Spongiform encephalopathy is a neurological disease of cats that affects the central nervous system.

Spongiform change in the central nervous system can involve the grey or white matter, or both, and is characterised by leucoencephalopathy, with the presence of vacuoles in the myelin sheaths, in the dendrites or axons in the neuropil, in the neuronal cell bodies or by swelling of astrocyte or oligodendrocyte cytoplasm.

Congenital spongiform degeneration of the grey matter has been described in cats and a suspected inherited encephalomyelopathy characterised by spongy change in the grey matter and a Wallerian-like degeneration in the spinal cord has also been described in five related Birman kittens. Transmissible spongiform encephalopathies cause spongiosis in humans and animals. This disorder in cats is referred to as feline spongiform encephalopathy (FSE) and has been recognised since 1990.

Nutritionally-induced leucoencephalopathy, with spongiform degeneration has been reported in cats fed gamma-irradiated commercial dry pet food but is not related to viral-FSE or congenital spongiform degeneration.

An encephalopathy in colony cats has also been reported in the United Kingdom characterised by a degeneration of axons and myelin with myelophages often seen within remnants of the fiber. These lesions affected long tracts in the spinal cord and brainstem, cerebral white matter, and optic pathways. There was an accompanying mild status spongiosis, increased numbers of astrocytes and microglial cells, and occasionally, swollen axons. Inflammatory changes were not a feature. Most severe lesions occurred in the spinal cord, especially involving larger diameter fibers (e.g., spinocerebellar and ventral tracts)^[1].

Spongiform encephalopathy usually occurs in young cats, though adult-onset disease has been reported in Ragdolls^[2]. Common clinical signs are ataxia, abnormal behavior, hyperaesthesia, and altered grooming. The presence of fibrils similar to those described in scrapie or bovine spongiform encephalopathy has also been described^[3].

Spongiform degeneration of the white matter has been reported in two Egyptian mau kittens with widespread vacuolation throughout the brain and spinal cord. The most severely affected areas were the cerebral subcortical, subependymal, cerebellar and brain stem white matter. Similar lesions have also been described in cats with experimental bromethalin toxicosis.

Congenital spongiform encephalopathies can be differentiated from FSE because of;

• early onset of spongiform encephalopathy which is usually under 6 months of age;
• location of lesions with spongiform encephalopathy usually affecting cerebral cortex, cerebellum, vestibular and some other brain stem nuclei whereas FSE usually affects the thalamus (medial geniculate nucleus), corpus striatum, and raphe, vagal and red nuclei.
• negative prion test (PrP-res immunolabelling)

References

1. ↑ Palmer AC, Cavanagh JB. (1995) Encephalomyelopathy in young cats. J Small Anim Pract 36:57-64
2. ↑ Comito B et al (2010) Adult-onset spongiform leukoencephalopathy in 2 Ragdoll cats. J Vet Intern Med 24(4):977-982
3. ↑ Salvadori, CS, et al (2007) Spongiform neurodegenerative disease in a Persian kitten. Journal of feline medicine and surgery 9:242-245