Hypothesis That BSE
Originated From A
Human TSE
From Terry S. Singeltary Sr.
Source: Spongiform Encephalopathy Advisory Committee (SEAC), Position Paper, 19 Oct 2005 [edited]
Hypothesis that BSE Originated from a Human TSE
1. Consideration of a hypothesis that BSE (bovine spongiform encephalopathy) was originally derived from a human TSE (transmissible spongiform encephalopathy) [see: part 4 of the ProMED-mail post archived as "CJD (new var.) update 2005 (09) 20050905.2627"].
2. The origins of BSE are unknown. Since the discovery of BSE, the Spongiform Encephalopathy Advisory Committee (SEAC) and others have considered a number of hypotheses about the origins of the disease. http://www.seac.gov.uk/summaries/summ_0901.htm http://www.seac.gov.uk/papers/paper_inf81-8.pdf
Recently a further hypothesis has been considered by SEAC, which suggests that BSE may have arisen as a result of UK importation, in the 1960s and 1970s, of mammalian bone and carcass material from the Indian subcontinent, for use in animal feed. Furthermore, this hypothesis suggests that this material may have been contaminated with human remains harbouring a strain of CJD (Creutzfeldt-Jakob Disease), which could have been transmitted to cattle [Colchester AC, Colchester NT (2005). The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet. 366, 856-61.]
Contamination of animal feed with human remains
3. It is not possible to establish with any certainty whether feed given to animals in the 1960s and 1970s was contaminated with human remains. However it is possible that carcass material, which may have inadvertently included human remains, was imported into the UK from the Indian subcontinent (particularly the Ganges region) during that period, and used in animal feed. Professor Colchester provides indirect evidence to suggest that this may have occurred.
4. It is likely that similar material was imported into other countries, such as Australia, that have not detected BSE in their livestock. Furthermore, the amount of human remains that may have contaminated animal feed would have been a very small fraction of the amount of sheep and cattle material that was incorporated into animal feed in the past. Thus, there was a much greater opportunity for cattle to have been exposed to an animal TSE rather than a human TSE. Current control measures implemented across the EU and in the UK have prevented the importation of such material for either animal feed or fertilizer.
Properties of BSE and other TSEs
5. BSE may have originated as a result of misfolding of the prion protein in cattle, the amplification via feed of a rare, new spontaneous mutation in cattle, or transmission of a TSE from another species. There are barriers to transmission from one host species to another, and there appears to be an appreciable barrier to transmission between cattle and humans. It is not currently possible to predict the ability, or likelihood, of transmission between species based on current understanding of strain characteristics.
6. Prion strains can be characterised by their properties in biochemical and infectivity tests. Generally, prion strains are transformed as a result of transmission to a new host, with consequent changes in their biochemical properties. However, BSE is somewhat unusual in that it appears to retain its strain characteristics when passaged through a new host. Experiments in transgenic mice expressing human, bovine and ovine forms of the prion protein gene have been designed to determine the likelihood of a strain passing to a new host but can also shed light on possible relationships between prion strains.
7. Nevertheless it is difficult, and often impossible with current technologies, to establish whether one strain is related to another following transmission to another species. It may therefore, never be possible to determine the true origin of BSE.
Summary Of SEAC's Discussion
8. SEAC considered it unlikely that the origins of BSE would ever be determined conclusively.
9. It is not possible to determine, from current knowledge of the characteristics of prion strains, whether BSE originated from CJD or other animal prion strains.
10. There was evidence to suggest that human remains may have been included in animal feed derived from the Indian subcontinent in the past, and the hypothesis presented by Professor Colchester was therefore considered plausible, but ultimately untestable.
11. Very much larger quantities of cattle and sheep remains historically had entered animal feed, compared with putative human remains. There is also likely to be a significant species barrier between humans and cattle, as there is known to be such a barrier in the opposite direction. It is therefore very much more likely that the origins of BSE are related to a TSE that originated in cattle or sheep, rather than a TSE from humans.
12. In conclusion, although Professor Colchester's hypothesis can never be ruled out, SEAC considered that, on the balance of possibilities, human TSE-contaminated material in animal feed was unlikely to have been the origin of BSE.
13. Although further experiments suggested by Professor Colchester would be of some scientific interest, SEAC did not consider them essential, as they are unlikely to yield conclusive results on the origin of BSE, and because current control measures now prevent possible transmission via the route proposed in this hypothesis.
--Terry S. Singeltary Sr.



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