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From: TSS (216-119-144-68.ipset24.wt.net)
Subject: SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the open session of the 84th meeting held on 28th September 2004
Date: October 22, 2004 at 2:29 pm PST

-------- Original Message --------
Subject: SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the open session of the 84th meeting held on 28th September 2004
Date: Fri, 22 Oct 2004 16:32:27 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


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

1
SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE
Draft minutes of the open session of the 84th meeting held on 28th
September 2004
At
The Conference Centre
Holiday Inn Bloomsbury
Coram Street
London
WC1N 1HT
Members: Professor C. Higgins (Chair)
Mr. J. Bassett
Dr. D. Brown
Mr. C. Browne
Professor G. Bulfield
Dr. J. Chambers
Professor N. Hooper
Professor J. Ironside
Mr P. Jinman
Dr. C. Lasmezas
Professor. J. Manson
Professor I. McConnell
Ms. D. McCrea
Dr. G. Medley
Dr. P. Rudge
Professor M. Stanley
Assessors: Mr A. Harvey (FSA)
Dr E. Lawrence (DH)
Technical Advisors: Dr P. Barrowman (Defra)
Ms. A. Conroy (FSA)
Dr S. Dixon (FSA)
Mr P. Soul (Defra)
Dr J. Stephenson (DH)
Dr D. Matthews (VLA)
2
SEAC Secretary: Dr C. Boyle
Secretariat: Dr T. Barlow
Mr M. Pemberton
Dr P. Keep
Dr C. Ravirajan
Ms T. Dale
Also in attendance: Professor A. McLean (Oxford University)
(Paper 84/2)
Professor N. Ferguson (Imperial College)
(Paper 84/2)
3
ITEM 1-CHAIRS INTRODUCTION
1. The Chair welcomed members of the public and those watching
via the web cast to the eighth open meeting of SEAC.
2. The Chair explained that the meeting was being filmed as part of
a one-year trial of web casting SEAC open meetings to assess
the potential benefits and uptake of viewing via this medium.
SEAC was the first UK government advisory committee to webcast
their meetings. The initiative allowed greater access to
meetings and continued SEACs commitment to expanding
openness. The Chair explained that for practical reasons, it was
necessary to register, via the SEAC web site, at least 24 hours in
advance of a meeting to determine whether the technology
available to the viewer would support access to the web cast. An
archive of meetings would also be available via the website for
which registration was also required.
3. The Chair welcomed Mr Peter Soul (Defra), Mr Alan Harvey
(FSA), Dr Danny Matthews (VLA) and Dr Angela McLean
(University of Oxford) who were presenting items to the
committee and Professor Neil Ferguson (Imperial College
London) who was invited to provide additional expertise for the
discussion of item 5. If required, officials from government
departments and the devolved administrations would be invited to
inform the committee of the research work sponsored by their
departments. Members were reminded of their obligation to
declare conflicts of interests at the start of each agenda item.
The Chair noted there were no apologies for absence. Members
were informed that the next SEAC meeting would be hosted by
the National Assembly for Wales in Cardiff.
4. The Chair noted that since the last meeting Professor Robin
Carrells term as a committee member had finished and he
recorded his thanks to Professor Carrell for his work on SEAC.
The Chair announced that the SEAC Secretary, Dr Catherine
Boyle, would leave at the end of November to take up a post as
Head of Science Strategy and International Research Policy in
Defra. A successor would be announced in due course. On
behalf of the Committee, the Chair thanked Dr Boyle for the firstrate
support she had given the committee and the Chair.
5. The Chair noted that because the open session of the last
meeting had been cancelled there were no minutes to approve.
4
ITEM 2  BSE UPDATE
6. Mr Peter Soul (Defra) presented an update on BSE in cattle in the
UK and worldwide. The committee was presented with figures
showing the annual numbers of BSE infected cattle in Great
Britain (GB) since 1988 and the reductions in the number of
cases after control measures1 had been introduced. In GB, the
BSE epidemic peaked in 1992, when over 36,500 cases were
confirmed, but thereafter the number of cases had declined very
considerably. In GB, a total number around 183,000 BSE cases
had been recorded to date.
7. Mr Soul explained that an active surveillance programme had
been in place since July 2001 following an EU legal requirement.
Figures from the programme showed a substantial decline in the
number of BSE cases in fallen stock and casualty animals over
