YERSINIA ENTEROCOLITICA: AN UNLIKELY CAUSE OF POSITIVE BRUCELLOSIS TESTS IN GREATER YELLOWSTONE ECOSYSTEM BISON (BISON BISON) Wade See, 1 William H. Edwards, 2 Stacey Dauwalter, 2 Claudia Almendra, 6 Martin D. Kardos, 1,7 Jennifer L. Lowell, 1 Rick Wallen, 3 Steven L. Cain, 4 William E. Holben, 1,7,8 and Gordon Luikart 1,5,6,7 1 Division of Biological Sciences, University of Montana, Missoula, Montana 59812, USA 2 Wyoming Game and Fish Wildlife Disease Laboratory, 1174 Snowy Range Rd., Laramie, Wyoming 82070, USA 3 National Park Service, P.O. Box 168, Yellowstone National Park, Wyoming, 82190 USA 4 Grand Teton National Park, USDI, P.O. Drawer 170, Moose, Wyoming 83012, USA 5 CIBIO, Centro de Investigac ¸a ˜ o em Biodiversidade e Recursos Gene ´ ticos, Campus Agra ´ rio de Vaira ˜ o, 4485-661 Vaira ˜ o, Portugal 6 Flathead Lake Biological Station, University of Montana, Missoula, Montana 59812, USA 7 Montana—Ecology of Infectious Diseases Program, University of Montana, Missoula, Montana 59812, USA 8 Corresponding author (email: bill.holben@mso.umt.edu) ABSTRACT: Yersinia enterocolitica serotype O:9 has identical O-antigens to those of Brucella abortus and has apparently caused false-positive reactions in numerous brucellosis serologic tests in elk (Cervus canadensis) from southwest Montana. We investigated whether a similar phenomenon was occurring in brucellosis antibody–positive bison (Bison bison) using Y. enterocolitica culturing techniques and multiplex PCR of four diagnostic loci. Feces from 53 Yellowstone bison culled from the population and 113 free-roaming bison from throughout the Greater Yellowstone Ecosystem (GYE) were tested. Yersinia enterocolitica O:9 was not detected in any of 53 the bison samples collected at slaughter facilities or in any of the 113 fecal samples from free-ranging bison. One other Y. enterocolitica serotype was isolated; however, it is not known to cause cross-reaction on B. abortus serologic assays because it lacks the perosamine synthetase gene and thus the O-antigens. These findings suggest that Y. enterocolitica O:9 cross-reactivity with B. abortus antigens is unlikely to have been a cause of false-positive serology tests in GYE bison and that Y. enterocolitica prevalence was low in bison in the GYE during this study. Key words: Bison, brucellosis, elk, Greater Yellowstone Ecosystem, perosamine synthetase, Yellowstone, Yersinia enterocolitica O:9. INTRODUCTION Yersinia enterocolitica is an enteric, gram-negative, pathogenic bacterium found in domestic animals, wildlife, and humans (Bottone, 1997). Yersinia enter- ocolitica serotype O:9 and Brucella abor- tus, the etiologic agent of brucellosis in elk (Cervus canadensis), bison (Bison bison), cattle (Bos taurus), and certain other ungulates, possess an identical O-antigen structure encoded by the gene perosamine synthetase (Godfroid et al., 2002). This genetic similarity is known to cause cross- reactivity between the two bacteria during serologic testing. As a result, infection with Y. enterocolitica serotype O:9 can lead to false-positive Brucella serology tests, mak- ing identification of Brucella-positive ani- mals difficult in livestock and wildlife populations including cattle, bison, and elk (Weynants et al., 1996; Munoz et al., 2005; Atkinson et al., 2007). In 2004–2005, staff from Montana Fish, Wildlife, and Parks detected high numbers of B. abortus antibody–positive elk (11.4%) in the Pioneer Mountains on the northwest perimeter of the Greater Yellowstone Ecosystem (GYE), ,100 km northwest of Yellowstone National Park where B. abor- tus occurs in bison and some elk (e.g., Beja- Pereira et al., 2009). In the Madison Valley Elk Management Unit, approximately 20 km east of the Pioneer Mountains, antibody prevalence in sampled elk rose to 6.9% in 2004–2005 and to 17.5% in 2005– 2006 samples (Atkinson, et al., 2007). Before 2004–2005, annual estimates of antibody prevalence were consistently less than 2% in both areas. The rise in antibody prevalence prompted further investigation to determine whether Y. enterocolitica O:9 Journal of Wildlife Diseases, 48(3), 2012, pp. 537–541 # Wildlife Disease Association 2012 537