No abstract

Detailed neuropathological findings in 222 cases of naturally occurring scrapie from Great Britain are described. The material consisted of formalin-fixed brain from eight breeds of sheep submitted between 1982 and 1991. Paraffin-embedded histological sections were made from several specified brain areas, including the medulla oblongata, cerebellum, pons, mesencephalon, diencephalon, septal area, basal ganglia and frontal cortex. Sections were examined by conventional and polarised light microscopy and the type and distribution of the lesions were recorded. Histologically, the lesions included vacuolation of neuronal perikarya and grey matter neuropil, neuronal degeneration (especially "dark' neurons) and loss, a reactive glial (predominantly astrocytic) response and amyloidosis. Vacuolar lesions were present in the cerebral cortex of 37 per cent of cases, centred around the superior frontal gyrus. Vacuolar lesions were detected in the neocortex for as long as sections have been taken from the superior frontal gyrus and are thus probably not a new feature of the disease. The distribution of vacuolation in the grey matter neuropil could be classified into seven patterns. Data from individual breeds of sheep showed that in some breeds there were significant differences in the age at which animals with different patterns of vacuolation died from scrapie.

The occurrence of bovine spongiform encephalopathy (BSE), recognition that it is a new scrapie-like disease epidemic in domestic cattle in the United Kingdom and concern of a remote zoonotic potential has, in four years, produced a plethora of documented information. While much of this information has been communicated outwith the scientific literature, this review attempts to summarise, from a neuropathological viewpoint, the main findings to emerge. The initial studies established the nosological homology of BSE with the subacute spongiform encephalopathies or "prion" diseases of animals and man. Epidemiological data are consistent with an extended common source epidemic originating from an abrupt change, commencing in 1981-82, in the exposure of domestic cattle to a scrapie-like agent in meat and bone meal incorporated into commercial animal feedstuffs. It is currently proposed that the method of production of meat and bone meal has contributed vital factors to the change in exposure. Invariability of the distribution pattern of vacuolar pathology in the natural disease and on primary transmission to cattle suggests a uniformity of the pathogenesis of BSE. Studies in mice suggest uniformity also of the biological properties of different BSE isolates but indicate that the properties differ from those of sheep scrapie isolates. Human health risks, although perceived to be negligible, have been addressed by various strategies including statutory measures and long term monitoring.

No abstract

Four of 17 cirl buntings (Emberiza cirlus) involved in a trial translocation in 2004 for conservation purposes died and were examined postmortem. Two of the cirl buntings showed intestinal and hepatic lesions, including necrotising enteritis, consistent with isosporoid coccidiosis, and a third had an intestinal infestation of isosporoid coccidia. Sporulated oocysts from faecal samples from the birds were identified as Isospora normanlevinei, a parasite previously detected in cirl bunting populations in continental Europe. In a subsequent translocation of 75 cirl buntings from Devon to Cornwall in 2006, each brood of birds was placed in strict quarantine at low stocking density, with improved hygienic precautions and detailed health surveillance, and each bird was treated prophylactically with toltrazuril in an attempt to control the disease but not eliminate the I normanlevinei parasites. Seventy-two of the 75 birds were successfully reared and released, and there were no apparent clinical or pathological signs of isosporoid coccidiosis in any bird. I normanlevinei was detected in the released population, an indication that it had been successfully conserved.