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From: Terry S. Singeltary Sr. (
Subject: SEAC Draft minutes of the open session of the 85th meeting held on 30th November 2004
Date: January 10, 2005 at 11:11 am PST

-------- Original Message --------
Subject: SEAC Draft minutes of the open session of the 85th meeting held on 30th
Date: Mon, 10 Jan 2005 09:16:41 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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

Draft 5 07/01/05 incorporating Bassetts comments 1
Draft minutes of the open session of the 85th meeting held on 30th
November 2004
The Hilton Hotel
CF10 3HH
Members: Professor C. Higgins (Chair)
Mr. J. Bassett
Dr. D. Brown
Dr. J. Chambers
Professor N. Hooper
Professor J. Ironside (Deputy Chair)
Mr. P. Jinman
Dr. C. Lasmezas
Professor J. Manson
Professor I. McConnell
Ms. D. McCrea
Professor G. Medley
Dr. P. Rudge
Assessors: Mr. A. Harvey (FSA)
Mrs. E. Lawrence (DH)
DA Assessors: Dr. M. Simmons (NAW)
Dr. P. Christie (SEHD)
Dr. A. Douglas (DARDNI)
Technical Advisors: Dr. P. Barrowman (Defra)
Dr. S. Dixon (FSA)
Dr. D. Matthews (VLA)
Dr. J. Stephenson (DH)
Draft 5 07/01/05 incorporating Bassetts comments 2
SEAC Secretary: Miss. K. Richards
Secretariat: Dr. T. Barlow
Mr. M. Pemberton
Dr. P. Keep
Dr. C. Ravirajan
Ms. T. Dale
Also in attendance: Dr. I. Hill (FSA) (Paper 85/2)
Dr. D. Bourne (Wildlife Information Network)
(Paper 85/2)
Draft 5 07/01/05 incorporating Bassetts comments 3
1. The Chair welcomed members of the public to the ninth open
meeting of SEAC and thanked the Welsh Assembly Government
for hosting the first open SEAC meeting to be held outside London.
2. The Chair explained that this was the second live broadcast of a
SEAC meeting over the internet, which is part of a one year trial to
assess the potential benefits and likely uptake of viewing via this
medium. To view the live broadcast, members must register, via
the SEAC web site, at least 24 hours in advance to ensure
technical compatibility. An archive of meetings would also be
available via the SEAC website for which registration was also
3. The Chair informed members that this would be Mr Colin Brownes
last meeting as a member of SEAC. The Chair thanked Mr
Browne, who could not attend the meeting, for his contribution to
SEAC. Apologies for absence had also been received from
Professors Bulfield and Stanley. The Chair also informed members
that Dr Mandy Bailey (Defras assessor) and Mr Peter Soul (Defras
technical adviser), both of whom could not attend the meeting,
would be retiring from Defra in the very near future and recorded
his thanks for their valued contribution to SEAC discussions.
4. The Chair welcomed Kate Richards, who had recently taken over
from Catherine Boyle as SEAC Secretary, to her first meeting. The
Chair also welcomed Dr Debra Bourne (Wildlife Information
Network), Dr Irene Hill (FSA), Mrs Eileen Lawrence (DH), Mr Alan
Harvey (FSA) and Dr Peter Barrowman (Defra) who were
presenting items to the committee.
5. The Chair thanked those members who had responded to the
secretariat regarding media training; this would be organised in due
course. Members were reminded of their obligation to declare
conflicts of interests at the start of each agenda item and were
informed that the next meeting would be held on 3rd March 2005 in
6. The minutes of the open session of the 28th September meeting
were agreed as a correct record subject to the following
Draft 5 07/01/05 incorporating Bassetts comments 4
" change paragraph 23 first sentence from &in July 20004& to
read &in July 2004&,
" change paragraph 25 first bullet point from &these would not
reduce scrapie in ARQ sheep, which may be more important than
to assumed in the modelling& to read &these would not reduce
scrapie in ARQ sheep, which may be more important than
assumed in the modelling&,
" change paragraph 45 first sentence from Professor Ferguson
noted that the 10-fold reduction in the quantity of duodenum and
jejunum entering the food supply& to read Professor Ferguson
noted that the 10-fold reduction in the infectivity from duodenum
and jejunum entering the food supply&, and
" change paragraph 47 line 2 from &it was only necessary to
consider large animal epidemics in a small number of flocks and
suggested that that a model& to read &it was only necessary
to consider large animal epidemics in a small number of flocks
and suggested that a model&.
