Two annual, random samples of clinically suspect cases of bovine spongiform encephalopathy (BSE) were taken in 1992-93 (year 1, 1500 cases) and 1993-94 (year 2, 1000 cases). From each sample, 100 positive cases were examined in detail to establish the severity of the vacuolation in 17 specific neuroanatomical locations. The resultant 'lesion profiles' were compared with the profile obtained from a similar sample of BSE-affected cattle from early in the epidemic (1987-89); the comparison showed that the distribution and severity of vacuolation in BSE has remained unchanged. The cases not confirmed as BSE on histological examination (172 in year 1 and 162 in year 2) were examined for evidence of any alternative neurohistological diagnosis. As in previous studies, the majority of these cases showed no significant lesions (61.6 and 61.7 per cent). The remainder consisted of bilateral focal spongiosis of unknown significance (26.7 and 21.0 per cent), inflammatory conditions (8.1 and 11.1 per cent) and a small number of cases with tumours, cerebrocortical necrosis or idiopathic brainstem neuronal chromatolysis. No evidence was found of any cases of BSE with an atypical distribution of lesions. These findings support the theory that the BSE epidemic is sustained by a single, stable strain of the BSE agent, and confirm that the existing statutory diagnostic criteria continue to be appropriate.
Heart rates of healthy cows and cows suspected of having bovine spongiform encephalopathy were measured by auscultation and by a portable cardiac monitor. Bradycardia was demonstrated in suspect cases which were confirmed histopathologically. Disturbances in cardiac rhythm were also evident in some cases. Healthy cows deprived of food exhibited bradycardia. The administration of pharmacological doses of atropine indicated that bradycardia in BSE was mediated by increased vagal influence, suggesting that the cardioinhibitory reflexes in the caudal brainstem were functionally altered by the disease.
Bovine spongiform encephalopathy (BSE) is a scrapie-like disease of cattle first recognized in the United Kingdom in 1986. The predominant pathology is a vacuolar degeneration of the central nervous system. In naturally affected cattle the severity and distribution of these vacuolar changes present an almost invariable pattern. The source of infection responsible for the current epidemic is considered to be commercially processed feed contaminated with a scrapie-like pathogen. A foodborne source of infection is also considered the likely origin of scrapie-like disease in other mammalian species, including the domestic cat and several species of exotic bovids and felids in zoological collections, which have occurred contemporaneously with the BSE epidemic. In common with other scrapie-like diseases BSE has been transmitted experimentally to several other species. The transmission of BSE to cattle by the oral dosing of calves with BSE-affected brain stem homogenate has been reported previously. Histopathological examinations of the brain based on the lesion profile system, developed originally for the characterization of scrapie in laboratory mice, were used to examine the distribution and severity of vacuolar changes in these cattle. The results were compared with the vacuolar profile in naturally affected cattle. The distribution of vacuolar changes in cattle dosed orally with BSE closely resembles that observed in naturally affected cattle providing experimental evidence that this route closely simulates natural infection and subsequent neural pathogenesis.
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