Degenerative Myelopathy and Vitamin a Deficiency in a Young Black-Maned Lion (Panthera Leo)

Abstract

Abstract. Degenerative myelopathy and vitamin A deficiency were diagnosed in a 1-year-old, female, black-maned lion (Panthera leo). Diffuse white matter degeneration characterized by dilated myelin sheaths, Wallerian degeneration, and reactive astrocytosis was present at all levels of the spinal cord. With luxol fast blue-cresyl echt violet stain, bilaterally symmetrical demyelination was observed in the fasciculus cuneatus of the cervical spinal cord and in peripheral white matter of cervical, thoracic, and lumbar segments. Additionally, the ventral gray columns and brain stem nuclei contained rare chromatolytic neurons with abnormal neurofilament accumulation. Leptomeninges of the cervical spinal cord were focally adhered to the dura and thickened by fibrosis and osseous metaplasia. Vitamin A deficiency was diagnosed based on hepatic vitamin A concentration of 1.71 mg/g dry weight. Adequate hepatic vitamin A concentration for yearling to adult domestic animals ranges between 150 and 1,000 mg/g dry weight. Lesions were distinct from those previously described in young captive lions with vitamin A deficiency, which had thickened skull bones and cerebellar herniation. The pathogenesis of vitamin A-associated myelopathy in this lion may be similar to that described in adult cattle, which is believed to result from spinal cord compression secondary to elevated pressure of cerebrospinal fluid.

Large felid leucoencephalomyelopathy in a Sumatran tiger (Panthera tigris sumatrae) from an Australian zoo

“…No aetiology for this white matter degeneration was found in the North American cases, but it was considered unlikely to be infectious, especially as there was no inflammatory reaction. Primary neurodegenerative diseases in large, non‐domestic felids are rare, being largely restricted to a leucomyelopathy of European cheetahs of unknown cause and degenerative myelopathies secondary to copper and vitamin A deficiencies. Because all the cheetahs in the USA study were fed a diet from a common commercial source, an environmental neurotoxin was suspected, a notion supported by cessation of cases when the feed source was changed.…”

Leukoencephalomyelopathy in Specific Pathogen-free Cats

“…13 The etiology of the syndrome, termed a leukoencephalomyelopathy, has not been determined, although the primarily degenerative nature of the lesions and their bilateral distribution suggest possible nutritional, metabolic, or toxic causes. The fact that the only significant difference between the affected cats in the SPF colony and their conventional status counterparts, moved out of the SPF colony at weaning, was the exclusive feeding of a gamma-irradiated diet and that no further cases of the condition were reported once supplemental or replacement pasteurized diets were introduced, provides circumstantial evidence that the ataxia may have a nutritional basis.…”

“…The relatively high dietary fat requirement of cats 12 may be significant in this context in that irradiation of this fat component could potentially generate higher concentrations of micronutrient-damaging free radicals than would be generated on irradiating laboratory animal diets of lower fat content. 22 Vitamin A deficiency has previously been implicated in ataxic syndromes in lions 13,14 and cheetahs. 17 In these reports, axonal degeneration was variously attributed to thickening of the cranial bones 14 or to elevations in CSF pressure, 13 leading to CNS compression.…”

MRI, CT and histopathological findings in a cat with hypovitaminosis A

“…Maratea and others29 have also reported thickening and focal adhesion of the cervical spinal cord leptomeninges, as well as osseous metaplasia and mineralisation, in a black maned lion with low hepatic vitamin A concentration.…”