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From: Terry S. Singeltary Sr. (216-119-144-33.ipset24.wt.net)
Subject: EIGHTY-FIFTH MEETING OF THE SPONGIFORM summary
Date: December 2, 2004 at 7:27 am PST

-------- Original Message --------
Subject: EIGHTY-FIFTH MEETING OF THE SPONGIFORM summary
Date: Thu, 2 Dec 2004 09:32:57 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

EIGHTY-FIFTH MEETING OF THE SPONGIFORM
ENCEPHALOPATHY ADVISORY COMMITTEE
The Spongiform Encephalopathy Advisory Committee (SEAC) held
its 85th meeting in Cardiff on 30th November 2004, when it
discussed the following matters:
CURRENT ISSUES
SEAC was updated on three current TSE issues:
• The FSA / SEAC milk working group, established to provide
advice to the FSA on research to develop diagnostic tests to
detect abnormal PrP in milk from cattle together with
assessment of results from tests of experimental samples, is
expected to complete its work in the early part of 2005. It is
anticipated that a report from the group will be provided at the
next SEAC meeting.
• A paper by Wadsworth et al (published 11 November 2004)
reporting 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.
• A European Commission press release (28 October 2004)
suggesting that a goat in France may have been naturally
infected with BSE. Following this announcement, the
Community Reference Laboratory expert group had
concluded (25 November 2005) 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.
CHRONIC WASTING DISEASE IN UK DEER
SEAC was asked by the FSA to consider the likelihood of chronic
wasting disease (CWD) being present in UK deer and, if it were
present, the possible risk posed to consumers from eating meat
from infected animals. CWD is an endemic transmissible
spongiform encephalopathy (TSE) of certain species of captive
and wild deer in areas of North America.
SEAC noted that CWD has never been found in the UK or
elsewhere in Europe but acknowledged that surveillance data on
TSEs in deer are very limited. Although the origins of the disease
are unknown, the committee considered there is good evidence
that it is transmitted laterally between animals, possibly via
contaminated environments, but the precise mechanisms are
unclear. Additionally, it is possible that at least some UK deer
species may be relatively susceptible to CWD, although red deer
may be the species most likely to be susceptible because they are
closely related to Rocky Mountain elk, one of the North American
species affected.
SEAC considered that, although incomplete, there is no evidence
from epidemiological or experimental studies to suggest that sheep
or cows are susceptible to natural infection with CWD.
Furthermore, the committee concluded there is no evidence of
transmission of CWD to humans from consumption of venison but
noted that data are extremely limited and it would be very difficult
to detect a low level of infection.
SEAC also considered that, although a theoretical possibility
existed, there is no evidence to suggest that BSE is present in UK
deer. It was noted that a study to look at the potential
susceptibility of red deer to BSE was at a very preliminary stage.
SEAC agreed to produce a position statement on CWD and UK
deer.
HORIZON SCANNING
The committee was informed by representatives from DH, FSA
and Defra about forthcoming issues that might require
consideration by SEAC, including:
• estimation of the size of the vCJD epidemic, minimisation of
the risks of secondary transmission of vCJD, development of
diagnostic tests for vCJD, age distribution and susceptibility of
vCJD infection (DH).
• development of diagnostic tests for BSE, possible public
health risks of TSEs in sheep, development of contingency
plans for TSEs in the food supply and changes to regulatory
controls for BSE (FSA).
• examination of BARB cases (BSE cases Born After the
Reinforced Ban), relaxation of BSE control measures and safe
disposal of animal by-products (Defra).
TERMINATION OF CATTLE BIOASSAYS
The committee noted the proposed termination of FSA-funded
cattle bioassays to examine the BSE infectivity in cattle tissues.
Members stressed the importance of archiving appropriate tissues
from the cattle bioassays to ensure maximum scientific information
can be obtained.
PUBLIC QUESTION AND ANSWER SESSION
The Committee answered questions from the public about TSEs
including the development of blood tests for TSEs, the number of
sCJD cases and their genetic make-up, and the recent finding of
possible BSE in a French goat.
MATERNAL TRANSMISSION OF vCJD
DH asked SEAC to consider the potential for maternal
transmission of vCJD. The item was discussed in a reserved
business session because it involved consideration of confidential
medical information and unpublished data.
SEAC concluded that there is no evidence for maternal
transmission of vCJD, but acknowledged that most of the relevant
information is indirect rather than direct. Therefore, although it
was considered that a hypothetical risk of maternal transmission is
likely to be low, a risk cannot be ruled out.