24 months old, both regarded as risk groups, as well as in
apparently healthy animals over 30 months old born both before
and after the reinforced ban. The combined BSE cases identified
by passive and active surveillance from January 1999 to August
2004 also show a sharp decline, indicating that UK control
measures are having a major effect on the number of cases of
the disease. Estimates of the future number of BSE cases from
2004 to 2010 predict a further annual decline from 285 cases in
2004 to around one in 2010. BSE cases have been reported in
many other EU countries and in some other countries outside the
EU.
8. Mr Soul explained that in the UK, and other EU countries, a
number of BSE cases born post August 1996 (BARB cases2) had
been reported. To date, a total of 97 BARB cases had been
identified in the UK, 84 in GB and 13 in Northern Ireland.
Research was underway to investigate the origin of the BARBs,
which remains uncertain.
9. A member noted that confidence in the figures from the active
surveillance programme depends on the number of animals
tested and asked how many animals were tested. Mr Soul
replied that a random selection of 10,000 animals/year born
before the reinforced ban, all animals over 42 months born after
1 Feed ban in July 1988; Specified Bovine Offal (SBO) ban in 1990;
Staining of Specified
Risk Material (SRM) in April 1995; Improved SRM controls in 1995;
Reinforced feed ban in
March 1996 and Fully Effective feed ban in August 1996.
2 Any animal born after 1 August 1996 is referred to as a BARB case
(Born After the
Reinforced Ban)
5
the reinforced ban, and all casualty animals going into the OTM
scheme were tested in the programme.
10. A member noted that a reduction in the number of confirmed
clinical cases of BSE had been observed and asked whether
differential diagnostic procedures were in place to allow the
detection of an altered form of BSE or another unknown disease.
Mr Soul acknowledged that there were cases of animals with
clinical signs consistent with BSE that were not confirmed as BSE
cases using the diagnostic tests applied. Although research
proposals had been received to examine such cases further they
had not been accepted because of the limited funds available.
Members considered that research on methods to allow
differential diagnosis of clinical cases of BSE was important
particularly in view of evidence on the phenotypic differences in
infection in humans and sheep.
11. One member asked what part of the brain was tested on postmortem.
Mr Soul responded that for the routine testing, the obex
was tested but lesion profiles across a large number of different
brain sections had been examined in animals early on in the BSE
epidemic and in early BARB cases.
ITEM 3  vCJD UPDATE
12. Professor James Ironside (National CJD Surveillance Unit)
updated the committee on the number of cases of vCJD in the UK
and worldwide. To date, the total number of definite and probable
vCJD cases in the UK was 149, of which five cases were still
alive. No significant gender difference had been observed in
vCJD cases, with 84 male and 65 female cases. Codon 129
analyses of 126 cases have shown all to be homozygous for
methionine at codon 129 of the PrP gene. The single case of
probable iatrogenic vCJD infection, not included in this analysis,
was heterozygous (methionine/valine) at codon 129.
13. Elsewhere, seven vCJD cases have been reported in France, and
a single case in each of Ireland, Italy, Canada and the USA. It
was noted that the vCJD cases reported in France and Italy had
not had a history of residence in the UK, unlike the cases
reported in Ireland, Canada and the USA that had a history of UK
residence during the late 1980s.
14. Professor Ironside explained that the age distribution in cases
had remained constant with the majority of cases in the 20-29
years age group and most cases occurring in the first four
6
decades of life with a single case over 70 years of age. Professor
Ironside considered it notable that the age distribution of vCJD
had not altered, in contrast to the increase in the average age of
cases observed in the BSE epidemic.
15. Professor Ironside explained that statistical models of vCJD
suggested that the incidence of onset of disease and of deaths is
in decline. In contrast, the number of deaths in the UK from sCJD
per annum had increased but this may reflect improved case
ascertainment. A similar increase in sCJD had been observed in
other countries. Seventy cases of sCJD were reported in 2003
and to date 30 cases have been reported in 2004 but additional
reports were expected later in the year.
