Yersinia pseudotuberculosis in a Closed Colony of Egyptian Fruit Bats (Rousettus aegyptiacus)
American Association of Zoo Veterinarians Conference 2004
Sara E. Childs-Sanford, DVM; Noha Abou-Madi, DVM, MSc; George V. Kollias, DVM, PhD, DACZM
Section of Wildlife Health, College of Veterinary Medicine, Cornell University, Ithaca, NY, USA

Abstract

Yersinia pseudotuberculosis, a gram-negative coccobacillus with a worldwide distribution, is an important cause of disease in captive animals.1,2,4 In June and July 2003, an outbreak of Y. pseudotuberculosis occurred in a colony of Egyptian fruit bats at the Rosamond Gifford Zoo in Syracuse, NY. Over a 6-wk period, 10 bats either died or were euthanatized due to severe clinical disease. Seven of these bats cultured positive for Y. pseudotuberculosis. Two of the Yersinia-positive bats exhibited the acute form of pseudotuberculosis, characterized by sepsis and multiorgan failure with rapid progression to death, while the remainder of the bats exhibited the chronic and debilitating form of the disease, characterized by necrotizing abscessation involving one or more organs, especially the liver, spleen, and mesenteric lymph nodes.

It is highly suspected that a wild rodent reservoir was the source of the Yersinia outbreak. The colony of bats, which contained 125 animals at the time of the outbreak, had been closed since its establishment from thirteen animals in 1986. In addition, primates in nearby exhibits had numerous enteric cultures for Yersinia, which were negative. Several mice trapped from the region of the exhibit have cultured negative for Y. pseudotuberculosis; however, they are still considered to be the most likely origin of the infection in this colony. Reported species differences in susceptibility to clinical disease from Y. pseudotuberculosis may indicate that fruit bats are predisposed.3 Furthermore, stress, which has been implicated as being an important element in precipitating outbreaks of Y. pseudotuberculosis,1,4 may have been a significant contributing factor in this colony, which was overpopulated and may have also had an inappropriate gender ratio (D. Heard, pers. comm.). This hypothesis is supported by the simultaneous diagnosis of several other diseases often associated with general debilitation and immunosuppression, including microsporidiosis, generalized cutaneous demodicosis, and mycobacteriosis.

Due to the suspected high prevalence of Y. pseudotuberculosis in the remaining bats in the colony, the close proximity of other animal exhibits, and the zoonotic potential of this pathogen, the entire colony was depopulated. Gross necropsy was performed on the 115 euthanatized bats, revealing that 80 (70%) of the bats exhibited gross evidence of potential infection with Y. pseudotuberculosis, especially hepatic abscessation, splenomegaly, and mesenteric lymphadenopathy.2,4 Studies are ongoing to document the prevalence of Y. pseudotuberculosis in this colony, characterize the pattern of gross lesions typical of this disease in Egyptian fruit bats, and describe the epidemiologic patterns involved in this outbreak.

Literature Cited

1.  Allchurch A.F. 2003. Yersiniosis in all taxa. In: Fowler, M.E. and R.E. Miller (eds.). Zoo and Wild Animal Medicine. 5th edition. Elsevier Science, St. Louis, Missouri. Pp. 724–727.

2.  Baskin G.B. 1980. Comparative aspects of Yersinia pseudotuberculosis infection in animals. In: R.J. Montali and G. Migaki (eds.). The Comparative Pathology of Zoo Animals. Proceedings: The Symposia of the National Zoological Park. Smithsonian Institution Press, Washington, DC. Pp. 219–223.

3.  Brice S. 1995. Screening a New World monkey colony for Yersinia and investigations of Y. pseudotuberculosis and soil. Dodo, J. Wildl. Preserv. Trust. 31:139–147.

4.  Gasper P.W. and R.P. Watson. 2001. Plague and yersiniosis. In: Williams E.S. and I.K. Barker (eds.). Infectious Diseases of Wild Mammals. 3rd edition. Iowa State University Press, Ames, Iowa. Pp. 313–329.

 

Speaker Information
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Sara E. Childs-Sanford, DVM
Section of Wildlife Health
Department of Clinical Sciences
College of Veterinary Medicine
Cornell University
Ithaca, NY, USA


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