry

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E mitis is recognized as pathogenic in the lower small intestine. Lesions are indistinct but may resemble moderate infections of E brunetti. E mitiscan be distinguished from E brunetti by finding small, round oocysts associated with the lesion.

Coccidiosis (site parasitized by Eimeria praecox), poultry

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E praecox, which infects the upper small intestine, does not cause distinct lesions but may decrease rate of growth. The oocysts are larger than those of E acervulina and are numerous in affected areas. The intestinal contents may be watery. E praecox is considered to be of less economic importance than the other species.

Coccidiosis (proposed site parasitized by Eimeria hagani), poultry

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Coccidiosis (proposed site parasitized by Eimeria mivata), poultry

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E hagani and E mivati develop in the anterior part of the small intestine. The lesions of E hagani are indistinct and difficult to characterize. However, E mivati may cause severe lesions similar to those of E acervulina. In severe infections, E mivati may cause reddening of the duodenum because of denuding of the villi. Some consider these species to be of dubious provenance, but work with molecular diagnostics seems to support their validity.

Turkeys:

Only four of the seven species of coccidia in turkeys are considered pathogenic: E adenoides, E dispersa, E gallopavonis, and E meleagrimitis. E innocua, E meleagridis, and E subrotunda are considered nonpathogenic. Oocysts sporulate within 1–2 days after expulsion from the host; the prepatent period is 4–6 days.

E adenoeides and E gallopavonis infect the lower ileum, ceca, and rectum. These species often cause mortality. The developmental stages are found in the epithelial cells of the villi and crypts. The affected portion of the intestine may be dilated and have a thickened wall. Thick, creamy material or caseous casts in the gut or excreta may contain enormous numbers of oocysts. E meleagrimitischiefly infects the upper and mid small intestine. The lamina propria or deeper tissues may be parasitized, which may result in necrotic enteritis ( see Necrotic Enteritis). E dispersa infects the upper small intestine and causes a creamy, mucoid enteritis that involves the entire intestine, including the ceca. Large numbers of gametocytes and oocysts are associated with the lesions.

Common signs in infected flocks include reduced feed consumption, rapid weight loss, droopiness, ruffled feathers, and severe diarrhea. Wet droppings with mucus are common. Clinical infections are seldom seen in poults >8 wk old. Morbidity and mortality may be high.

Game Birds:

The Chinese ringneck pheasant, the chukar partridge, and the bobwhite quail, extremely popular as game birds, are reared in large numbers under conditions similar to those of chickens. Losses in these birds from coccidiosis often exceed 50% of a flock. In pheasants, the common species are E phasiani, E colchici, E duodenalis, E tetartooimia, and E pacifica. Chukars are infected by two species: E kofoidi and E legionensis. Bobwhite quail are infected mainly by E lettyae, E dispersa, and E coloni. Treatment and control of these coccidia are similar to that in poultry; however, amprolium appears to be of little use. Monensin and salinomycin are the approved drugs for quail, and lasalocid and sulfadimethoxine/ormetoprim are the approved drugs for chukars.

Ducks:

A large number of specific coccidia have been reported in both wild and domestic ducks, but validity of some of the descriptions is questionable. Presence of Eimeria, Wenyonella, and Tyzzeria spp has been confirmed. T perniciosa is a known pathogen that balloons the entire small intestine with mucohemorrhagic or caseous material. Eimeria spp also have been described as pathogenic. Some species of coccidia of domestic ducks are considered relatively nonpathogenic. In wild ducks, infrequent but dramatic outbreaks of coccidiosis occur in ducklings 2–4 wk old; morbidity and mortality may be high.

Geese:

The best known coccidial infection of geese is that produced by E truncata, in which the kidneys are enlarged and studded with poorly circumscribed, yellowish white streaks and spots. The tubules are dilated with masses of oocysts and urates. Mortality may be high. At least five other Eimeriaspp have been reported to parasitize the intestine of geese, but these are of lesser importance.