7. Under matters arising, the Chair informed members that he had
presented the outcome of SEACs discussion at the meeting on 28th
September 2004 relating to BSE and sheep to the FSA Board, who
are considering their contingency arrangements should BSE ever
be found in sheep.
8. At the meeting on 28th September 2004, members noted that a
there had been a number of cases of animals with clinical signs
consistent with BSE that were not confirmed as BSE using
diagnostic tests. In view of these cases and the phenotypic
differences of TSE infection in sheep and humans, members had
suggested that research on methods to allow differential diagnosis
of clinical cases of BSE was important. One member asked
whether any progress had been made relating to this issue. The
Chair agreed to pursue the matter with Defra.
9. The Chair explained that this would be a regular agenda item to
update members of the committee on current TSE issues that had
arisen since the previous meeting.
Draft 5 07/01/05 incorporating Bassetts comments 5
FSA / SEAC Milk Working Group
10. A joint FSA / SEAC milk working group had been established to
provide advice to the FSA on research to develop diagnostic tests
to detect abnormal PrP in milk from cattle. The Chair informed
members that he had discussed this work with Professor Chris
Bostock, Chair of the milk working group, who had explained that
the assessment of results from tests of experimental samples was
currently incomplete and that a discussion at SEAC would have
been premature. It is anticipated that a report from the group will
be provided at the next SEAC meeting on 3rd March 2005.
Wadsworth et al (2004) paper
11. The Chair informed members that a very recent paper by
Wadsworth et al (2004)1 suggested that the phenotype and
transmission of vCJD and BSE in transgenic mice expressing
human PrP were profoundly influenced by polymorphisms at codon
129 of the PrP gene. Animals with homozygous valine at codon
129 were associated with i) altered molecular and
neuropathological phenotypes of vCJD infection, ii) a partial barrier
to primary infection, and iii) a large barrier to secondary infection
compared with methionine homozygous animals. Given the
potential implications for human health, consideration would be
given on how best to take this forward at the next SEAC meeting.
Possible BSE in a French goat
12. The Chair provided members with the background to this particular
case. In 2002, a single healthy goat, from a flock of 300, tested
positive for a TSE as part of a French surveillance programme.
The results appeared different from normal scrapie strains. All the
goats from the flock were destroyed and no product from the flock
entered the human food supply. Studies to investigate the type
TSE are almost complete and have led to the suspicion of BSE.
The results had been passed to the Community Reference
Laboratory expert group who concluded that, although the data
available are consistent with BSE, a definitive interpretation could
not be provided until further data from mouse bioassays were
available in approximately two months. The European Food Safety
Authority (EFSA) was now considering the implications of these
1 Wadsworth et al. Human prion protein with valine 129 prevents
expression of variant CJD
phenotype. Science. (2004) 306, 1793-1796.
Draft 5 07/01/05 incorporating Bassetts comments 6
13. In response to members questions, Dr Danny Matthews (VLA)
confirmed that the goat was a mature milking goat, although there
remained some confusion over its exact age, which the French
authorities were trying to clarify. The Chair explained that it was
possible the goat could have been exposed to infected mammalian
meat and bone meal (MMBM) before the EU wide feeding ban.
14. Members asked what was likely to happen once the further results
were known and should BSE be confirmed. Mr Alan Harvey (FSA)
explained that decisions regarding risk management measures
would be taken at EU level following consideration by the Standing
Committee on Food Chain and Animal Health. Dr Matthews added
that a TSE working group was being held in Brussels on 30th
November 2004 to consider the implications of the findings. It was
expected that the working group would make recommendations on
increased surveillance and further SRM controls. The committee
considered it important that, in the event of confirmation of BSE in
the goat, possible risk management measures were identified in
15. The Chair informed the committee that the FSA had asked SEAC to
advise on the potential public and animal health risks of chronic
wasting disease (CWD). As SEAC had not considered CWD
previously, a position statement would be drafted on the basis of
the discussion and, if it was considered necessary, the committee
could discuss the issue further at the next meeting. There may also
be an opportunity to invite an external expert for that discussion.
