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From: TSS (
Subject: SEAC Statement 18th January 2005 Position statement - Chronic wasting disease in UK deer SEAC Statement
Date: January 20, 2005 at 6:58 am PST

-------- Original Message --------
Subject: SEAC Statement 18th January 2005 Position statement - Chronic wasting disease in UK deer SEAC Statement
Date: Thu, 20 Jan 2005 08:54:21 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

##################### Bovine Spongiform Encephalopathy #####################

SEAC Statement

18th January 2005


Position statement - Chronic wasting disease in UK deer


1. The Food Standards Agency asked SEAC to consider the possible public
and animal health implications of chronic wasting disease (CWD), in
particular the level of risk posed to consumers of meat from infected
animals. The committee also considered the possibility that BSE may be
present in UK deer.


2. CWD has emerged as an endemic transmissible spongiform encephalopathy
(TSE) in certain captive and free-ranging species of cervid (deer) in
some areas of North America. The disease is characterised by weight loss
and behavioural changes in infected animals, usually over a period of
weeks or months leading to death. CWD has not been found in the UK or
elsewhere in Europe. No definitive or suspected cases of transmission of
CWD to humans have been reported.

3. SEAC considered a review of the published, and some unpublished,
research on CWD, together with surveillance data on TSEs in European
cervids and information on UK cervid populations (1


4. The origins of CWD are unknown. On the basis of epidemiological data,
it is highly improbable that CWD originated from the recycling of
mammalian protein in processed feed. It has been suggested that CWD may
have arisen from transmission and adaptation of scrapie from sheep to
cervids, as a result of a spontaneous change of endogenous prion protein
(PrP) to an abnormal disease-associated form, or from an unknown source.

5. Data supporting any of these possible origins of CWD are either
absent or equivocal. Although CWD could have originated from scrapie,
the differing properties of the two prion diseases in strain typing
bioassays, whilst limited, do not support this hypothesis. Evidence for
multiple strains of CWD is equivocal. It seems most likely that CWD
arose from a spontaneous change of endogenous PrP resulting in a
disease-associated and laterally-transmissible form of PrP, although
direct data to support this hypothesis are lacking.

Host range

6. The known natural hosts for CWD are mule deer (Odocoileus hemionus
hemionus), black-tailed deer (Odocoileus hemionus columbianus),
white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk
(Cervus elaphus nelsoni). The prevalence and geographical distribution
of CWD in these species appears to be increasing in North America in a
manner which is unlikely to be due simply to increased surveillance.

7. There are no direct data relating to the transmissibility of CWD to
UK cervid species. However, comparison of a limited number of PrP codons
indicates some homology in the endogenous PrP gene of European and North
American cervid species. Thus, the possibility that UK cervids may be
susceptible to CWD cannot be excluded, in particular red deer (Cervus
elaphus elaphus) which are closely related to elk.

8. There is no evidence to suggest that CWD is present in UK cervids.
However, because surveillance in the UK is very limited, a low level
prevalence of CWD cannot be ruled out. The committee endorsed the
opinion of the European Food Safety Authority on CWD surveillance in the
European Union (2004)

9. Transmission studies using parenteral routes of administration to
cattle, sheep and a single goat, together with data from in vitro PrP
conversion experiments, suggest that a significant barrier to CWD
transmission to these species may exist. No transmission has been
evident so far in an on-going oral transmission study in cattle after
six years. Furthermore, no signs of infection have been observed from
monitoring of cattle co-habiting areas with infected cervids, or in
cattle, sheep or goats in close contact with infected cervids in
research facilities. Thus, although the data are limited, there is
currently no evidence to suggest that CWD can be transmitted naturally
to cows, sheep or goats, and it is likely that there is a strong species
barrier to such transmission.

Routes of transmission

10. Epidemiological data indicate that lateral transmission between
infected and susceptible cervids occurring naturally is sufficiently
effective to maintain epidemics in both captive and free-living
populations. There is good evidence from studies of cervids inhabiting
paddocks previously inhabited by infected animals or contaminated with
infected carcases, that CWD can be transmitted laterally between animals
via the environment. The precise mechanism of transmission is unclear.
It is possible that the infectious agent is shed in the saliva, faeces
or urine or as a result of decomposition of infected carcases and
transferred to other cervids grazing the contaminated areas. It is also
possible that some maternal transmission occurs.

