The Bse Epizootic

First recognized in November of 1986, with retrospective histological evidence of the first case dating from November 1985, the BSE epizootic peaked in 1992 with more than 1000 cattle cases confirmed per week (see Fig. 2). Reviews of archived tissue samples from cattle with undiagnosed disease have failed to identify any unrecognized cases prior to 1985 (1,6).

40,000 35,000 30,000

25,000 20,000 15,000 10,000 5,000 0

Figure 2. Confirmed cases of BSE in UK cattle by year.

Epidemiological studies suggest that UK cattle became infected through exposure to contaminated MBM feed supplements in 1981 to 1982 (6). Although the original source of the contamination is unknown, the most accepted theory proposes that sheep scrapie prions completed a species jump and induced normal cattle prion protein to become distorted (6-9). This distorted cattle prion protein distorts others, eventually resulting in clinical disease. Affected animals were slaughtered or died, rendered, and the resulting MBM containing abnormal cattle prion protein was fed to other cattle. The UK sheep population has a high enzootic rate of scrapie, and a high ratio of sheep to cattle (45 million to 12 million). This resulted in sheep representing 14% of rendered products, compared with 0.6% in the United States. The higher level of MBM supplements fed to young calves in the UK (2-4% MBM in rations) may explain the high incidence of BSE as compared with other EU countries (30).

A second theory suggests that cattle have always had a low incidence of BSE, perhaps at a rate similar to the l:l,000,000/year incidence of CJD found in humans, which was unrecognized (31). Changes in rendering practices in the late 1970s and early 1980s no longer destroyed infec-tivity sufficiently to prevent accumulation of the necessary infectious dose.

A third hypothesis, offered in an effort to explain the rapid appearance and spread of the epizootic, theorizes importation of the agent to the UK in MBM containing abnormal proteins from an unknown ruminant other than cattle (32). The original source would have to be a country or countries lacking the infrastructure necessary to identify clinical cases and with rendering systems inadequate to destroy the agent. The imported material would need to be in sufficient quantity, or commingled with domestic MBM, to result in the volumes of contaminated product with infectious dose levels necessary to account for the epizootic.

Whatever the original source, changes in British rendering methods in the late 1970s and early 1980s are proposed to have played a role in the widespread amplification of the disease (6-8). The solvent extraction step with steam recovery was eliminated, and a liquid slurry process was introduced (33). Both changes may have resulted in decreased exposure of materials to heat during rendering. Critics note that TSEs such as scrapie have been demonstrated to be resistant to solvents, and the temperatures used (about 100°C) are too low to inactivate the agent (23,24,32). The impacts from these changes in the rendering system on the epizootic are unknown. The use of MBM in cattle rations as a source of supplemental protein had been a common practice for decades prior to the emergence of BSE, and scrapie is known to have been endemic in the UK for more than 250 years.

BSE has been confirmed in native cattle in Ireland, France, Portugal, the Netherlands, and Switzerland. Exported British cattle have been found with the disease in Oman, the Falkland Islands, Germany, Denmark, Canada, and Italy (1). The export of rendered animal feed products from the UK is considered the source of the disease outbreaks in native cattle in other countries. There are concerns that the number of cattle, and the amount of feed, exported should have resulted in significantly more disease than reported (30). There is confusion about whether the expected cases failed to occur for unknown reasons, went unrecognized within the surveillance systems in place, or were unreported.

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