The Chair reminded members of the advice sought from the
16. Dr Irene Hill (FSA) provided a background to the FSA request. The
FSA recognised the potential risks to human health should BSE be
found in deer. However, the human health risks of CWD in deer
are unknown. Therefore, the FSA has asked the committee to
consider the possible human health risks should CWD be found in
UK deer. Although no TSEs have been found in deer in the UK to
date, surveillance is limited and given the origins of the disease are
unknown, the presence of CWD in deer cannot be ruled out. A
recent EFSA opinion made recommendations on the scope of TSE
surveillance in deer. As a result, it is likely deer surveillance will
increase in the future. Should a positive result be found from such
surveillance, the FSA will need to consider what action it could take
to reduce the possible risks to consumers of venison. With this in
mind, the FSA is seeking advice from SEAC on whether CWD
Draft 5 07/01/05 incorporating Bassetts comments 7
should be considered a risk to human health should it be found in
UK deer. However, it was acknowledged that most of the
information on CWD is derived from research on North American
deer and there are few data on UK species or human health
17. Dr Debra Bourne (Wildlife Information Network) summarised the
current knowledge of CWD. CWD is present in certain North
American species of cervid (deer). It is the only prion disease
known in free-living animals. In North America, there are concerns
about the negative impact that CWD may have on free-ranging
cervid populations and on the deer hunting and farming industries.
Concerns have also been expressed about the possibility of CWD
transmission to other types of livestock and to humans from
consumption of infected meat. The disease was first evident in
mule deer in a Colorado research facility in the early 1960s but it
has since been found in other types of free-living and captive
cervids (mule, white-tailed and black-tailed deer, and Rocky
Mountain elk) in other areas of the USA and Canada. A small
number of cases have occurred in farmed elk imported to South
Korea from Canada. CWD has not been found in cervids in Europe
but surveillance has been limited.
18. Dr Bourne explained that the origins of CWD are unknown.
However, it may have arisen from a spontaneous change of PrP to
a disease-associated form, from scrapie, or from an unknown
source, but data on these possible origins are either absent or
equivocal. Feed-borne or familial origins for CWD appear highly
unlikely. CWD has been successfully transmitted to a range of
non-cervid species by intracerebral inoculation. However, via the
oral route, it has only been transmitted to cervids. The incubation
period is generally more than one year. Following oral challenge,
PrPCWD is detectable in the gut associated lymphoid tissues before
other lymphoid tissues or wide-spread accumulation in the central
nervous system, although in many elk it is not found in the
retropharyngeal lymph nodes and tonsils. Clinically, CWD is
characterised by weight loss and behavioural changes, usually over
a period of weeks or months. At the microscopic level, the nature
and distribution of tissue lesions are similar to those found in
scrapie. Definitive diagnosis of CWD is usually made on the basis
of detection of abnormal PrP in brain or lymphoid tissues by IHC
but western blot, ELISA and conformation-dependent immunoassay
(CDI) tests have also been used.
19. Dr Bourne explained that CWD is transmitted laterally between
animals, possibly via environments that become contaminated with
Draft 5 07/01/05 incorporating Bassetts comments 8
infectious agent. The agent might be shed from animals in the
saliva, faeces or urine or as a result of decomposing carcases. The
possibility of some maternal transmission has not been ruled out.
Although polymorphisms in the cervid PrP gene have been
identified, the influence of these polymorphisms on susceptibility to
CWD is unclear. It is possible that European cervid species may
be relatively resistant to CWD, although red deer, which are closely
related to elk, are more likely to be susceptible. There is no
evidence for natural transmission to cattle or sheep co-habiting with
CWD infected cervids. Inefficient transmission to cattle, sheep and
goats following intracerebral inoculation, as well as the results of in
vitro PrP conversion experiments, suggest a significant species
barrier. In humans, there is no evidence of transmission from
studies that examined possible links between consumption or
handling of cervid tissues and human cases of prion disease.
Additionally, the incidence of CJD in areas of the USA affected by
CWD is similar to areas from which CWD is absent. Although, the
results from in vitro PrP conversion experiments are equivocal,
experiments in transgenic mice expressing human PrP, whilst
incomplete, suggest some species barrier to infection of humans.
