Naturally occurring transmissible spongiform encephalopathies (TSE) ha
ve been identified in several species including sheep, mink, captive d
eer, cattle, and humans. In 1990 a similar disease was recognised in a
domestic cat in England.1 These diseases are characterised clinically
by progressive locomotor and behavioural abnormalities which are unre
sponsive to therapy. Diagnosis depends upon histopathological examinat
ion of central nervous tissues after death. The presence of widespread
grey matter neuropil vacuolation, neuronal vacuolation, and a glial r
eaction are pathognomonic of the TSE. In addition, the demonstration o
f scrapie-associated fibrils (SAF) and PrP (known both as protease res
istant protein and as prion protein) are often also of diagnostic valu
e.2