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Asian Small-Clawed Otter Husbandry Manual (1998)

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Concurrent infection with calicivirus or picornavirus, as well as poor air quality with high ammonia levelshas been implicated as predisposing factors in the pathogenesis of the disease. Bacterins composed ofall four stereotypes are available for use. (United Vaccines, Harlan Sprague Dawley Inc., Madison, WI53711 and American Scientific Labs., Elkhorn, Nebraska).Botulism--Most species of mustelids are susceptible to type C toxin (and to a lesser extent types A, B,and E) produced by Clostridium botulinum. Usually animals are found dead but some may exhibitparalysis and dyspnea before dying. There are no postmortem lesions. The disease is caused by eatinguncooked or contaminated meat. Animals not on a commercially prepared diet should be vaccinatedannually.Tuberculosis--Many mustelids are susceptible to bovine, avian and human strains of tuberculosis. Thedisease has been reported in the domestic ferret, mink, otters, and the European badger. It is usuallyacquired by eating contaminated food, however in the European badger, transmission can occur frommother to cub, by aerosol, or through bite wounds. Clinical signs may include weight loss, enlargedlymph nodes, chronic respiratory disease, and mastitis. Tuberculin skin testing is unreliable. Serologicaltests used to identify European badgers with Mycobacterium bovis have also been unreliable. Mustelidcaretakers should be tested annually for TB.Anthrax has been reported in the European badger, the honey badger (Mellivora capensis), and mink.Clinical signs include acute death with blood draining from body cavities. Postmortem findings includesubcutaneous and subserosal edema, hepatomegaly, and splenomegaly.Campylobacteriosis--Diarrhea caused by Campylobacter jejuni and C. coli has been reported indomestic ferrets and mink. Fever and leucocytosis often accompany infections. Abortion and otherreproductive problems occur in both mink and ferrets when they are inoculated with C. jejuni duringpregnancy. Ferrets can be asymptomatic carriers. Clinical disease is most common in animals less thansix months of age. Special techniques are required to culture the organism from the feces. Humans arealso susceptible to infections with C. jejuni. Erythromycin, the drug of choice in humans, does noteliminate the carrier state in ferrets. Raw meat diets appear to predispose mink to C. jejuni infection.Campylobacter-like organisms (C.L.O.) have been cultured from the gastric mucosa of both normaland diseased ferrets. The role they play in the pathogenesis of gastritis and gastric ulcer disease isunclear at this time.Proliferative colitis is a syndrome described in young domestic ferrets characterized bymucohemorrhagic diarrhea, weight loss, and partial prolapse of the rectum. Occasionally it isaccompanied by C.N.S. signs. The disease causes a profound thickening of the mucosa and muscularwall of the colon, which can be palpated per rectum. Pathological lesions are similar to those found inhamsters with "wet tail" and swine with proliferative ileitis, except lesions in the ferret are in the colon notthe ileum. Campylobacter jejuni and Campylobacter-like organisms have frequently been isolated inthe feces of affected animals, but their role in the disease is uncertain. Experimental inoculation of minkand ferret kits with C. jejuni causes enterocolitis but not proliferative colitis.<strong>Asian</strong> <strong>Small</strong>-<strong>Clawed</strong> <strong>Otter</strong> <strong>Husbandry</strong> <strong>Manual</strong>/Health Care-35-

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