16. One member asked whether the current decline in the numbers of
post mortem examinations may influence figures on the age
range of vCJD cases because of a reduction in the number of
cases that may be detected. Professor Ironside responded that
the lower number of post-mortem examinations of elderly people
with neurological conditions might affect the age distribution
figures of vCJD. Additionally, given that recent cases of vCJD
infection have been identified in the absence of clinical
symptoms, it is possible that some cases may not be detected.
17. In response to a question on whether pathologists may be
reluctant to conduct post-mortem examinations of possible vCJD
cases, Professor Ironside indicated neuropathologists in the UK
supported the National Surveillance Program well and autopsy
had been performed on all the cases for which consent for
autopsy had been obtained.
18. A member asked for information on the basis of the diagnosis of
vCJD in the patient over 70 years of age. Professor Ironside
explained that the patient had clinical symptoms typical of vCJD
but he recognised that the differential diagnosis of vCJD in
younger adults may be more straightforward than for older adults
because in older adults other neurological diseases could
produce similar symptoms.
19. A member pointed out that there appears to be an age-related
susceptibility to vCJD in humans such that human adolescents
are more susceptible to vCJD infection than older age groups.
Professor Ironside considered that it was possibility that there
was an age-related susceptibility but pointed out that, even if an
age-related susceptibility existed, a shift in the age distribution of
cases to older ages would be expected if it was assumed that
7
exposure had occurred at a specific point in time. This has not
been observed. Alternatively, the lack of a shift in the age
distribution of vCJD may indicate that exposure may have
occurred over a much wider period of time than originally
suspected.
20. One member asked whether there are studies of vCJD that
include random testing of humans who died for reasons other
than possible TSE infection to establish whether there is a
background level of vCJD or whether there are clinical symptoms
of the disease that may be being missed. Professor Ironside
explained that a tonsil and appendix survey had been looking for
PrP in a sample of the UK population. Additionally, a study to
examine the brains of young individuals who died from a range of
causes, and a study of brains in older individuals who died with
neurological illnesses, are also under consideration but ethical
issues relating to the use of human tissues had limited progress
of the projects.
21. One member asked whether diagnosis of sCJD had improved.
Professor Ironside explained that there is more awareness of
sCJD generally, and this had aided ascertainment, along with the
establishment of a National CSF Laboratory in NCJDSU for
14.3.3 protein analysis (to detect this protein in cerebrospinal fluid
(CSF) as a marker of disease).
ITEM 4: REPORT BACK FROM THE SEAC SHEEP SUB-GROUP
22. The Chair informed the committee that the SEAC sheep subgroup
(SSG) had considered two issues relating to the National
Scrapie Plan (NSP) this year. The SSG had considered, via
correspondence, the impact of reports of PrPSc in the brains of
ARR homozygote sheep, previously thought to be naturally
resistant to scrapie, on the NSP. The SSG had concluded that
the scientific rationale behind the NSP strategy remains
appropriate but should be kept under review.
23. The SSG had also considered, at a meeting in July 20004, the
impact of four options to breed TSE resistance into the national
sheep flock as part of a Defra consultation on NSP. Professor
McConnell summarised the four options (A-D).
24. On the basis of modelling work examining the impact of the four
options, the SSG had considered that a solution close to Option D
was the most scientifically desirable. However, at the request of
the SSG, two additional options (E and F) had been modelled and
8
their impact was considered. The SSG had agreed that Option D
remained the most scientifically desirable but given high voluntary
take-up; options E and F would also be expected to increase TSE
resistance.
25. SEAC endorsed the SSG statement but requested that the
following minor amendments be considered by the SSG:
" change paragraph 3 line 5 from ..these would not reduce
scrapie in ARQ sheep.. to read ..these would not reduce
scrapie in ARQ sheep, which may be more important than
to assumed in the modelling, ..
" change paragraph 3 line 6 from .. BSE in sheep which