20. Members considered the possibility that CWD is present in UK
deer. Surveillance of CWD in Europe is very limited with the most
extensive European surveillance programme, in Germany, capable
of detecting a one percent incidence of CWD. Thus, members
agreed that, although it has not yet been found, it is not possible to
conclude that CWD is absent in the European deer population. It
was considered that some UK deer species may be susceptible to
CWD, particularly red deer, which are a subspecies of elk. There
are currently no data from transmission studies of CWD to
European cervid species.
21. In response to a suggestion that all slaughtered deer could be
tested in the UK, Dr Matthews noted that, although the number of
deer slaughtered in the UK was small, it would be very difficult to
test each slaughtered animal because of the practical difficulties in
obtaining samples from all the animals killed in remote
geographical locations. Members suggested that surveys of
farmed red deer may be the most practicable way of determining
whether CWD is present in UK deer because of the relatively high
concentration of animals, the putative susceptibility of red deer to
CWD, and the opportunity to observe these animals closely.
Members also suggested that, given the experience of cross
infection between farmed and wild cervids in the USA, it would be
unlikely that CWD would be present in wild deer but absent in
farmed deer. SEAC noted that EFSA had issued an opinion on
Draft 5 07/01/05 incorporating Bassetts comments 9
TSE surveillance in deer and members endorsed the EFSA
22. One member, who had worked with researchers in Colorado
investigating CWD, explained that most cervid samples tested in
Colorado were derived from hunter-killed animals and the incidence
of CWD infection in these animals was very low with most infected
animals being asymptomatic. Thus, it was suggested that in wild
populations the apparent increased prevalence of CWD may reflect
increased surveillance rather than a real increase in the prevalence
of the disease. Dr Bourne agreed but pointed out that some
American researchers were of the opinion that the incidence of
CWD was increasing and the disease was becoming more widespread.
Additionally, in enclosed populations of deer, the
prevalence of CWD was much higher due to the relatively high
concentration of animals facilitating greater exposure to the
infectious agent. It was noted that deer are susceptible to stress
and that this may influence the disease in farmed animals.
23. One member explained that some researchers in the USA had
suggested that the prevalence of CWD could be modified by levels
of trace elements in the environment, such as copper and
manganese, which when absorbed could influence PrP conversion.
The Chair asked whether the member considered that this theory
might provide an alternative to lateral transmission as a mechanism
of propagation of the disease. In response, the member explained
that in a feeding study in elk, dietary copper had reduced the
incidence of CWD in an experimental herd compared with a control
herd. Thus, it is possible that trace elements could either reduce
the severity of the symptoms or prevent infection. The committee
noted that there was strong evidence for lateral transmission of
CWD via the environment, from studies of cervids inhabiting
paddocks previously inhabited by infected animals or contaminated
with infected carcases.
24. Members considered the possibility that CWD could have
originated from scrapie. However, the differing properties of these
prion diseases in strain typing bioassays, whilst limited in scope, do
not support this hypothesis. It seems most likely that CWD arose
from a spontaneous mutation of the endogenous PrP gene
resulting in a disease-associated and horizontally-transmissible
form of PrP.
25. Members noted that the pathogenesis of CWD is similar to scrapie.
Abnormal PrP is found initially in the gut associated lymphoid tissue
before spreading more widely within lymphoid tissues and then to
Draft 5 07/01/05 incorporating Bassetts comments 10
the brain. However, in some naturally and experimentally infected
elk, an absence of abnormal PrP in the retropharyngeal lymph
nodes and tonsils has been observed despite it being found in the
26. Members asked whether there is evidence for multiple strains of
CWD. Dr Bourne explained that a recent report had shown that
samples from mule deer and elk had similar properties when
inoculated into transgenic mice expressing cervid PrP although a
further sample from a different mule deer had behaved differently.
Thus, it is unclear whether multiple strains of CWD exist. Further
studies to investigate this possibility were underway. Dr Matthews
(VLA) indicated that there was some evidence of different CWD
strains from CDI experiments.
