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"Management and Control of Goat Coccidia (Part 2)"

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USDA Rural Information Center

Management and Control of Goat Coccidia (Part 2)

By: A. David Scarfe, Ph.D., D.V.M., Tuskegee University
About the Author

The schizont undergoes asexual reproduction producing a large number of daughter cells called merozoites. The number of merozoites produced within each meront varies from about a dozen to more than a hundred thousand, depending upon the species of coccidia involved. Each of the merozoites released from a schizont has the capability to enter a new host cell where a new schizont is once more formed and, subsequently, another generation of merozoites. The number of generations of meront formation is unique to each coccidian species. After a predetermined number of generations, the merozoites differentiate into male and female gametes and fertilization of fusion of these gametes form an oocyte within a host cell. The oocyte is then passed in the feces, completing the life cycle in about 2 weeks.

Various species of coccidia parasitize different areas of the intestinal tract, utilizing specific types of host cells. Some invade only mature epithelial cells, others only cells of underlying tissues. Each species has different reproductive patterns. There are varying numbers of generations of asexual reproduction, and if more merozoites are produced per meront, then more host cells are invaded. It is for these reasons that some species of coccidia are much more likely to cause disease than others.

Pathological Changes Induced by Coccidia
The damage done to the host is essentially that of intestinal cell destruction, which occurs when any coccidian stage leaves the host cell. Potentially, one oocyst ingested may lead to the production of a million or more oocysts which are passed in the feces 2 to 3 weeks later. This also means that one oocyte ingested potentially destroys millions of intestinal cells. The host cells affected most often are epithelial cells lining the gut which transport nutrients and fluids into the body. If these cells are damaged, blood or plasma may leak into the lumen of the gut. The damage may also allow bacteria from the intestine to enter the blood stream and invade other tissues. If the individual does not die of blood loss, dehydration, or bacterial septicemia, the cells will be replaced at least to some extent by scar tissue or by a increased turnover of epithelial cells. The latter form short, flattened villi or large polyps with rapidly proliferating epithelial cells that are not as efficient in absorbing nutrients from the intestine. This causes the host to become unthrifty.

Clinical Signs of Coccidiosis
As with other parasitic diseases, the clinical signs may vary between animals and on occasion may appear vague. In general, two forms of the disease should be recognized: the acute (or clinical) form and the chronic (subclinical) form. In the clinical form, obvious signs of the disease are suddenly seen. In the subclinical form, progressive, but slow and unseen, damage is done. In reality there is a continuum between these forms and occasionally animals will be seen to occasionally spontaneously break with clinical signs which then resolve themselves without intervention. In these cases, acute disease is seen while chronic coccidiosis is continuously occurring. Acute coccidiosis
The primary clinical signs of disease are directly related to the degree of intestinal mucosa (lining) destruction. The first signs of disease are usually a sudden onset of severe diarrhea with foul smelling, fluid feces often containing mucus and blood. The blood may appear as a dark tarry staining of the feces or as streaks. In particularly severe cases, the stool may consist almost entirely of large clots of blood. The perineum and tail are usually stained with blood-stained feces. Occasionally severe straining may be seen, with possible rectal prolapse.

Affected animals may also have a slightly evaluated body temperature but usually the temperature is normal or subnormal (under 104F). Depending on the loss of blood from enteric hemorrhage, the animal may be anemic with pale nucosa (mucus membranes), be weak, stagger and, occasionally, have difficulty breathing. Dehydration is common, but may not be severe if animals continue to drink.

There is usually a decrease in appetite in animals with clinical coccidiosis. Decreased appetite and, occasionally, failure to eat may last 5-6 days during the acute phase of disease. Some animals undergo a long convalescent period during which feed consumption and body weight gains are subnormal. In mild cases which may not show dysentery, some diarrhea and a reduced growth rate is usually seen. Subclinical cases (those showing no diarrhea) show inferior growth rates and chronic anemia. In groups of kids raised and fed in crowded conditions, the symptoms over a 1-3 week period may include inferior growth rates, gradual onset of weakness, inappetence, recumbency, emaciation and sometimes death. Signs of diarrhea may not be obvious.

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