John and Dizzy
Carrot Top Stud



Enterotoxemia:

Enterotoxemia is an explosive diarrheal disease, primarily of rabbits 4-8 wk old. It occasionally affects adults and junior stock. Signs are lethargy, rough coat, a perineal area covered with greenish brown fecal material, and death within 48 hr. Often, a rabbit looks healthy in the evening and is dead the next morning. Necropsy reveals the typical lesions of enterotoxemia, ie, a fluid-distended intestine with hemorrhagic petechiae on the serosal surface. The primary causative agent is Clostridium spiroforme , which produces an iota toxin. Little is known about transmission of the organism; it is assumed to be a commensal that is normally present in low numbers. The type of diet seems to be a factor in development of the disease; enterotoxemia is seen less often when high-fiber diets are fed. Because lincomycin, clindamycin, and erythromycin induce Clostridium -related (eg, C difficile ) enterotoxemia due to their selective effect on normal gram-positive bacteria, they are contraindicated in rabbits. Enterotoxemia is a consideration for most antibiotic therapy, and it has been seen after administration of penicillins and cephalosporins. The incidence rate is 40-80% after oral penicillin therapy, which should be considered contraindicated in rabbits. These diarrheas are remarkably similar to those that occur naturally (described above as enterotoxemia). Treatment of colony rabbits is seldom attempted because of the rapidity of death. However, when population size permits, cholestyramine has been used with promising results, both as a preventive and a treatment. Reducing stress of the young rabbits (weaning, etc) and ad lib feeding of hay or straw are helpful in prevention. Adding 250 ppm of copper sulfate to the diet of young rabbits also helps prevent enterotoxemia. Individual animal treatment for enterotoxemia should include supportive fluid therapy. There is little evidence that antibiotics are helpful. Diagnosis depends on history, signs, lesions, and demonstration of C spiroforme . Centrifugation of intestinal contents at 20,000 g for 15 min followed by culture of the supernatant-pellet interface will reveal the organism. For a definitive diagnosis, the presence of iota toxin in the supernatant of centrifuged cecal contents can be demonstrated by in vivo or in vitro assays.

 

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