Leukoencephalopathy in Cheetahs
American Association of Zoo Veterinarians Conference 1999
Linda Munson1, DVM, PhD; Alexander de Lahunta2, DVM, PhD; Scott B. Citino3, DVM; Robin W. Radcliffe4, DVM; Don L. Neiffer5, VMD; Richard J. Montali6, DVM; Ilse Stalis7, DVM, PhD

1Deptartment of VM-PMI, University of California, Davis, CA, USA; 2Deptartment of Anatomy, New York State College of Veterinary Medicine, Cornell University, Ithaca, NY, USA; 3White Oak Conservation Center, Yulee, FL, USA; 4Fossil Rim Wildlife Center, Glen Rose, TX, USA; 5Pittsburgh Zoo, Pittsburgh, PA, USA; 6National Zoological Park, Smithsonian Institution, Washington, D.C., USA; 7San Diego Zoo, San Diego, CA, USA


During the past 2 yr, 27 adult cheetahs (Acinonyx jubatus) in United States zoos developed an unusual progressive degenerative neurologic disease that resulted in the euthanasia of 24 cheetahs. Clinically, the disease is characterized by blindness, incoordination, and lack of normal responsiveness to the environment. Pathologic findings in all cases have been similar and characterized by a remarkable reactive astrocytosis in the cerebral cortical white matter with symmetric degeneration and necrosis. The lesions appear to begin in the corona radiata as a reactive astrocytosis, but more advanced lesions have demyelination, axonal loss, and leukoencephalomalacia. In terminal stages, there is marked cavitation of the cerebral cortical white matter with secondary hydrocephalus. In all lesions, the astrocytes are hypertrophied with bizarre nuclei and abundant, sometimes vacuolated cytoplasm. Inflammatory changes have been absent in most cases.

The unique character and location of lesions is unlike any previously recognized disease. These lesions were not noted in cheetahs before 1996 and have not been reported previously in any other species. The epidemiology of the disease also is unusual in that it has affected only older animals (7-yr-old or older) and has emerged in the population at multiple facilities throughout the U.S. during this 2-yr period. Many different founder lines have been affected suggesting that it is not a familial disease. Also, a single confirmed case in England suggests that the disease is not due to some factor only in U.S. diets.

Attempts to identify potential causative infectious agents in the lesions such as feline corona virus, canine distemper virus, JC polyoma virus, and prions, have been unsuccessful to date. Because the lesions are most similar to those caused by mycotoxins or vitamin B deficiencies, serum and tissue levels of these compounds are being assayed in affected animals. Potential reactions to vaccines or medications also are being investigated. This important emerging disease has had a major impact on the captive breeding program and adds to the list of major health problems in this endangered species.


Speaker Information
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Linda Munson, DVM
Department of VM-PMI
University of California
Davis, CA, USA

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