Members of the genus Clostridium are widely recognized as enteric pathogens of humans, domestic animals, and wildlife. Their array of proven and putative virulence attributes is impressive, and infections take a variety of forms in mammalian and avian hosts. C. perfringens may be the most widely occurring pathogenic bacterium and is certainly the most important cause of clostridial enteric disease in domestic animals.3 Some types of C. perfringens (mainly type A) are consistently recovered both from the intestinal tracts of animals and from the environment, while others (types B, C, D, and E) are less common in the intestinal tracts of animals.2 As many as 17 exotoxins of C. perfringens have been described in the literature. A definitive role in the induction of disease in humans and animals has only been demonstrated for a few of these toxins.4
A clinical syndrome, similar to Clostridium perfringens enterotoxicosis (CPE) described in other species, has been identified in approximately 15% of recently captured North American river otters (Lontra canadensis) involved in an ongoing population restoration project in New York state. Otters with CPE die peracutely (<6 hr post capture), acutely (<60 hr post capture), or develop soft to watery mucoid diarrhea (±blood), and or marked reduction in normal grooming behavior, hypophagia and hypodipsia, profound hypothermia, and in some cases coma at 24–72 hr post capture.
Otters administered a regimen of oral metronidazole, oral or parenteral electrolyte solution, equine hyperimmune antiserum, and general supportive care (e.g., correcting hypothermia, hand feeding) following recognition of the clinical signs/problems described above, have a high rate of recovery, and no recurrence of this problem over a 14–21 day period.1
River otters that die have mild to severe intestinal lesions consistent with CPE, including superficial mucosal necrosis and vascular congestion. In some otters, C. perfringens toxin-induced autolysis was hypothesized to have “masked” typical microscopic lesions observed in intestinal sections postmortem.
In all cases, CPE is confirmed by anerobic culture of fresh feces, in vitro detection of type A (putative) Clostridium perfringens exotoxin, clinical signs, and gross necropsy and histopathologic findings.
CPE is currently thought to be minimized by adhering to the treatment protocol (with modifications), described above, to all recently captured otters involved in this population restoration project.
1. Kollias GV. 1998. Health assessment, medical management and pre-release conditioning of translocated North American river otters (Lontra canadensis). In: Miller RE, ME Fowler, ed. Current Vet Therapy IV - Zoo and Wildlife Medicine. W.B. Saunders Co., Philadelphia, PA (in press).
2. McDonel JL. 1986. Toxins of Clostridium perfringens type A, B, C, D, and E. In: Dorner F, H Drews, eds. Pharmacology of Bacterial Toxins. Pergamon Press, Oxford, England. Pp 477–515.
3. Songer JG. 1996. Clostridial enteric disease of domestic animals. Clin. Micro. Rev. 9:216–234.
4. Walker PD. 1990. Clostridium. In: Carter GR, JR Cole, Jr., ed. Diagnostic Procedure in Veterinary Bacteriology and Mycology. 5th Edition, Academic Press, San Diego, CA, Pp. 229–251.