27. The Chair asked whether diagnostic tests could distinguish CWD
from other prion diseases both in the natural hosts and other
species. Dr Bourne explained that strain typing bioassays and
glycoform patterns in western blots had shown distinct differences
between samples of CWD and other TSEs. However, because the
number of scrapie strains which have been tested is relatively
small, it is possible that CWD is indistinguishable from other prion
strains. Additionally, because of a lack of samples, comparative
experiments of CWD in non-cervid species have not been
conducted. However, it was noted that certain antibodies against
abnormal PrP appeared to be effective in analysis of samples from
a range of ungulate species, including cervids. Members
expressed caution on relying on glycoform patterns in western blots
for strain typing analysis and considered that bioassays enhanced
the reliability of strain typing TSEs.
28. In response to questions about the possible transmission of CWD
to cows and sheep, Dr Bourne explained that transmission of CWD
by intracerebral inoculation of cows and sheep was inefficient. In
addition, an oral transmission experiment of CWD to cows, whilst
incomplete, had not shown transmission of the disease after six
years. Additionally, no signs of infection were found from
surveillance of cows living in a CWD endemic area for a number of
29. In response to questions about the human epidemiological data, Dr
Bourne explained that studies of young people with CJD had found
no evidence of a link between CJD and consumption of venison
from known CWD endemic areas and that there had been no
unusual clinical or biochemical features in the analysis of these
cases. One member added that a review of these cases by the
Draft 5 07/01/05 incorporating Bassetts comments 11
NCJDSU had concluded that they were indistinguishable from
sCJD. However, it is not known what the clinical symptoms of a
CWD infection of humans would be. Dr Bourne also noted that a
study of three older men with neurological illnesses who were
known to partake in wild game feasts, showed that only one of the
subjects had CJD and that this was indistinguishable from sCJD.
30. Dr Bourne explained that the age adjusted death rates of CJD in
the CWD endemic areas of Wyoming and Colorado were 0.8 and
1.2 cases per million people, respectively. Whilst members were
reassured that there was no noticeable difference between the
prevalence of CJD in these areas and other areas of the world, they
expressed caution about drawing firm conclusions about the
apparent lack of transmission to humans because of the possible
long incubation period of the disease and the difficulty in detecting
a low level of increase in such a rare disease. In addition, because
comprehensive CJD surveillance in the USA had started relatively
recently, it was considered possible that not all CJD cases had
been identified. Members noted that UK surveillance of prion
diseases incorporated an assessment of venison consumption and
handling of deer.
31. Members asked what form of human PrP was expressed in the
transgenic mice used in transmission experiments and whether
preclinical signs of infection had been noted in the mice. Dr Bourne
explained that this information was not yet available but understood
that none of the mice had yet developed clinical disease. The
Chair asked the Secretariat to contact the researchers to ask for
further information. Members expressed caution about the
interpretation of the findings from transgenic mice experiments as
the results may be influenced by the expression level of PrP and
therefore, may not accurately predict the human situation.
Additionally, members noted that the results of in vitro experiments
examining the conversion of human PrP by abnormal forms of PrP
including PrPCWD were equivocal and were difficult to directly
extrapolate to the in vivo situation.
32. The committee noted that most of the imports of venison into the
UK were from New Zealand, which had no reported cases of CWD.
The UK imported very little venison from North America. It was
noted that there are no specified risk material controls for venison
but that tissues other than muscle are not normally consumed.
33. The committee noted that there are no known imports of cervids
from North America to Europe that could act as a source of CWD
infection to European deer. For this reason, members considered
Draft 5 07/01/05 incorporating Bassetts comments 12
that the TSE risk in European cervids is more likely to arise as a
result of BSE in cervids from feed contaminated with MMBM prior
to the MMBM ban followed by lateral transmission of the disease.
The committee noted that a study to look at the potential
susceptibility of red deer to BSE after ic or oral challenge had
shown no signs of transmission of the disease but the study was at
a very preliminary stage.
34. In conclusion, it was agreed by the Committee that, given the scope
of the discussion and the limited data available, it would not be
necessary for the committee to consider the issue at the next
meeting. A draft position paper would be prepared and circulated
for approval. The Committee noted that:
" the prevalence and geographical distribution of CWD appears
to be increasing in North America.
" there is no evidence to suggest CWD is present in UK deer but
surveillance data are limited.
" diagnostic tests are available which appear to distinguish
CWD from other prion diseases, but are limited by the paucity
of reference materials.
