- Source: Spongiform Encephalopathy Advisory Committee
(SEAC), Position Paper, 19 Oct 2005 [edited]
-
- http://www.seac.gov.uk/statements/state191005.htm
-
- Hypothesis that BSE Originated from a Human TSE
-
- Issue
-
- 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"].
-
- Background
-
- 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.
- flounder9@verizon.net
|