targets the ARQ alleles.. to read .. BSE in sheep which
appears to preferentially target the ARQ alleles..
" replace paragraph 4 so that it reads The subgroup
recognised there were potential practical difficulties with
option D and therefore, recommended that an additional
option, Option E (mandatory Option B combined with
voluntary Option D) be considered. This option, together
with a further option, Option F (Option E combined with
voluntary ewe genotyping and removal of VRQ ewes) were
modelled. The subgroup considered the outcome of the
additional modelling work and agreed that Option D
remains the most scientifically desirable. Option F offered
no significant advantage over Option E. Members agreed
that Option E, given high voluntary take up, could also be
regarded as precautionary from a risk reduction
perspective.
ITEM 5  BSE AND SHEEP: THE FSAS CONTINGENCY POLICY
26. The Chair informed the committee that the FSA would shortly
review its contingency policy on action to take should BSE ever
be found in sheep. To assist with this review, the FSA
commissioned two modelling studies (a) to estimate the possible
prevalence of BSE in sheep and (b) to estimate the likely impact
of different risk reduction strategies should BSE be found in
sheep. SEAC were asked to advise on the underlying scientific
assumptions and approaches adopted in both studies, taking any
uncertainties into account. Members were reminded that the
Annexes of the paper contained unpublished information that
should be regarded as confidential.
9
27. Mr Alan Harvey (FSA) provided a background to the FSA
contingency policy. In 2000, an FSA review of BSE controls
concluded that, although BSE had never been found in sheep,
there remained a theoretical possibility that it could be present
because, in the past, some sheep consumed the same feed that
infected cattle. Although these sheep are no longer alive, it is
possible that following an initial infection, BSE may have been
transmitted within flocks. In 2002, the FSA formulated a
contingency policy that should BSE be found in sheep, only
animals demonstrated to be free of BSE would enter the food
chain. At the time, it was acknowledged that, because the
necessary testing mechanisms were not available,
implementation of this policy would prevent all UK sheep from
entering the food chain. The FSA is reconsidering whether, in the
light of scientific developments, this contingency policy remains
proportionate. To inform its consideration, the FSA has asked for
SEACs opinion on the modelling studies it commissioned.
TSE testing
28. Dr Danny Matthews (VLA) presented a summary of the western
blot and immunohistochemical methods used at VLA to detect
TSEs and to discriminate between scrapie and BSE infection in
sheep. The methods had been used in two studies conducted by
the VLA to monitor TSEs in sheep: a retrospective study from
January 1998 to October 2001 and a prospective study from
November 2001 to May 2004. Of a total of 2367 TSE cases
examined, 2316 cases gave positive results for scrapie infection
but 51 samples had given equivocal results. In the course of the
prospective study, two additional samples had given unusual
(atypical) test results and had been reanalysed as part of a
Community Reference Laboratory ring-trial by VLA and other
laboratories. On the basis of the combined results from these
analyses, it was concluded that the samples did not precisely
resemble known strains of either scrapie or BSE in sheep but
reflected a TSE infection, possibly by an unknown scrapie strain.
No cases of clear-cut BSE in sheep had been identified in the two
studies. Of the scrapie cases identified, 2147 cases could be
traced back to 450 flocks with almost half of these cases coming
from 34 flocks. The origin of 220 cases could not be determined
and were excluded from the data set. A statistical analysis of
these data, using an approach similar to that of Gravenor et al.
(2003)1, which assumed a skewed distribution in the data, had
1 Gravenor et al. (2003) Searching for BSE in sheep: interpreting the
results so far. Vet. Rec.
152, 298-299.
10
provided two estimates of the possible proportion of the scrapie
cases that could be BSE: 0.14% based on the number of scrapie
cases and 0.66% based on the number of flocks.
29. The Chair sought clarification on when the Community Reference
Laboratory ring trial would be completed. Dr Matthews explained
that, with the exception of a conformation-dependent
immunoassay (CDI) test, all the other reference laboratories had
submitted their test results. The Chair emphasised the