" it is possible that many UK deer species are relatively resistant
to CWD, although the red deer, which is closely related to elk,
is the species most likely to be susceptible. It is possible that
trace metals or other environmental factors may affect the
susceptibility of cervids to CWD infection.
" the origins of CWD are unclear. CWD is unlikely to have been
directly derived from scrapie. Most likely CWD arose as the
result of a spontaneous change in PrP but there is no direct
" there is good evidence that CWD is transmitted laterally
between animals, possibly via contaminated environments,
and natural transmission is sufficiently effective to maintain
epidemics in both captive and free-living cervid populations.
However, the precise mechanisms of transmission are
" the pathogenesis of CWD appears similar to scrapie.
Therefore, some of the precautionary measures that have
been applied to infection in sheep and goats may also be
appropriate to cervids.
" there is no evidence that CWD can be orally transmitted to
cows and there is some evidence to suggest a significant
species barrier to infection of cows, sheep and goats.
" there is no evidence of transmission of CWD to humans from
consumption of venison but data are extremely limited and it
would be very difficult to detect a low level of infection.
Draft 5 07/01/05 incorporating Bassetts comments 13
Additionally, although there are few data, there is some
evidence to suggest the presence of a species barrier to
transmission to humans. Studies of transgenic mice
expressing human forms of PrP may give more information
about a possible species barrier.
" modelling studies of the geographical distribution and make-up
of deer populations and of venison imports and consumption
may help to inform assessment of surveillance programmes
and exposure estimates.
" although a theoretical possibility exists, there is no evidence to
suggest that BSE is present in UK deer. However, it is
important to closely monitor the findings of an on-going study
to look at the potential susceptibility of red deer to BSE.
35. The Chair explained this agenda item had been included to give the
assessors from DH, FSA and Defra an opportunity to provide SEAC
with brief overviews of topics that might require the committees
consideration in the future.
Department of Health
36. Mrs Eileen Lawrence (DH) explained that protection of public health
was the key priority for DH and this was reflected in the
departments recently published research strategy on TSEs.
Important research areas that may require input from SEAC in the
future included the advancement of the treatment and care of vCJD
patients, the development of diagnostic tests for vCJD, surveillance
to provide more accurate estimates of the size of the vCJD
epidemic and measures to reduce the risks of secondary
transmission by medical procedures. As part of this work the
Health Protection Agency (HPA) was in the process of setting up an
archive of tonsil tissues for research and surveillance of human
TSEs. Research was also in progress to develop a diagnostic test
for abnormal PrP, as earlier detection of the disease might facilitate
better treatment and prevent secondary transmission of the
disease. Additionally, advisory groups had been set up to look at
developing more effective methods of decontamination for surgical
instruments and the effectiveness of changes to decontamination
procedures. Furthermore, the National Institute for Clinical
Excellence (NICE) was currently developing guidance, which would
be available next year, on vCJD risks during surgery and the
Committee on the Microbiological Safety of Blood and Tissues was
continuing to look at the potential risk of transmission of vCJD from
Draft 5 07/01/05 incorporating Bassetts comments 14
blood and tissues. Although these groups were looking at specific
measures, it is likely that aspects of their work would require risk
analysis from SEAC.
37. In addition, DH would continue to ask SEACs opinion on the
implications of new research findings on the epidemiology of vCJD.
For example, the recent research findings that suggested possible
age and genotype related differences in susceptibility to vCJD.
Similarly, SEACs view may also be sought on research on other
human and animal TSEs that may inform understanding of vCJD.
Food Standards Agency
38. Mr Alan Harvey (FSA) noted that there were a number of crosscutting
issues for FSA, DH and Defra such as the development of
non-invasive TSE tests. Thus, there would be occasions where
advice on a particular aspect of TSE science may be sought by
more than one department. Mr Harvey explained that the Agency
would continue to ask SEAC to carry out risk assessments on food
safety issues to enable government to make risk management
decisions. SEACs view would also be sought on new findings on
sheep TSEs and the theoretical possibility of BSE in sheep as well
as the implications of new research on contingency plans to protect
public health from emerging TSE risks. A subgroup comprising key
FSA stakeholders and members of SEAC might also be convened
to discuss emerging research results, which could inform
contingency plans.
