Neurodegenerative Disorders in Snow Leopard Cubs (Uncia uncia)
American Association of Zoo Veterinarians Conference 2003
Nadia Robert1, DVM, DACVP; Brice Lefaux2, DVM; Claire Dally3, DVM; Emmanuelle Collilieux4, DVM; Stephane Blot5, DVM, DECVN; Catherine Botteron6, DVM, PhD, DECVP
1Center for Fish and Wildlife Health, Berne University, Berne, Switzerland; 1Parc Zoologique, France; 3Service d’Histologie et Anatomie Pathologique, Ecole Nationale Veterinaire d’Alfort, Maisons-Alfort, France; 4Clinique Veterinaire, Angerville, France; 5Unitede Neurologie, Ecole Nationale Veterinaire d’Alfort, Maisons-Alfort, France; 6Neurocenter, Department of Clinical Veterinary Medicine, Berne University, Berne, Switzerland


This report presents the clinical features and pathologic findings of two neurologic disorders affecting young snow leopard (Uncia uncia) cubs born recently in different zoological institutions in Switzerland and France. The first disorder was diagnosed in snow leopard cubs born to three breeding pairs in one Swiss and two French zoological institutions (Pare d’Auneau and Zoo de Thoiry) between 1997 and 2002. The disorder appeared in two or three consecutive litters from each breeding pair and all cubs born in the affected litters developed neurologic signs. Beginning at the age of 2–4 months, the cubs developed locomotional disorders characterized by a swaying gait, hypermetria and weakness of the hind limbs, associated with progressive muscle atrophy of the hindquarters. The interpretation of the neurologic assessment was very difficult; however, the spinal reflexes of the pelvic limbs (patellar and flexor reflexes) were present. Due to the progressive nature of the symptoms most cubs were euthanatized within 1 year of age. Necropsies were performed on five animals and did not reveal any gross lesions. Histopathologic examination revealed degenerative lesions in the cervical, thoracic and lumbosacral segments of the spinal cord. The lesions were confined to the lateral and ventral columns, with the dorso-lateral and ventro-medial peripheral aspects being most severely affected. The changes were characterized by the dilation of myelin sheaths containing preserved axons, myelinophages or axonal debris, occasional axonal swelling, and decreased density of myelin and axons associated with astrocyte proliferation and perivascular gitter cell cuffs. The severe Wallerian-type degeneration of the axons was better appreciated in the longitudinal sections.

A second neurologic syndrome was diagnosed in three of four cubs born in July 2002 at the Zoo of Doue-la-Fontaine, France. The first cub drowned at 2 weeks of age during an accidental flooding of the building. At the age of 3–5 weeks the three remaining cubs started to show clinical neurologic symptoms characterized by head and body tremors, swaying gait, followed by inability to stand and paresis of hind limbs. Additional clinical findings were loss of body weight and a shaggy hair coat. Due to the progression of the neurologic symptoms all three cubs were euthanatized at the age of 9–11 weeks and necropsies performed. Gross examination revealed severe emaciation. The hair coat appeared shaggy due to the presence of small dystrophic, hyperkeratotic hair. No lesions were observed in the other organs. Histopathologic investigation of the nervous system revealed lesions characterized by the presence of chromatolytic neurons in the spinal cord, predominantly located in the proprioceptive nucleus thoracicus in the proximal lumbar segments with associated microgliosis. Evidence of neuronal necrosis and neuronophagia was not evident. In one animal there was also distinct myelin sheath dilation and axonal degeneration in the corresponding thoracic and cervical spinocerebellar tracts (dorso-lateral). No changes were seen in the brain, spinal ganglions and peripheral nerves.

The cases from Switzerland, Auneau, and Thoiry appear to be clinically and pathologically similar to a previously described neurologic disorder of snow leopard cubs at the Helsinki zoo.1 In Helsinki, snow leopard cubs presented with spastic paresis. Pathologic lesions from these cubs were characterized by myelin and axonal loss associated with astrocytic proliferation without inflammatory reaction, predominantly in the thoracic and lumbosacral segments of the spinal cord. These cases also resemble the degenerative myelopathy described in cheetahs, an emerging disease which severely affects the European cheetah population.3,4 To date, the cause of the degenerative lesions in these two species could not be determined.

The cases from Doue are clearly distinct. Not only are the age of onset, the clinical symptoms and histopathologic features distinct, but also the fact that this was an isolated litter from a breeding pair that had already produced several normal litters. This contrasts the situation in the three other institutions where afflicted litters were repeatedly produced.

Neurodegenerative diseases characterized by spinal white matter degeneration or neuronal chromatolysis have been described in human and in several animal species, including cheetahs and snow leopards, but the cause is mostly unknown.1-4 Some of these diseases have been shown to have a hereditary basis, but nutritional deficiencies, intoxication or metabolic disorders were suggested as other etiologies. The genetic basis of captive snow leopards is narrow. Going back one to five generations, a preliminary pedigree analysis showed that all affected snow leopards from Switzerland, Auneau, Thoiry and Doue have common ancestors. This may indicate a possible genetic predisposition, but whether this is the sole etiology remains to be elucidated.

Literature Cited

1.  Haltia, M. and C. Wahlberg. 1984. Spastic paraparesis in young snow leopards (Panthera uncia). Int. Pedigree Book Snow Leopard. 4: 105–107.

2.  Junge, R.E., Skip, J. and W.A. Carlton. 1986. Leukoencephalomyelopathy in a snow leopard (Panthera uncia). Proc. Am. Assoc. Zoo Vet. Pp. 150–152.

3.  Walzer, C. and A. Kiibber-Heiss. 1995. Progressive hind limb paralysis in adult cheetahs. J. Zoo Wild. Med. 26: 430–435.

4.  Walzer, C., A. Uri, ,N. Robert, A. Kiibber-Heiss, R. Nowotny, and P. Schmid. 2003. Acute onset ataxia in cheetah cubs. J. Zoo Wild. Med. 34: 36–46.


Speaker Information
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Nadia Robert, DVM, DACVP
Center for Fish and Wildlife Health
Berne University
Berne, Switzerland

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