Bovine spongiform encephalopathy: epidemiological studies on the origin.

The results of further epidemiological studies of bovine spongiform encephalopathy (BSE) support the previous findings that the onset of exposure of the cattle population to a scrapie-like agent, sufficient to result in clinical disease, occurred in 1981/82. The onset of this exposure was related to the cessation, in all but two rendering plants, of the hydrocarbon solvent extraction of fat from meat and bone meal. A further possible explanation, related to the geographical variation in the reprocessing of greaves to produce meat and bone meal, was identified for the geographical variation in the incidence of BSE.     

Bovine spongiform encephalopathy: epidemiological features 1985 to 1990.

Following the identification of bovine spongiform encephalopathy (BSE) in the British cattle population in 1986 epidemiological studies were launched. This paper provides an updated account of the epidemiological features of BSE from 1985, when the first cases, based on clinical histories, occurred, until 1990. The number of cases up to December 1989 represents an annual incidence of 3.9 confirmed cases per 1000 adult animals in Great Britain. Many more dairy herds were affected than beef suckler herds, a difference attributable to the difference in feeding practices between the two herd types. The geographical variation in incidence previously described has persisted with the highest incidence in the south and east of England. Other features of the epidemiology, including the low within-herd incidence, remained unaltered from the earlier findings. The results support the previously suggested hypothesis that the outbreak of BSE was due to the sudden exposure of the cattle population to a scrapie-like agent in 1981/82. There was no evidence of direct transmission between cattle during the period considered.     

Bovine spongiform encephalopathy and related diseases: an epidemiological overview

Following the recognition of the novel disease bovine spongiform encephalopathy in Great Britain in 1986, epidemiological and other research studies were initiated. The initial results of these studies revealed that bovine spongiform encephalopathy was caused by a scrapie-like agent and the vehicle of infection was meat-and-bone meal incorporated into cattle feedstuffs as a protein source. The British cattle population became effectively exposed in 1981-82 and this was associated with a dramatic reduction in the use of hydrocarbon solvents for the extraction of fat in the production of meat-and-bone meal. The feeding of ruminant-derived protein to ruminants was statutorily banned in July 1988 to prevent further exposure from the food-borne source. This paper reviews the epidemiological aspects of bovine spongiform encephalopathy and the occurrence of transmissible spongiform encephalopathies in other species.     

Bovine spongiform encephalopathy: a review

Transmissible Spongiform Encephalopathies are a group of chronic, always fatal diseases affecting the central nervous system of humans and animals. They occur in all species and are probably caused by agents called prions. In this minireview, a first part provides an overview of the various disease forms, a second part is devoted to the molecular biology of transmissible spongiform encephalopathies, and a last part deals with the specific problems of the Bovine Spongiform Encephalopathy.     

Bovine spongiform encephalopathy in Northern Ireland: epidemiological observations 1988-1990.

This study describes the epidemiological features of bovine spongiform encephalopathy (BSE) in Northern Ireland where the first case occurred in November 1988. They were very similar to those observed in Great Britain except that the annual incidence of BSE in 1990 in Northern Ireland, 2.3 confirmed cases per 10,000 adult cows, was approximately one 10th of that in Great Britain. The findings were also consistent with the current hypothesis that affected cattle had been exposed to a scrapie-like agent via cattle feedstuffs containing ruminant-derived protein. However, a preliminary investigation of the potential sources of infection for cattle in Northern Ireland did not provide any conclusive evidence.     

Bovine spongiform encephalopathy and human health

Because bovine spongiform encephalopathy (BSE) has probably been caused by accidental transmission of the transmissible agent of sheep scrapie there is concern that humans may be at risk from BSE. Epidemiological and experimental evidence is examined which suggests that this is unlikely.     

Feline spongiform encephalopathy: fibril and PrP studies.

The brains from 18 cats were examined for the presence of the fibrils and modified PrP protein which are molecular diagnostic markers for scrapie-like diseases. Thirteen cats were referred with clinical neurological signs potentially indicative of feline spongiform encephalopathy (FSE). Of these, five had histopathological changes of FSE, five had other lesions of the central nervous system, and in three the brain was normal. The remaining five cats had no clinical neurological signs and were selected as controls. Fibrils and modified PrP protein were found in the brains of the five cats with FSE and in one of the cats with neurological signs but no histopathological changes in the central nervous system. Fibrils were present in the absence of modified PrP in the brains of two cats, one with neurological signs and a histologically confirmed meningioma, and one with no neurological signs and a histologically normal brain.     

Bovine spongiform encephalopathy in a cow in the United Kingdom

Bovine spongiform encephalopathy (BSE) was diagnosed in a cow with a history of behavioral change, apprehension, hyperesthesia to auditory and tactile stimuli, wide-based stance, and marked hind limb hypermetria. Myoclonus involving individual muscles was observed in the shoulder region, ventral cervical region, and upper portion of the hind limb. Clonus was observed in the forelimbs. Clinicopathologic findings were normal, except for high serum globulin concentration, which was attributable mainly to an increase in the gamma-globulin fraction. Results of electroencephalography revealed almost continuous high-amplitude complexes in the occipital leads, interspersed with short runs of normal activity. There were generalized discharges, but these were not periodic. Current theory implicates the scrapie agent (prion) as the causal agent for BSE. The presence of scrapie in, and the possible entry of prion into bovine feedstuffs could result in the emergence of BSE in the United States.