Feline spongiform encephalopathy

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Feline spongiform encephalopathy is a disease that affects the brains and livers^{[citation needed]} of felines. It is caused by proteins called prions.

1 Disease
2 Clinical signs
3 Epidemiology
4 Diagnosis
5 Treatment
6 See also
7 References
8 External links

[edit] Disease

Feline spongiform encephalopathy (FSE) is a prion disease thought to be related to Bovine spongiform encephalopathy (BSE). This disease is known to affect domestic and captive feline species. Lezmi S. et al (2003), suggested that this infectious agent might be spread by both haematogenous and nervous pathways. Like BSE, this disease can take several years to develop. It is probable, but not proven, that the affected animals contract the disease by eating contaminated bovine meat.

[edit] Clinical signs

Ataxia was observed to last for about 8 weeks in the affected animals. The ultimate result is death of the infected animals.

[edit] Epidemiology

This disease was first reported in the United Kingdom in 1990. Up until about 5 years ago, there were reports of 87 FSE cases (only domestic cats) in the UK, one in Norway, one in Northern Ireland and one in Switzerland. However, since 1990, other feline species in zoos were reported to have contracted this disease.

[edit] Diagnosis

This disease can only be confirmed at the post-mortem, which includes identification of bilaterally symmetrical vacuolation of the neuropil and vacuolation in neurones. Lesions are likely to be found in basal ganglia, cerebral cortex and thalamus of the brain.

[edit] Treatment

Unfortunately this is a terminal condition and there is currently no specific treatment for the disease.

[edit] See also

Bovine spongiform encephalopathy

[edit] References

http://www.provet.co.uk/petfacts/healthtips/fse2.htm
Lezmi S., Bencsik A., Monks E., Petit T., Baron T.; First case of spongiform encephalopathy in a captive cheetah born in France:PrP(sc) analysis in various tissues revealed unexpected targeting of the kidney and adrenal gland; Histochem. Cell Biology; 2003; 119(5): 415-422