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USGS · 2001121

Intestinal coccidiosis

Abstract

Coccidia are a complex and diverse group of protozoan (single-celled organisms) parasites; the coccidia group contains many species, most of which do not cause clinical disease. In birds, most disease-causing or pathogenic forms of coccidia parasites belong to the genus Eimeria. Coccidia usually invade the intestinal tract, but some invade other organs, such as the liver and kidney (see Chapter 27). Clinical illness caused by infection with these parasites is referred to as coccidiosis, but their presence without disease is called coccidiasis. In most cases, a bird that is infected by coccidia will develop immunity from disease and it will recover unless it is reinfected. The occurrence of disease depends, in part, upon the number of host cells that are destroyed by the juvenile form of the parasite, and this is moderated by many factors. Severely infected birds may die very quickly. Often, tissue damage to the bird’s intestine results in interrupted feeding; disruption of digestive processes or nutrient absorption; dehydration; anemia; and increased susceptibility to other disease agents. In cranes, coccidia that normally inhabit the intestine sometimes become widely distributed throughout the body. The resulting disease, disseminated visceral coccidiosis (DVC) of cranes, is characterized by nodules, or granulomas, on the surface of organs and tissues that contain developmental stages of the parasite. Collectively, coccidia are important parasites of domestic animals, but, because each coccidia species has a preference for parasitizing a particular bird species and because of the self-limiting nature of most infections, coccidiosis in freeranging birds has not been of great concern. However, habitat losses that concentrate bird populations and the increasing numbers of captive-reared birds that are released into the wild enhance the potential for problems with coccidiosis.

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BibTeXRIS

M. Friend, J. C. Franson. 1999. Intestinal coccidiosis. https://pubs.usgs.gov/publication/2001121

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