importance of the CDI test as part of the evaluation of the
methods generally as, unlike all the other tests used by
laboratories taking part in the ring trial, CDI was not dependent on
differential digestion by proteinase K. It represented an important
confirmatory and possibly powerful discriminatory test. The Chair
also emphasised the importance of continued evaluation of the
two atypical samples, particularly the need for infection studies.
30. Members asked whether all the unusual scrapie cases had been
tested using the mouse bioassay. Dr Matthews explained that
the 51 samples, which had given equivocal results in the test,
were not part of the bioassay programme, although mice were
currently being bred for inoculation with material from the two
atypical cases, next month.
31. Members asked whether there were plans to apply the
discriminatory tests to random cattle samples to see whether
variants of BSE exist in cattle. Dr Matthews explained that the
western blot method had been applied to all cattle samples
routinely for the past 18 months and, so far, no variation in test
results had been found. A proposal from VLA for a retrospective
immunohistochemical examination of cattle to test for phenotypes
different to those already recognised is under consideration.
Members considered it important to test a number of historical
BSE cases by the western blot method.
32. The Chair noted that the two atypical cases could either be i) a
variant form of scrapie with no implications for human health, ii)
an unknown variant of BSE, iii) another as yet uncharacterised
TSE, or iv) an unusual phenotype resulting from a combination of
a TSE and a particular sheep genotype. Members emphasised
the urgency of strain typing by transmission studies as the only
validated way of discerning one strain from another in terms of
biological properties and ascertaining possible health and welfare
implications of the 'atypical' TSEs.
11
33. In concluding this part of the discussion, SEAC noted that:
" The analytical methods used to detect TSEs in sheep, and
distinguish BSE from scrapie, were becoming more robust;
" The results from the on-going ring trial were important to
fully assess the robustness of the methods. The analysis
of the final data from the CDI method was considered
particularly important because, unlike all the other methods
used in the ring trial, it does not rely on differential enzyme
(proteinase K) digestion of PrP; and
" Although no unambiguous case of BSE in sheep had yet
been detected, this conclusion cannot be considered
absolute because of the limitations of the test methodology
and the relatively small numbers of samples that could be
tested.
" The two 'atypical' cases could not yet be defined as either
scrapie or BSE variants, and follow up studies on these
'atypical' TSEs should be pursued with some urgency.
Possible prevalence of BSE in sheep
34. In respect of the modelling work to estimate the prevalence of
BSE in sheep, members expressed concern about the extent to
which cases based on the total sample size of 450 flocks
represented a random selection. Dr Matthews responded that
they were a non-random selection but represented all cases
presented to the VLA, primarily via passive surveillance.
35. Professor Ferguson raised a concern about the use of the
passive surveillance data, which may lead to a selective
ascertainment bias and, therefore, an under-estimate of the
maximum prevalence of BSE in sheep. Professor Ferguson
suggested a more conservative approach would be to use the
active surveillance results, although he acknowledged that this
limited the amount of data that could be used in the analysis. He
suggested that data from the 2002 scrapie postal survey, relating
to the distribution of cases on scrapie affected farms, could be
compared with the passive surveillance data in order to assess
the possible effect of the sample bias.
36. Professor Ferguson provided further comments on two of the
assumptions used to model the prevalence of BSE in sheep.
12
Firstly, that the expected survival rate for sheep with BSE is
assumed to be similar to that for scrapie, and secondly, whether
BSE is likely to be identified as a TSE in the passive surveillance
programme. Professor Ferguson considered that both these
assumptions could be better addressed using the active
surveillance data.
37. The Chair sought clarification on whether the uneven distribution
of scrapie cases within the 450 flocks sampled had been taken
into account as part of the modelling study. Professor Wilesmith
believed that it had been taken into account but noted that the