http://www.seac.gov.uk/papers/301104summary.pdf

Greetings,

I see by this summary they are so worried about the increase of
sporadic CJD and the findings of BASE with molecular similarity
with sCJD that they forgot to go into any kind of detail about it.
I see at least someone from the public brought it up at the Q/A.
maybe it will be burried in the full text somewhere's when it comes
out (sorry Ralph, just how i feel, they can ignore it all they want,
but it will not go away. UNTIL they bring sporadic CJD to the fore
front of research, they have simply missed the bigger picture, and
the agent continues to spread). If i understand SEAC correctly, they
say that this meeting will be available from Wednesday 1st Dec. on
at;

85th Meeting of SEAC - 30.11.04
This event took place on Tuesday 30th November and was broadcast live on
the internet. The archives will be available from Wednesday 1st December
2004. Please check back then.

Agenda & more information


HOWEVER, in the USA, they do not even mention these studies.
ITs all BSE/nvCJD or nothing, while the agent continues to spread.
Ignorance is bliss, but this ignorance will continue to spread this agent
from border to border and sea to sea...

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan
Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah
E. Lloyd, Jonathan D.F. Wadsworth and John Collinge1

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology, University College, Queen Square, London WC1N 3BG, UK 1
Corresponding author e-mail: j.collinge@prion.ucl.ac.uk


Received August 1, 2002; revised September 24, 2002; accepted October
17, 2002

Abstract

Variant CreutzfeldtJakob disease (vCJD) has been recognized to date
only in individuals homozygous for methionine at PRNP codon 129. Here we
show that transgenic mice expressing human PrP methionine 129,
inoculated with either bovine spongiform encephalopathy (BSE) or variant
CJD prions, may develop the neuropathological and molecular phenotype of
vCJD, consistent with these diseases being caused by the same prion
strain. Surprisingly, however, BSE transmission to these transgenic
mice, in addition to producing a vCJD-like phenotype, can also result in
a distinct molecular phenotype that is indistinguishable from that of
sporadic CJD with PrPSc type 2. These data suggest that more than one
BSE-derived prion strain might infect humans; it is therefore possible
that some patients with a phenotype consistent with sporadic CJD may
have a disease arising from BSE exposure...

http://embojournal.npgjournals.com/cgi/content/full/21/23/6358

THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease

http://www.pnas.org/cgi/content/abstract/0305777101v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

Sarah E. Lloyd, Jacqueline M. Linehan, Melanie Desbruslais,
Susan Joiner, Jennifer Buckell, Sebastian Brandner,
Jonathan D. F. Wadsworth and John Collinge

Correspondence
John Collinge
j.collinge@prion.ucl.ac.uk

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology,
University College, London WC1N 3BG, UK
Received 9 December 2003
Accepted 27 April 2004