39. Mr Harvey noted that as BSE continues to decline across Europe,
surveillance programmes and associated control measures may be
reviewed and the FSA would ask SEAC for advice on any new
proposals in these areas from the European Commission.
40. Dr Peter Barrowman (Defra) explained that Defra was working
towards both a reduction of scrapie cases by 40% and eradication
of BSE by 2010. It would continue to ensure that animal byproducts
such as tallow, were disposed of in an environmentally
sound and safe manner. It was anticipated that advice from SEAC
would be sought on aspects of this work. SEAC would also be
asked to advise on the risks associated with possible future
relaxation of various BSE control measures, such as Specified Risk
Materials (SRM) legislation and the feed ban. In addition, Defra
had recently initiated an independent review of BARB cases (BSE
cases Born After the Reinforced Ban) and SEAC would be asked to
Draft 5 07/01/05 incorporating Bassetts comments 15
comment on the findings of this review. SEAC would also continue
to be presented with the findings from Defra research into possible
BSE in sheep and goats, the possibility of different strains of BSE,
the resistance of sheep genotypes to scrapie and the atypical
scrapie cases.
41. The Chair thanked the assessors and requested that the
departments continue to liaise with the secretariat to ensure that
the committee had sufficient advance notice of issues that would
require consideration by SEAC.
42. The Chair explained that at SEACs 75th meeting, the FSA had
agreed to notify the committee when a cattle bioassay study, to
define the pathogenesis of BSE in cattle, would be terminated.
43. Mr Harvey informed the committee that the FSA planned to
terminate the cattle bioassays it was funding at the VLA, both on
grounds of animal welfare and to focus funding on research to
develop non-invasive live animal diagnostic tests. Members were
informed that the initial challenge groups in the cattle bioassay
studies were reaching 8 years post inoculation (p.i.) and that the
original proposal indicated that 7 years p.i. would be the anticipated
end point for the study. Analyses by Wells et al provided at Annex
1 of SEAC paper 85/3 showed that termination of the studies at
approximately 7 years p.i. would not result in any measurable loss
of data. A culling strategy was planned to start in December 2004
and would be completed in March 2007 as each of the challenge
groups reached 7 years p.i.. A series of tissues would be archived
to include brain, spinal cord (cervical, thoracic and lumbar), distal
ileum, Peyers patches and tonsil. Members were asked to
comment on the scientific rationale for termination of the study.
44. The committee was content with the scientific rationale for
termination of the cattle bioassays but stressed the importance of
archiving appropriate tissues for further study.
45. The Chair invited members of the public who had submitted
questions in advance of the meeting to ask their questions and then
invited questions from the floor.
Draft 5 07/01/05 incorporating Bassetts comments 16
Question 1
46. With reference to the case of probable transmission of vCJD via
blood transfusion, the committee was asked if there had been any
control studies in subjects of a similar age and clinical condition to
assess the possible presence of abnormal prion protein in spleen
47. On behalf of the committee, Professor Ironside explained that this
particular patient had been traced through the Transfusion
Medicine Epidemiology Review (TMER) study funded by DH. As
part of this study, spleen tissue from post mortem of normal
controls and patients with other neurological diseases had been
performed and in none of these cases was abnormal PrP detected,
although the cases were limited in number. Also, no abnormal PrP
had been found in other DH-funded studies to examine the brain
and other tissues collected from autopsies of elderly and younger
Question 2
48. In view of recent findings from studies of transgenic mice
expressing forms of human prion protein, which suggested BSE
infection may be influenced by polymorphisms at codon 129 of PrP
gene, the committee was asked for data on the number and
genotype of sporadic CJD cases, and if the pattern had changed
within the last 15 years.
49. In answer, Professor Ironside presented information on sCJD
deaths from 1985 to 29 November 2004 that indicated the number
of sCJD deaths per annum in the UK was increasing, but explained
that this was possibly due to better case ascertainment, particularly
in the elderly. Comparable data have been obtained in European
countries and Australia, which showed similar changes in the
incidence of sporadic CJD. France, Germany and Italy had higher
relative mortality rates for sCJD than the UK, over the period
examined (1 Jan 2004 to 30 September 2004).
50. Professor Ironside explained that during the period 1 May 1990 to
29 November 2004 there were 756 sCJD cases (dead and alive),
with genotype data available from 476 cases. The codon 129
genotype genotype distribution was 65% MM (310 cases), 17% MV
(80 cases) and 18% VV (86 cases).