prevalence data was based on a simple statistical analysis rather
than a complex modelling study. Professor Ferguson commented
that by basing the prevalence on sheep flocks rather than
individual cases, the clustering of scrapie cases within flocks had
to some extent been taken into account.
38. SEAC generally accepted the approach used to model the
possible prevalence of BSE in sheep, but noted that:
" The model depended on the ability of the tests used to
effectively detect and discriminate between scrapie and
BSE;
" Using the number of TSE affected flocks in the calculation
of prevalence was preferable to using individual TSE cases
Impact of risk reduction strategies
39. Dr Angela McLean (University of Oxford) summarised the main
assumptions, data and methodology used in a study to
mathematically model the amount of infected material that could
enter the human food chain as a result of a BSE epidemic in
sheep. Due to the paucity of data available, it had been
necessary to make a large number of assumptions.
40. Dr McLean explained that the possible number of sheep flocks
with BSE had been based on the estimate of the proportion of
scrapie cases that could be BSE presented earlier and the data
from a postal survey of scrapie in sheep flocks. To model the
distribution of BSE in these flocks, it had been necessary to
greatly simplify the demography and genotype of sheep flocks
and to assume that the time course of a BSE epidemic would be
similar to a scrapie epidemic. It had also been assumed that
sheep of the ARR/ARR genotype were completely resistant to
infection.
13
41. Dr McLean explained that the accumulation of BSE infectivity in
sheep within flocks had been inferred using the limited
experimental data available on the susceptibility, incubation
period and accumulation of infectivity in scrapie infected sheep,
combined with the very limited data on the tissue distribution of
BSE in sheep. These data, together with information on sheep
tissues used in the food chain, were used to model BSE infectivity
that could enter the food chain.
42. Dr McLean noted that a key result from the modelling was the
suggestion that the total infectivity entering the food chain from a
single sheep, about one year prior to the onset of clinical disease,
would represent a very large dose of BSE infectivity.
43. Dr McLean explained that the modelling work had been used to
assess the impact of risk reduction strategies to reduce the
potential for infected material to enter the food chain. The
strategies were based on testing sheep prior to entry into the food
chain, removal of certain specified risk materials, or restriction of
sheep of certain PrP genotypes and age from entering the food
chain. The modelling suggested that strategies based on sheep
PrP genotype perform better than the other strategies.
44. The Chair invited Professor Neil Ferguson (Imperial College
London) to comment on the study. Professor Ferguson
acknowledged the difficulties in modelling BSE in sheep and the
large number of assumptions that were required. In view of this,
it was important to stress that the magnitude of the relative
reductions in risk between strategies suggested from the
modelling should not be regarded as absolute. In respect of the
data presented on the level of infection in the peripheral nervous
system, which assumes zero infectivity until 36 months post
infection, Professor Ferguson understood that infection peaked at
an earlier stage of the incubation period. It was noted that an
earlier peak in infection would impact on the efficacy of the
various SRM risk reduction strategies presented.
45. Professor Ferguson noted that the 10-fold reduction in the
quantity of duodenum and jejunum entering the food supply
differed considerably from the much larger estimate of the level of
infectivity entering the food supply in a previous study undertaken
by Imperial College in 2001. It was acknowledged that the
estimates used in the 2001 study were subject to debate at the
time. A member considered the effective removal of all lymph
nodes assumed in the modelling was unrealistic. Professor
14
Ferguson also noted that the modelling suggested that the total
infectivity entering the food supply from a single BSE infected
sheep would be very large compared with the amount of
infectivity that could enter the food supply from a BSE infected
cow.
46. Professor Ferguson commented on the assumption made in the
model that sheep with the ARR/ARR genotype were completely
resistant to naturally occurring BSE and suggested that other risk
reduction strategies should be considered that assumed some
