BSE and the Emergence of vCJD

    There are a few major theories regarding the emergence of prion diseases. Many sources agree that the consumption of a scrapie infected sheep led to BSE, which in turn led to vCJD through human consumption of infected beef (WHO, CDC, Environmental Literacy Council). The spread of BSE can largely be attributed to the practice of feeding the ground up remains of infected cows to other cows (especially due to changes in the processing of meat and bone meal). The practice of air-injection stunning to slaughter the cattle may have then facilitated the contamination of beef eaten by humans.

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    Studies have also found that chronic wasting disease can be transmitted indirectly through paddocks contaminated with infected carcasses or infected waste. Though prions could not be directly demonstrated in soil, the results suggest that deer can be infected by foraging and consuming soil in contaminated vicinities. A similar phenomenon may have lead to the original spread of scrapie in sheep. Along the same lines as the BSE contaminated feed theory, most sources agree that Kuru spread through a traditional funerary ritual of the Fore people of Papua New Guinea in which relatives consume specific body parts of their deceased kin. A single case of spontaneous CJD could thus have been amplified into a high rate of vCJD in the population. This theory explains the prevalence of the disease among women (who were the primary participants in the cannibalistic ritual) and also the sudden decline in Kuru following the influence of missionaries in the 1950s.

    Despite the attractiveness of these theories, there is also another school of thought regarding the emergence of TSEs. This school contends that BSE, and possibly even Kuru, might be due to chemical exposure rather than contaminated tissue consumption. Organophosphate pesticides were widely used on livestock in the UK prior to the BSE outbreak of the 80s and 90s to kill warble flies. It is possible that these chemicals could bind to and cause changes in the conformation of proteins. Another chemical, containing manganese, could be to blame for Kuru. This theory would account for the increase in spontaneous CJD that accompanied the sharp rises in vCJD among the Fore. The role of genetic predisposition may also come into play. However, despite its attractiveness, most recent research supports the contaminated tissue consumption theory and there is little concrete data to back up the organophosphate theory.