11. There have also been suggestions that the lateral transmission of
CWD may be influenced by environmental factors.


12. Information on the pathogenesis of CWD is limited. The data show
that, following oral challenge, PrPCWD is first detected in the oral and
gut-associated lymphoid tissues before spreading more widely within the
lymphoid system and then to the brain. Involvement of the
retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur
in some elk. At the microscopic level, the nature and distribution of
the tissue lesions are similar to those found for scrapie. The available
data suggest the pathogenesis of CWD is similar to scrapie.

BSE in UK deer

13. Both captive and free-ranging cervids in the UK may have been
exposed to contaminated feed prior to the reinforced mammalian meat and
bone meal ban instituted in 1996. A study to look at the potential
susceptibility of red deer to BSE has shown no signs of transmission of
the disease by the oral route, but it is at a very preliminary stage.
Although a theoretical possibility exists, there is no evidence from the
very limited surveillance data to suggest that BSE is present in the UK
cervid population.

Human health implications

14. Epidemiological data on possible CWD infection of humans are very
limited. The possibility that clinical symptoms of CWD in humans differ
from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There
is no significant difference between the prevalence of CJD in CWD
endemic areas and other areas of the world. However, because CJD
surveillance in the USA is relatively recent, not all CJD cases may have
been identified. Additionally, detection of a small increase in
prevalence of such a rare disease is very difficult. Investigation of
six cases of prion disease in young people (< 30 years of age) in the
USA found no definite causal link with consumption of venison from known
CWD endemic areas. The disease characteristics in these cases were
indistinguishable from sporadic CJD or Gerstmann-Sträussler-Scheinker
syndrome. Likewise, in a study of three hunters (> 54 years of age)
diagnosed with sporadic CJD, no link with consumption of venison from
CWD endemic areas was found. No causal link was found in an
investigation of three men with neurological illnesses who were known to
partake in wild game feasts. Only one of these subjects was found to
have a prion disease and this was also indistinguishable from sporadic CJD.

15. Preliminary results from transmission experiments in transgenic mice
expressing human PrP suggest the presence of a significant species
barrier to transmission of CWD to humans. However, these findings must
be interpreted with caution as they may not accurately predict the human
situation. Data from in vitro experiments on conversion of human PrP by
disease-associated forms of PrP, including PrPCWD, are equivocal.

16. The committee concluded there is no evidence of transmission of CWD
to humans from consumption of venison, and that there may be significant
barriers to transmission. Nevertheless, as the data are extremely
limited a risk cannot be ruled out should CWD enter UK herds.


17. There is no evidence that CWD (or BSE) is present in the UK cervid
population. However, because only limited surveillance is conducted in
the cervid population, a low level prevalence of CWD cannot be ruled
out. It is recommended that further surveillance of TSEs in UK cervids
is conducted.

18. There is no evidence of transmission of CWD to humans from
consumption of meat from infected cervids. Although epidemiological and
experimental data on potential transmission of CWD are extremely
limited, they suggest that there may be a significant species barrier.
It would be helpful if further studies were available assessing the
potential species barrier for transmission to humans.

19. Although limited, there is no evidence CWD can be transmitted to
cattle, sheep or goats by natural means.

20. In summary, it appears that CWD currently poses relatively little
risk to human health, or to the health of cattle, sheep or goats in the
UK. Nevertheless, as a risk cannot be excluded a watching brief should
be maintained.

January 2005

1. The information considered by the committee
is available.


Chronic Wasting Disease in UK deer

Alan Harvey (FSA).Wildlife Information Network.

85/2 *(pdf)
Annex 1 (pdf)
Annex 2 (pdf):
Annex 3 (incl. appendices)
Annex 4 (pdf)
Annex 5 (pdf):


######### ##########

[[In summary, it appears that CWD currently poses relatively little
risk to human health, or to the health of cattle, sheep or goats in the

SOUNDS like a broken record. THIS is what was said about BSE, until
they finally got around to proving it would transmit to humans.

CWD transmits to primates, humans are primates.

CWD TEST have NEVER been performed on humans...

In Confidence - Perceptions of unconventional slow virus diseases
of animals in the USA - APRIL-MAY 1989 - G A H Wells


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