level of susceptibility for sheep with the ARR/ARR genotype.
Members agreed that even if the ARR homozygous genotype is
not completely resistant to infection, there were still advantages
of this genotype compared with the other genotypes.
47. Professor Ferguson noted that the model assumed a selfsustaining
BSE epidemic in a small number of farms. Given that
sheep would have been exposed to infected feed approximately
20 years ago, Professor Ferguson disagreed with the assumption
that it was only necessary to consider large epidemics in a small
number of flocks and suggested that that a model of a selfsustaining
transmission of BSE in a sheep flock was inconsistent
with the data on the possible prevalence of BSE in sheep
considered earlier. Professor Ferguson considered epidemics in
smaller flocks to be more consistent with the data on the
prevalence of BSE in sheep. Dr McLean agreed that the
presence of large-scale epidemics on a small number of farms
was unlikely but evidence from flock-to-flock modelling studies
and the slow dynamics of BSE meant that this was not
inconceivable.
48. Members asked whether any studies were underway to
reproduce natural transmission of BSE in sheep. Dr Matthews
responded that natural transmission studies were underway at
both the VLA and the IAH.
49. Dr Matthews commented on the assumption made in the
modelling that sheep were easy to infect with BSE. Attack rate
studies at both IAH and VLA had not shown infectivity in sheep
for animals orally challenged with less than 0.5g of infected
material. Based on studies relating to the susceptibility of various
genotypes orally challenged with 0.5g of infected material, Dr
Matthews considered the inputs on attack rate used in the model
to be pessimistic. Dr McLean explained that challenge data had
been used to establish relative susceptibility between genotypes,
15
but these data were not used to model transmission rates
between sheep
50. Members considered it important to note that, in contrast to
assumptions made in the modelling, sheep breeds were
heterogeneous and methods of husbandry differed considerably.
Also, it may not be appropriate to generalise about the
prevalence and distribution of PrP genotypes in sheep because
PrP genotype can be extremely variable between sheep breeds.
Dr McLean acknowledged the concerns expressed about the
modelling not taking account of the heterogeneity of breeds and
PrP genotype and differences in husbandry. The model did,
however, take account of some differences relating to flock size
and husbandry, as reflected by the proportion of homebred
sheep. This was considered important given the results of the
scrapie postal survey, which suggested that home breeding flock
farms were more likely to report scrapie.
51. Members considered that if sheep had been infected with BSE,
infection would have been most likely to occur before the
reinforced feed ban and noted that since the ban one and a half
life cycles in sheep would have passed. Thus, the likelihood of
BSE infection now must be very small. Dr McLean agreed but
pointed out that the model represented BSE infection in a very
small number sheep flocks.
52. SEAC generally accepted the modelling approach undertaken
and acknowledged the large number of assumptions that had to
be used; in particular the assumption that the pathogenesis of
BSE in sheep is similar to scrapie, which is largely unknown.
Taking into account the various assumptions and caveats relating
to the modelling study, SEAC noted that:
" The model of BSE infectivity in sheep tissues suggested
that a single BSE infected sheep entering the food supply
could present a significantly greater risk to public health
compared with the current risk associated from a single
infected bovine entering the food supply;
" Although there was no evidence of a large, self-sustaining
epidemic of BSE in sheep, the presence of small epidemics
in a few flocks cannot yet be ruled out;
" the model suggests that strategies based on control of
specified risk material or TSE testing are currently unlikely
to be very effective in minimising risk of human infection,
16
although the committee noted that should the sensitivity of
TSE tests be improved they may be effective in the future;
and
" the model suggests that strategies based on PrP genotype
of sheep would be the most effective in reducing risk of
human infection. However, the committee stressed that the
magnitude of the relative reductions in risk between the
various strategies modelled could not be regarded as
absolute.
ITEM 6: AOB
53. There was no other business to discuss.

