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Until recently, the United States appeared to have at least approached the ideal by having a large national herd, an adequate testing program, and an apparently small risk for contamination by imported cattle or cattle feed. Obviously, the ideal country in which to examine the question of sporadic BSE would have a large national herd that was guaranteed never to have been exposed to environmental sources of infection. In this article we consider the importance of atypical BSE within the overall concept of sporadic (spontaneous) disease and whether such cases, if they exist, could account for at least some cases of apparently sporadic Creutzfeldt-Jakob (CJD) in humans. Thus, the phenomenon of spontaneous disease remained in limbo until the recent discovery of "atypical" strains of BSE reopened the question. The pros and cons of these competing ideas have been argued elsewhere ( 2, 3), and neither will ever be convincingly proved or disproved. These measures have been extraordinarily successful, to the extent that no new countries have been added to the list during the past year and the number of new cases has dramatically diminished in most countries in which BSE has appeared (the situation in some countries with insufficient surveillance remains unclear).Īlthough the origin of the epidemic is thought to have been caused by a species-crossing contamination by sheep scrapie during the course of rendering and recycling carcass meat and bone meal as cattle feed, an alternative hypothesis suggested an origin in a similarly recycled case of spontaneously occurring disease in cattle. By 2006, 20 years after its first appearance in the United Kingdom, the disease had been reported in an additional 24 countries ( 1).īeginning toward the end of the 1980s in the United Kingdom, and in the 1990s in other countries, numerous regulations were enacted to minimize the entry of contaminated tissues into both the animal and human food chains and to eliminate the international spread of disease. Because of continuing exportation of both live cattle and meat and bone meal rendered from the carcasses of slaughtered cattle, the disease spread throughout most of Europe and a few non-European countries. Such a link might yet be established by the discovery of a specific molecular marker or of particular combinations of trends over time of typical and atypical BSE and various subtypes of sporadic CJD, as their numbers are influenced by a continuation of current public health measures that exclude high-risk bovine tissues from the animal and human food chains.īovine spongiform encephalopathy (BSE) was first recognized in 1986 in the United Kingdom and quickly reached epidemic proportions, affecting >30,000 cattle per year by 1992.
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A link between BSE and sporadic CJD has been suggested on the basis of laboratory studies but is unsupported by epidemiologic observation.
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To achieve 95% statistical confidence that the prevalence for sporadic BSE is no greater than 1 per million (i.e., the annual incidence of sporadic Creutzfeldt-Jakob disease in humans) would require negative tests in 3 million randomly selected older cattle. Strategies to investigate the possible existence of sporadic bovine spongiform encephalopathy (BSE) require systematic testing programs to identify cases in countries considered to have little or no risk of orally acquired disease or to detect a stable occurrence of atypical cases in countries in which orally acquired disease is disappearing.