51. Professor Ironside noted there had been increases in the VV and
MV proportion of cases over time but believed this to be largely due
Draft 5 07/01/05 incorporating Bassetts comments 17
to increased surveillance in young patients, presenting with a
variety of neurological signs and sypmtoms, with a higher
proportion of VV or MV genotypes. Between 1 May 1990 and 31
Dec 1995, 75% of sCJD deaths were genotype MM (96 cases),
11% were MV (14 cases) and 13% were VV (17 cases). Between 1
Jan 96 and 31 Dec 2003, 62% of sCJD deaths were genotype MM
(191 cases), 19% were MV (59 cases) and 19% were VV (58
52. Professor Ironside commented that in the UK, clinical, biochemical,
pathological and genetic analysis was performed for each case of
CJD. Additionally, material from many of the cases, particularly
from younger patients, had been experimentally transmitted to mice
to investigate the possibility that a BSE strain may be responsible
for the disease, but so far this had been negative. However, it was
not assumed that vCJD would necessarily be the only manifestation
of BSE-associated disease in humans, particularly in those people
with different genotypes of PrP. However, it was reassuring that
the PrP western blot profile of the second blood transfusionassociated
case in an individual of the MV genotype was clearly
identifiable as vCJD and was similar to that found in MM
Question 3
53. The committee was asked when a non-invasive blood test for vCJD
would be available for the haemophilia community. The Chair
referred to DH for comment.
54. Dr John Stephenson (DH) replied that a diagnostic non-invasive
blood test was a research priority for DH. However, no test was
currently available. DH was also in liaison with companies working
on such tests. Dr Stephenson indicated that Professor Christine
Lee at the Royal Free Hospital, London was co-ordinating the
surveillance of haemophiliac patients in the UK and could be
approached for further details.
Question 4
55. The committee was asked whether the ethical issues had been
considered if a blood test for vCJD became available.
56. Dr Stephenson explained that the National Blood Centre was
setting up a test assessment facility to prepare the blood services
for the introduction of such testing. In addition, DH had asked the
Health Protection Agency and the Nuffield Council for Bioethics to
Draft 5 07/01/05 incorporating Bassetts comments 18
set up a workshop to consider the ethical issues of blood testing for
vCJD infection.
Question 5
57. The committee was asked if research on immune system reactions,
which may be an early marker of TSE disease, was being pursued.
58. Dr Steve Dixon (FSA) explained that the FSA is funding work to
search for metabolic biomarkers of TSE infection and to look at the
use of erythroid differentiation-related factor (EDRF) as marker of
TSE disease. Dr Barrowman indicated that results of a Defra
funded metabolomics study of BSE infection at the Institute for
Grassland Research may be available later this year. Dr Matthews
indicated that an infra red spectroscopy TSE test is being validated
by EFSA on post mortem tissue from clinically-affected BSE cases.
If successful, the test would be evaluated using samples from
animals with preclinical disease.
Question 6
59. In response to a question received in advance of the meeting about
the case of possible BSE in a French goat, the Chair explained that
this issue had been covered earlier in the meeting, under item 3
(paragraphs 12-14 above).
60. The committee had also been asked by the questioner if it
endorsed the 26 November 2004 European Food Safety Authority
(EFSA) statement on goat milk2. The Chair replied that SEAC had
not changed its view that goats milk from healthy animals is unlikely
to pose a significant risk to human health, and that therefore the
EFSA statement was consistent with previous advice from SEAC.
61. The questioner had also asked whether new EC legislation required
that samples from goats and sheep that had tested positive for a
TSE be tested by bioassay. Dr Matthews explained that from 31
January 2005 all cases in small ruminants that had initially tested
positive would then be tested by discriminatory western blot or
ELISA. If an abnormal result was obtained, the samples would be
submitted to a ring trial using ELISA, western blot and IHC. Only if
the outcome from all these tests was unusual would a bioassay be
2 Statement of the EFSA Scientific Expert Working Group on BSE/TSE of
the Scientific Panel
on Biological Hazards on the health risks of the consumption of milk and
milk derived
products from goats E F S A | European Food Safety Authority


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