91 research outputs found
Feline Spongiform Encephalopathy: A Study of the Clinical Presentation and Pathology
No full textFeline Spongiform Encephalopathy (FSE) was first reported in 1990 by Wyatt et al., over three years after Bovine Spongiform Encephalopathy (BSE) was first identified. At present only limited published clinical and pathological descriptions of FSE are available. The aims of this thesis are therefore to review the current literature on FSE and describe the clinical and pathological features of the cases in this study. The nine naturally occurring cases of FSE included in this thesis were presented to Glasgow University Veterinary School during the period of June 1990 to April 1998. A set of clinical criteria was identified allowing a presumptive ante-mortal diagnosis of FSE. These included: progressive behavioural changes, hyperaesthesia, ataxia, hypersalivation and intermittent pupillary dilatation, although not all where present in every' case. No evidence of a breed or sex predilection, geographic clustering, reliable routine diagnostic test or successful treatment modality could be identified. The nature and distribution of the pathological changes are very similar in all cases in this series, with the significant changes confined to the central nervous system (CNS). The changes include vacuolation of grey matter neuropil, vacuolation of individual neurones, Wallerian-type degeneration and a reactive astrocytosis. Neuropil vacuolation is widespread, but certain regions (including the cerebellar granule cell layer, deep cerebral layers, thalamus, basal nuclei and septal nuclei) appear to be preferentially affected. Vacuolation of individual neurones is selectively present in the dorsal nucleus of the vagal nerve and raphe nuclei, and occasionally present in the hypoglossal nucleus, vestibular nuclei and reticular formation. Characteristic patterns of pathological PrP accumulation in the CNS are evident on PrP immunocytochemistry, using monoclonal antibody 3F4 raised against hamster PrP. Aspects of the spongiform changes and PrP immunocytochemistry in these cases bear strong similarities to new variant CJD (vCJD), although with some differences. These similarities are consistent with circumstantial evidence suggesting that both FSE and vCJD originated from ingestion of material contaminated with the infective agent responsible for BSE (Bruce et al. 1997; Collinge et al. 1996)
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