An introduction to the issue of bovine spongiform encephalopathy

Most of these infected animals were slaughtered for human consumption before there were any clinical signs of BSE.

Even while some European countries were clamouring for bans on British beef, they were ignoring warnings from the European Commission about how to avoid the spread of BSE in their own herds. The origin of the epidemic of BSE following the first case is much clearer and, although some uncertainties remain, the recycling of bovine tissues back to cattle in feed is the most plausible explanation for the fuelling of the epidemic and this provided the key to controlling the spread of the disease through restrictions placed on such recycling.

An introduction to the issue of bovine spongiform encephalopathy

In contrast, the incidence of vCJD in humans is low and it is unclear whether a peak incidence has occurred Fig. PrP was identified as a susceptibility factor for cross-species transmission experiments with PrP transgenic mice where expression of hamster PrP was found to render transgenic mice susceptible to hamster-specific scrapie strains Prions can accumulate in the brains of cattle after 24 months of infection. After this adaptation, on-going intra-species recycling caused the BSE epidemic in British cattle [ 35 , 47 ]. At present only the infectious agent causing Classical BSE has been demonstrated to be transmissible to humans. Further evidence in support of this hypothesis was the higher incidence of BSE in dairy cattle than in beef cattle. However, it remains unclear whether BSE originated by adaptation from an unusual strain of sheep scrapie or from an unrecognised bovine TSE case. More recent studies showed that expression of PrPsen is required for susceptibility to TSE diseases, and propagation of infectivity is eliminated in the absence of the PrP gene At present, the means of acquisition of TSE agent in these patients remains a mystery. This was more effective than The Bovine Spongiform Encephalopathy Order as it was more far reaching and did not merely address animal feed for ruminants.

The incubation period for TSEs in mice can be up to 18 months. In the United States, the CDC has refused to impose a national requirement that physicians and hospitals report cases of the disease.

To control potential transmission of vCJD within the United States, the American Red Cross has established strict restrictions on individuals' eligibility to donate blood. While scrapie is common in sheep, recorded CJD is very rare in man.

Origin of bse

There is an optimised Western Blot approved for use by the European Union in which takes 6 to 8 hours to complete. In addition, it is legal for ruminants to be fed byproducts from some of these animals. The incubation period or latent period time from exposure to the agent until clinical onset is long, ranging from 2 years to greater than 10 years. BSE infectivity levels of CNS tissue from clinically diseased cattle have been titrated in cattle, and there is evidence that 0. There are also a further two types of atypical BSE reported in Japan and Belgium that have yet to be classified. Once the infection had been introduced into cattle, it seems highly likely that it was recycled to other cattle through MBM in the same way as happened in the UK. In both species, the incidence of CWD in contaminated game farms can be much higher than in wild populations, and the commerce in live farmed deer and elk appears to account for the rapid spread to new sites in the US and Canada which are not always geographically contiguous with previous areas of infection Fig. Nevertheless, there continues to be a paucity of information concerning the structure and composition of the infectious agent. Cattle and feed exported from the UK have seeded smaller epidemics in other European countries, where control measures were applied later. Current hypotheses include exposure to an as yet unidentified virus, spontaneous generation of a non-viral agent through somatic cell mutation of PrP in each diseased individual, and stochastic initiation of spontaneous PrPres formation without PrP mutation. This was because the feed ban would not have impacted on cases of BSE due to maternal transmission.

Clinical variability occurs even within individual patients of the same family, suggesting that genes other than PrP or non-genetic factors also influence these diseases 45 — To date, the incidence of both forms is negligible and estimated to approach zero cases per million cattle. Although the mechanism of these effects is not certain, the susceptibility of sheep with these allelic variants to scrapie correlates with the relative efficiencies with which the respective PrPC molecules convert to PrPres in in vitro systems Ruminant-derived MBM was still permitted to be fed to pigs and poultry as these animals were not thought to be susceptible to infection with the BSE agent.

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Bovine spongiform encephalopathy : OIE