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Digestive System
Coccidiosis
Coccidiosis of Goats
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Chapters in Digestive System
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  • Diseases of the Mouth in Large Animals
  • Diseases of the Esophagus in Large Animals
  • Gastrointestinal Ulcers in Large Animals
  • Diseases of the Ruminant Forestomach
  • Diseases of the Abomasum
  • Acute Intestinal Obstructions in Large Animals
  • Colic in Horses
  • Intestinal Diseases in Ruminants
  • Intestinal Diseases in Horses and Foals
  • Intestinal Diseases in Pigs
  • Gastrointestinal Parasites of Ruminants
  • Gastrointestinal Parasites of Horses
  • Gastrointestinal Parasites of Pigs
  • Fluke Infections in Ruminants
  • Hepatic Disease in Large Animals
  • Malassimilation Syndromes in Large Animals
  • Abdominal Fat Necrosis
  • Diseases of the Mouth in Small Animals
  • Diseases of the Esophagus in Small Animals
  • Diseases of the Stomach and Intestines in Small Animals
  • The Exocrine Pancreas
  • Gastrointestinal Parasites of Small Animals
  • Hepatic Disease in Small Animals
  • Vomiting
Topics in Coccidiosis
  • Overview of Coccidiosis
  • Coccidiosis of Cattle
  • Coccidiosis of Sheep
  • Coccidiosis of Goats
  • Coccidiosis of Pigs
  • Coccidiosis of Cats and Dogs
     
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    Coccidiosis of Goats

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    Numerous species of Eimeria are found in goats in North America and elsewhere. The Eimeria spp are host-specific and are not transmitted from sheep to goats.

    E arloingi, E christenseni, and E ovinoidalis are highly pathogenic in kids. Clinical signs include diarrhea with or without mucus or blood, dehydration, emaciation, weakness, anorexia, and death. Some goats are actually constipated and die acutely without diarrhea. Usually, stages and lesions are confined to the small intestine, which may appear congested, hemorrhagic, or ulcerated, and have scattered pale, yellow to white macroscopic plaques in the mucosa. Histologically, villous epithelium is sloughed, and inflammatory cells are seen in the lamina propria and submucosa. In addition, there have been several reports of hepatobiliary coccidiosis with liver failure in dairy goats. Diagnosis of intestinal coccidiosis is based on finding oocysts of the pathogenic species in diarrheal feces, usually at tens of thousands to millions per gram of feces. It is not unusual to find oocyst counts as high as 70,000/g of feces in kids without overt disease, but weight gain may be affected.

    Angora and dairy goats, raised under different management practices, may have similar patterns of exposure of kids. Just after parturition, nursery pens and surrounding areas may be heavily contaminated with oocysts from does. Resistance to infection is decreased just after shipping, changing rations, introducing new animals, or mixing young with older animals. Coccidiostats can be administered to a herd immediately after diagnosis or as a preventive in predictable situations such as those mentioned above.

    Diagnosis and treatment are similar to those for cattle and sheep. Sulfadimidine at 55 g/tonne is also effective for the control of coccidiosis in goats. In nonlactating goats, adding monensin to the feed at 18 g/tonne is preventive.

    Last full review/revision March 2012 by Peter D. Constable, BVSc (Hons), MS, PhD, DACVIM

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