Distinct prion strains can be distinguished by differences in incubation
period, neuropathology
and biochemical properties of disease-associated prion protein (PrPSc)
in inoculated mice.
Reliable comparisons of mouse prion strain properties can only be
achieved after passage in
genetically identical mice, as host prion protein sequence and genetic
background are known
to modulate prion disease phenotypes. While multiple prion strains have
been identified in
sheep scrapie and CreutzfeldtJakob disease, bovine spongiform
encephalopathy (BSE) is
thought to be caused by a single prion strain. Primary passage of BSE
prions to different lines
of inbred mice resulted in the propagation of two distinct PrPSc types,
suggesting that two
prion strains may have been isolated. To investigate this further, these
isolates were
subpassaged in a single line of inbred mice (SJL) and it was confirmed
that two distinct prion
strains had been identified. MRC1 was characterized by a short
incubation time (110±3 days),
a mono-glycosylated-dominant PrPSc type and a generalized diffuse
pattern of PrP-immunoreactive
deposits, while MRC2 displayed a much longer incubation time (155±1 days),
a di-glycosylated-dominant PrPSc type and a distinct pattern of
PrP-immunoreactive deposits
and neuronal loss. These data indicate a crucial involvement of the host
genome in modulating
prion strain selection and propagation in mice. It is possible that
multiple disease phenotypes
may also be possible in BSE prion infection in humans and other animals.

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique
Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

THE recent discoveries of previously unidentified strains of
Scrapie such as 221C44 and the Nor9845;

2.5.2 The existence of distinct strains was recognised when sources of
sheep scrapie were serially transmitted to mice. A single inbred line of
mice, in which all
individuals make the same PrPC, can propagate several different strains
of scrapie, each with
its own distinctive incubation period, pattern of damage in the brain
and PrPSc
properties42, 43. Strain variation also occurs in natural scrapie, and
the recent discoveries of
previously unidentified strains, such as 221C44 and Nor9845, suggests
that the
spectrum of different strains may change with time. Since different
strains can have very
different patterns of pathology and distribution of PrPSc, their
presence may be missed by the
application of standard sampling and testing protocols used for
surveillance45.
Although a single strain of BSE appears to be responsible for the vast
majority of cases around the
world46, 47, evidence is emerging that suggests that there may be other
strains which
have different properties when transmitted to mice48 or result in
different pathology
or properties of PrPSc in infected cattle49, 50.

FULL TEXT APPRX. 91 PAGES

UK Strategy for Research and
Development on Human and Animal
Health Aspects of Transmissible
Spongiform Encephalopathies

2004-2007

http://www.mrc.ac.uk/pdf-uk_strategy_v5.2.pdf

WHEN in fact, the findings from Marsh and the findings at
MISSION, TEXAS support even further evidence that there
are furthers strains of TSE in the USA besides that one
accidently documented BSE case in Washington on
Dec. 23, 2003;

In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - Report of a visit to the USA - April-May 1989 - G A
H Wells [head of England's main veterinary lab]

2. Meeting with USDA, BSE Task Force

This group comprises Alex Thierman (USDA-APHIS, International Programs)
(Chairman), Roger Breeze (USDA-ARS Director, Plum Island), Bill Hadlow
(Neuropathologist - retired, formerly of NIH Rocky Mountain Laboratory,
Hamilton, Montana), John Gorhan and Mark Robinson (USDA-ARS, Pullman,
Washington) and Dick Marsh (Dept. Vet. Science, Univ Wisconsin - Madison).
The objectives of the group are to assess the implications of the
occurrence of BSE for US cattle particularly the risk of BSE occurrence
in the US in relation to endemic scrapie agent.
The purpose of my invitation to this meeting was to discuss aspects of
research which are of common interest and to identify a tentative USDA
research programme including any potential collaborative projects. The
discussions were informal and there was no agenda.
The general opinion
of those present was that BSE, as an overt disease phenomenon, could
exist in the USA but if it did it was very rare. The need for improved
and specific surveillance methods to detect it was recognised. Clinical
similarities between BSE and rabies suggested one means of sampling the
cattle population which might increase the probability of detection of
BSE. It was clear that the bovine rabies negative rate would vary
greatly between States but initially this should be determined and as it
would inevitably be high relative to positive cases, some differential
diagnosis carried out.

The work of Wilbur Clarke at Mission, Texas was discussed briefly. the
results of this study in which 10 calves were inoculated with scrapie
has not been published and perhaps would not be published. USDA are
sensitive regarding publicity of the results of the study which remain
far from conclusive. Apparently only 3 of the inoculated animals
developed neurological signs. The neuropathology of the affected cattle
has not been examined in any depth but Hadlow has the material. Marsh
indicated the requirement to obtain the fresh brain material from this
study in order to perform PrP extractions.

