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.     

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.     

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 (BSE) safety measures in Japan

Since the first identification of bovine spongiform encephalopathy (BSE) in Japan in September 2001, a series of safety measures was introduced by the Ministry of Agriculture, Forestry and Fisheries, the Ministry of Health, Labour and Welfare and the Food Safety Commission of the Cabinet Office. These measures included blanket BSE testing and removal of specified risk materials at slaughterhouses, surveillance of risk animals and a ban on the use of meat-and-bone meals and traceability on all farms. The Japanese experience over the past five years has shed light on several issues in countries that have a low BSE incidence.     

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 and the safety of milk from Canadian dairy cattle

The detection of bovine spongiform encephalopathy (BSE) in beef cattle closed Canadian beef export markets to 30 countries, including the USA, with devastating financial losses. The detection and confirmation of the fifth and seventh BSE-infected animals but first infected dairy cows extended the problem of risk management to Canadian dairy farmers. As the public are concerned about the safety not only of beef but also of milk and milk products that may contain disease-causing prions, this review examines the evidence for the safety of milk from studies on prions in milk or colostrum and their vertical and lateral transmission in various animal systems. The evidence indicates that the risk of contracting new variant Creutzfeldt-Jakob disease through the consumption of milk is negligible.     

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: diagnostic significance of vacuolar changes in selected nuclei of the medulla oblongata

The adequacy of a histopathological diagnosis of bovine spongiform encephalopathy (BSE) based exclusively on observations of neuroparenchymal vacuolation in three specific neuroanatomic nuclei was tested by using a standard coronal section of medulla oblongata cut at the obex. The agreement between the observations and the definitive histopathological diagnosis was assessed in each of 684 bovine brains - 563 confirmed cases of BSE, 20 with changes which did not diagnose BSE conclusively and 101 in which the lesions of BSE were not detected. When the assessment was confined to the solitary tract nucleus and the spinal tract nucleus of the trigeminal nerve a positive result was obtained in 99.6 per cent of confirmed cases of BSE and only 1 per cent of brains in which lesions of BSE were not detected gave a false positive result. Thus an initial examination of the single section, together with an examination of representative areas of the rest of the brain when no unequivocal lesion was found, provided a satisfactory method for the routine diagnosis of BSE.     

Bovine spongiform encephalopathy: detection of fibrils in the central nervous system is not affected by autolysis

The effect of autolysis on the electron microscopic detection of the characteristic abnormal fibrils, originally called 'scrapie-associated fibrils', was investigated in four different areas of the central nervous system (CNS) from 10 clinically suspect BSE cattle after post mortem delay and compared with the histopathological diagnosis. The tissues for fibril detection were subjected to controlled incubations to simulate autolysis. Fibril detection in all areas sampled from nine animals in which BSE was confirmed by histopathology was not affected by combined post mortem delays and specific controlled treatments. Detection of fibrils from the cervical spinal cord was no less sensitive than from brain areas. Fibrils were not detected in the one suspect case in which histopathology did not reveal lesions of BSE. The study confirms that fibril detection is of diagnostic value in BSE when post mortem autolysis renders CNS material unsuitable for histopathology.