http://www.seac.gov.uk/minutes/draft84.pdf

Greetings,

> 10. A member noted that a reduction in the number of confirmed
> clinical cases of BSE had been observed and asked whether
> differential diagnostic procedures were in place to allow the
> detection of an altered form of BSE or another unknown disease.
> Mr Soul acknowledged that there were cases of animals with
> clinical signs consistent with BSE that were not confirmed as BSE
> cases using the diagnostic tests applied. Although research
> proposals had been received to examine such cases further they
> had not been accepted because of the limited funds available.
> Members considered that research on methods to allow
> differential diagnosis of clinical cases of BSE was important
> particularly in view of evidence on the phenotypic differences in
> infection in humans and sheep.


MOST disturbing.

> In contrast, the number of deaths in the UK from sCJD
> per annum had increased but this may reflect improved case
> ascertainment. A similar increase in sCJD had been observed in
> other countries.


i do not agree with this _assumption_!

i believe there are multiple routes and sources for this agent
and they are going ignored, while being called 'sporadic'.

and by all means i would ignore all the latest studies that show that
indeed sporadic CJD is tied to some strain of TSE in cattle and sheep,
and that there are more than one strain of TSE in cattle. no need to look
any further in that is there...

> 8
> ITEM 5  BSE AND SHEEP: THE FSAS CONTINGENCY POLICY
> 26. The Chair informed the committee that the FSA would shortly
> review its contingency policy on action to take should BSE ever
> be found in sheep. To assist with this review, the FSA
> commissioned two modelling studies (a) to estimate the possible
> prevalence of BSE in sheep and (b) to estimate the likely impact
> of different risk reduction strategies should BSE be found in
> sheep. SEAC were asked to advise on the underlying scientific
> assumptions and approaches adopted in both studies, taking any
> uncertainties into account. Members were reminded that the
> Annexes of the paper contained unpublished information that
> should be regarded as __confidential__.


MORE disturbing, back to the same-old, same-old i see.
ISN't this secrecy crap what got us in this mess.
IT seems to me the likelyhood of BSE in sheep is very real,
SO what's the hold up here, how much longer will we discuss this
BSE AND SHEEP: THE FSAS CONTINGENCY POLICY
before taking action? the longer you wait, the more the agent spreads
in the sheep population. course the regular scrapies transmit to primates,
and there has never been transmission studies on man, so i am sure that
there is no need to worry there either?

> The methods had been used in two studies conducted by
> the VLA to monitor TSEs in sheep: a retrospective study from
> January 1998 to October 2001 and a prospective study from
> November 2001 to May 2004. Of a total of 2367 TSE cases
> examined, 2316 cases gave positive results for scrapie infection
> but 51 samples had given equivocal results. In the course of the
> prospective study, two additional samples had given unusual
> (atypical) test results and had been reanalysed as part of a
> Community Reference Laboratory ring-trial by VLA and other
> laboratories. On the basis of the combined results from these
> analyses, it was concluded that the samples did not precisely
> resemble known strains of either scrapie or BSE in sheep but
> reflected a TSE infection, possibly by an unknown scrapie strain.
> No cases of clear-cut BSE in sheep had been identified in the two
> studies.

> 32. The Chair noted that the two atypical cases could either be i) a
> variant form of scrapie with no implications for human health, ii)
> an unknown variant of BSE, iii) another as yet uncharacterised
> TSE, or iv) an unusual phenotype resulting from a combination of
> a TSE and a particular sheep genotype. Members emphasised
> the urgency of strain typing by transmission studies as the only
> validated way of discerning one strain from another in terms of
> biological properties and ascertaining possible health and welfare
> implications of the 'atypical' TSEs.

WHAT more do you expect.
SEEMS the same thing has happened with those VERMONT sheep
that tested 'atypical' here in the USA that were imported from Belgium.
Dr. Detwiler said that the UK fumbled the football on this one too.
THIS is why the testing of those sheep has been put off for 2+ YEARS,
they simply are mortified over the final results.

> " The two 'atypical' cases could not yet be defined as either
> scrapie or BSE variants, and follow up studies on these
> 'atypical' TSEs should be pursued with some urgency.


after floundering for some 20+ years on this issue, i would say
indeed they must move forward with some urgency. but i don't
think they know what the word 'urgency' means.

all in all, seems like the same old BSeee to me...

TSS

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