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IV. Enterotoxemia
A. Etiology: Clostridial species, principally C. difficile and C. spiroforme, proliferate and produce toxins to induce this disease. Clostridial exotoxins induce secretory and vascular effects. A history of antibiotic therapy with broad spectrum antibiotics including oral ampicillin, clindamycin or lincomycin, may be associated with this disease. Clostridial enteritis may occur in rabbits that have not been treated with any antibiotics. Diets high in carbohydreates enhance the overgrowth of Clostridium species. Change in gut flora and other stressors leading to anorexia may predispose to disease.
B. Clinical Signs: Sudden death with no previous signs of illness or watery diarrhea 2 to 3 days prior to death are the usual signs. This disease affects all ages, but primarily targets recently weaned rabbits.
C. Pathology: Prominent gross lesions observed include in a large, fluid-filled edematous cecum with serosal congestion and hemorrhage and watery mucoid feces in the colon (A.). Microscopically, severe lesions include a necrotic erosive or ulcerative typhlitis with swelling and loss of enterocytes and pseudomembrane formation (B.). The mucosa and submucosa are infiltrated with heterophils and there is submucosal edema and hemorrhage. Large Gram-positive bacilli with spores can often be observed on the mucosal surface.
D. Diagnosis: Diagnosis is achieved by the history of antibiotic treatment or environmental/dietary stressors, and isolation or PCR amplification of Clostridium species from cecal contents. An antigen capture ELISA is available for cytotoxins A and B of C. difficile. C. spiroforme may be seen as a spiral bacillus on a direct smear.
E. Treatment: Due to the acute course of the disease, there is usually no treatment. Supportive fluid therapy, kaopectate, and yogurt may be helpful.
F. Control: Do not use lincomycin or clindamycin in rabbits. Eliminate extreme dietary changes and minimize environmental stressors. |