Amyloidosis in the Black-Footed Ferret (Mustela nigripes)
American Association of Zoo Veterinarians Conference 2004
Michael M. Garner1, DVM, DACVP; James T. Raymond1, DVM, MS, DACVP; Timothy D. O’Brien2, DVM, PhD, DACVP; Robert W. Nordhausen3, MA
1Northwest ZooPath, Monroe, WA, USA; 2Department of Veterinary Population Medicine, Veterinary Diagnostic Laboratory, College of Veterinary Medicine, University of Minnesota, St. Paul, MN, USA; 3The Animal Health and Food Safety Laboratory, University of California-Davis, Davis, CA, USA

Abstract

The black-footed ferret (Mustela nigripes) is among the most critically endangered mammals in North America.1,12 Populations of this highly specialized predator were adversely impacted when its primary prey, the prairie dog (Cynomys spp.), was targeted as a nuisance species and largely eradicated from some of its home ranges by human development and land conversion.1 Sylvatic plague has also played a role in decimating large populations of prairie dogs.1 These factors combined to produce a well-documented genetic bottleneck in the wild black-footed ferret population in the 1980s.1,12 The last isolated wild ferret population also experienced epidemics of plague and distemper that further restricted the gene pool.9-11 The last wild population was subsequently captured for captive breeding programs. Although captive propagation has been successful, the bottleneck has resulted in decreased genetic diversity in the remaining population.12

A number of infectious processes have been reported in wild or captive black-footed ferrets, including distemper,3,7,10,11 plague,9,11 gastritis due to Clostridium perfringens type A,8 and enteritis due to enterotoxigenic E. coli2. A few cases of neoplasia4,6 and a single case of diabetes mellitus5 have also been reported. In none of these studies has amyloidosis been reported as a primary or concurrent lesion in affected animals. A literature search could find no reference to amyloidosis occurring in mustelids. Furthermore, aside from black-footed ferrets, amyloidosis has rarely been diagnosed among mustelid cases submitted to Northwest ZooPath in the past 10 yr. (Garner, unpublished data). This study describes amyloidosis occurring in 26 black-footed ferrets from eight U.S. zoological institutions.

Of the 26 study ferrets, six were females, 18 were males and sex was unknown for two. Age of affected ferrets ranged from 0.5 yr to 8 yr, with average age=5.1 yr. The most common clinic signs were inappetance (11), diarrhea (5), “renal disease” or azotemia (4), and lethargy (4). Ten were euthanatized, 13 died, and manner of death was not known for three. The most common gross findings were hepatic cysts (14), abnormalities in renal morphology (11), hemorrhage in various organs (9), and thin or emaciated body condition (8).

Histologically, homogenous amphophilic deposits in all tissues were positive for amyloid using the Congo red stain. The most common sites for amyloid deposition were kidney (26), intestine (15), stomach (11), gallbladder (9), blood vessels (8), and pancreas (8). In 25/26 animals, the most severe amyloid deposition occurred in the kidney, and the glomeruli and tubular basement membranes were equally affected. In the kidney, severity of amyloid deposition in the glomeruli positively correlated with number of tubules that contained protein casts. The most common concurrent disease processes were miscellaneous inflammatory conditions (16), miscellaneous neoplastic conditions (13), biliary cysts or tumors (12), cholecystitis/cholangiohepatitis (10), bacterial sepsis (7), and chronic gastroenteritis (7).

The common occurrence of an otherwise uncommon mustelid disease in a bottlenecked population of black-footed ferrets suggests that these animals may be genetically predisposed to development of amyloidosis. Because all animals had concurrent disease processes, particularly inflammatory or neoplastic diseases, it is considered possible that amyloid deposition was precipitated by other disease processes. Further characterization of the type of amyloid may provide more insight into the pathogenesis of this condition. Additional cytochemical, immunohistochemical and electron microscopic characterization of the amyloid deposits in these ferrets is currently being performed. Because glomerular amyloidosis with protein casts is a consistent finding in affected ferrets, urinalysis that includes measurement of protein:creatinine ratio may be a helpful test for identifying affected animals.

Acknowledgments

The authors acknowledge the cooperation of the following institutions regarding submission of cases for this study: the Hogle Zoo, the San Antonio Zoo, the Cheyenne Mountain Zoo, the Akron Zoo, the Lee Richardson Zoo, the Fort Worth Zoo, the Louisville Zoological Gardens, and the Elmwood Park Zoo.

Literature Cited

1.  Biggins D.E., and J.L. Godbey. 2003. Challenges to reestablishment of free-ranging populations of black- footed ferrets. C.R. Biol. 326 Suppl 1: S104–11.

2.  Bradley G.A., K. Orr, C. Reggiardo, and R.D. Glock. 2001. Enterotoxigenic Escherichia coli infection in captive black-footed ferrets. J. Wildl. Dis. 37:617–20.

3.  Carpenter J.W., M.J. Appel, R.C. Erickson, and M.N. Novilla. 1976. Fatal vaccine-induced canine distemper virus infection in black-footed ferrets. J. Am. Vet. Med. Assoc. 169:961–4.

4.  Carpenter J.W., J.P. Davidson, M.N. Novilla, J.C. Huang. 1980. Metastatic, papillary cystadenocarcinoma of the mammary gland in a black-footed ferret. J. Wildl. Dis. 16:587–92.

5.  Carpenter J.W., and M.N. Novilla. 1977. Diabetes mellitus in a black-footed ferret. J. Am. Vet. Med. Assoc. 171:890–3.

6.  Lair S., I.K. Barker, K.G. Mehren, and E.S. Williams. 2002. Epidemiology of neoplasia in captive black- footed ferrets (Mustela nigripes), 1986–1996. J. Zoo Wildl. Med. 33:204–13.

7.  Pearson G.L. Vaccine-induced canine distemper virus in black-footed ferrets. 1977. J. Am. Vet. Med. Assoc. 170:103, 106, 109.

8.  Schulman F.Y., R.J. Montali, and P.J. Hauer. 1993. Gastroenteritis associated with Clostridium perfringens type A in black-footed ferrets (Mustela nigripes). Vet. Pathol. 30:308–10.

9.  Williams E.S., K. Mills, D.R. Kwiatkowski, E.T. Thorne, and A. Boerger-Fields. 1994. Plague in a black- footed ferret (Mustela nigripes). J Wildl. Dis. 30: 581–5.

10.  Williams E.S., E.T. Thorne, M.J. Appel, and D.W. Belitsky. 1988. Canine distemper in black-footed ferrets (Mustela nigripes) from Wyoming. J. Wildl. Dis. 24:385–98.

11.  Williams E.S., and E.T. Thorne. 1996. Infectious and parasitic diseases of captive carnivores, with special emphasis on the black-footed ferret (Mustela nigripes). Rev. Sci. Tech. 15:91–114.

12.  Wisely S.M., S.W. Buskirk, M.A. Fleming, D.B. McDonald, E.A. Ostrander. 2002. Genetic diversity and fitness in black-footed ferrets before and during a bottleneck. J. Hered. 93:231–7.

 

Speaker Information
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Michael M. Garner, DVM, DACVP
Northwest ZooPath
Monroe, WA, USA


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