Because of the successful transmission of the Brecke (Stetsonville)
isolate of TME to cattle and the subsequent passage history in mink it
was generally considered important that comparisons be made with BSE
isolates in mink. Is BSE like scrapie in mink? Is BSE like the Brecke
isolate of TME?

Very little was said about CWD but some present considered that its
occurrence may indicate a sylvatic origin of agent. It was also agreed
that the role of possible subclinical infection in the
epidemiology of transmissible spongiform encephalopathies could well
be important but was unknown.
Marsh remarked on the possibility that
BSE was due to an extremely thermostable strain of agent. His
experience in the past with one particular Wisconsin isolate of TME
(Hayward strain) suggested that i/c biopsy needles could not be
effectively "scrapie sterilised", even employing an experimental
autoclave system capable of 60 psi and 300"C+ for 5 hours. This
experience led him to the policy that in scrapie or TME transmission
studies re-use of instruments or glassware that had contained agent was
an unacceptable protocol.

I was given confidential access to sections from the Clarke scrapie-
cattle transmission experiment. Details of the experimental design were
as supplied previously by Dr Wrathall (copy of relevant information
appended). Only 3 animals (2 inoculated with 2nd pass Suffolk Scrapie
and 1 inoculated with Angora goat passaged scrapie) show clinical signs.

Clinical signs were characterised by weakness, "a stilted hindlimb
gait", disorientation, ataxia and, terminally,
lateral recumbency. The two cattle from which I examined material were
inoculated at 8 months of age and developed signs 36 months pi (goat
scrapie inoculum) and 49 months pi (one of the Suffolk scrapie
inoculated) respectively.
This latter animal was killed at 58 months
of age and so the clinical duration was only 1 month. The neuropathology
was somewhat different from BSE or the Stetsonville TME in cattle.
Vacuolar changes were minimal, to the extent that detection required
careful searching. Conversely astrocyte hypertrophy was a widespread and
prominent feature. The material requires detailed neuropathological
assessment but whether or not this will be done remains in question.

Appendix I

VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE

1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has
successfully transmitted ovine and caprine scrapie to cattle. The
experimental results have not been published but there are plans to do
this. This work was initiated in 1978. A summary of it is:-

Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a
2nd Suffolk scrapie passage:-

i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.

1/6 went down after 48 months with a scrapie/BSE-like disease.

Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus
2/6 went down similarly after 36 months.

Expt C Mice inoculated from brains of calves/cattle in expts A & B were
resistant, only 1/20 going down with scrapie and this was the reason
given for not publishing.

Diagnosis in A, B, C was by histopath. No reports on SAF were given.

Dr Warren Foote indicated success so far in eliminating scrapie in
offspring from experimentally (and naturally) infected sheep by ET. He
had found difficulty in obtaining emhryos from naturally infected sheep
(cf SPA).

3. Prof. A Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr A Thiermann showed the picture
in the "Independent" with cattle being incinerated and thought this was
a fanatical incident to be avoided in the US at all costs. BSE was not
reported in USA.

4. Scrapie incidents (ie affected flocks) have shown a dramatic increase
since 1978. In 1953 when the National Control Scheme was started there
were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.

5. Scrapie agent was reported to have been isolated from a solitary fetus.

6. A western blotting diagnostic technique (? on PrP) shows some promise.

7. Results of a questionnaire sent to 33 states on the subject of
the national sheep scrapie programme survey indicated;

17/33 wished to drop it
6/33 wished to develop it
8/33 had few sheep and were neutral

Information obtained from Dr Wrathall's notes of a meeting of the U.S.
Animal Health Association at Little Rock, Arkansas Nov. 1988.

CONFIDENTIAL TRANSMISSION (Day 4)

6.1 BSE to pigs

snip...end

full text ;

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


TSS

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