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From: TSS ()
Subject: BSE/TSE/SRM POKER AND POLITICS it's simply not about science or human health anymore
Date: June 3, 2005 at 7:18 am PST

BSE/TSE/SRM POKER AND POLITICS it's simply not about science or human health anymore

European Food Safety Agency proposes increase in cattle age for removal of SRM

Editorial team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office

The age at which specified risk materials (SRM, tissue such as brain and spinal cord) are removed from cattle slaughtered for food was set at 12 months in all European Union (EU) member states (except for the United Kingdom) in 2000. This measure was designed to protect consumers of beef from the risk of bovine spongiform encephalopathy (BSE) [1,2].
New information supplied by the World Organization for Animal Health (OIE), surveillance data and scientific research was recently considered by members of the European Food Safety Authority Biological Hazards Panel. Based on this evidence and a review of previous discussions, the panel recognised that the bovine central nervous system is unlikely to become infectious until an infected animal is considerably older than 12 months. [3].

The average age of cattle with BSE in the EU has increased between 2001 and 2004, from 86 months to 108. Only 4 cases in cattle under 35 months have been reported since 2001. The lowest age of animals with BSE rose from 28 to 42 months between 2001-4.

From pathogenesis studies of infectivity distribution throughout the incubation period, and the earliest age of clinical manifestation, it was concluded that a bovine central nervous system would not become infectious until at least 26 months of age, as it appears that only during the last quarter of the incubation period does the disease become detectable.

The panel concluded that setting the age for SRM removal at 21 months would allow a reasonable safety margin. Based on this opinion, the European Commission will consider whether changes to the existing legislation should be proposed. There is currently no scientific basis for raising the age limit for bovine tonsil and intestine.


References:
Official Journal of the European Communities. Commission Decision of 29 June 2000 regulating the use of material presenting risks as regards transmissible spongiform encephalopathies and amending Decision 94/474/EC. L158/76. 30 June 2000. (http://forum.europa.eu.int/irc/sanco/vets/info/data/oj/00418ec.pdf)
Chalus T, Peutz I. BSE : the European regulatory context. Euro Surveill 2000; 5(10): 107-12 (http://www.eurosurveillance.org/em/v05n10/0510-223.asp)
European Food Safety Authority. EFSA provides new scientific assessment on the age limit for the removal of specified risk materials from cattle with regard to BSE. Press release. 26 May 2005. (http://www.efsa.eu.int/science/biohaz/biohaz_opinions/938_en.html)
http://www.eurosurveillance.org/ew/2005/050602.asp#4


107

Vet Pathol 42:107–108 (2005)

Letters to the Editor

Editor:

Absence of evidence is not always evidence of absence.

In the article ‘‘Failure to detect prion protein (PrPres) by

immunohistochemistry in striated muscle tissues of animals

experimentally inoculated with agents of transmissible spongiform

encephalopathy,’’ recently published in Veterinary

Pathology (41:78–81, 2004), PrPres was not detected in striated

muscle of experimentally infected elk, cattle, sheep, and

raccoons by immunohistochemistry (IHC). Negative IHC,

however, does not exclude the presence of PrPSc. For example,

PrPres was detected in skeletal muscle in 8 of 32

humans with the prion disease, sporadic Creutzfeldt-Jakob

disease (CJD), using sodium phosphotungstic acid (NaPTA)

precipitation and western blot.1 The NaPTA precipitation,

described by Wadsworth et al.,3 concentrates the abnormal

isoform of the prion, PrPres, from a large tissue homogenate

volume before western blotting. This technique has increased

the sensitivity of the western blot up to three orders

of magnitude and could be included in assays to detect

PrPres. Extremely conspicuous deposits of PrPres in muscle

were detected by IHC in a recent case report of an individual

with inclusion body myositis and CJD.2 Here, PrPres was

detected in the muscle by immunoblotting, IHC, and paraf-

fin-embedded tissue blot. We would therefore caution that,

in addition to IHC, highly sensitive biochemical assays and

bioassays of muscle are needed to assess the presence or

absence of prions from muscle in experimental and natural

TSE cases.

Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi

Institute of Neuropathology

University Hospital of Zurich

Zurich, Switzerland

References

1 Glatzel M, Abela E, et al: Extraneural pathologic prion

protein in sporadic Creutzfeldt-Jakob disease. N Engl J

Med 349(19):1812–1820, 2003

2 Kovacs GG, Lindeck-Pozza E, et al: Creutzfeldt-Jakob

disease and inclusion body myositis: abundant diseaseassociated

prion protein in muscle. Ann Neurol 55(1):

121–125, 2004

3 Wadsworth JDF, Joiner S, et al: Tissue distribution of protease

resistant prion protein in variant CJD using a highly

sensitive immuno-blotting assay. Lancet 358:171–180,

2001

=========================

THE findings from the cow in Japan with tissue infectivity in the
peripheral nerve tissue, suprarenal gland,
First time from non-Specified Risk Material ;


Japan Consumer Press online
Nippon shouhisha shinbun
http://www.jc-press.com/eg.htm
http://www.jc-press.com/En/Latest%20News/200411/20041109BSE%20death%20cow%27s%20anomalous%20prion.htm
Last modified, 11/09/2004 13:42:49
BSE death cow's anomalous prion detected from peripheral nerve tissue,
suprarenal gland
First time from non-Specified Risk Material, or SRM
By JCPRESS
National Institute of Animal Health Animal announced on November 1 that
it had detected the anomalous prion protein that was the etiologic agent
of the mad cow disease, or BSE, or bovine spongiform encephaalopathy,
from the peripheral nerve tissue and the suprarenal gland of the cow of
the age in the mad cow disease for the dying infection 94 months on
March 9 this year.
Japan is obligating the removal of the Specified Risk Material, or SRM
such as the head, the spinal cord, the vertebral columns, and the small
intestines that accumulate the anomalous prion protein easily as a BSE
(bovine spongiform encephaalopathy) measures.
Because the mad cow disease etiologic agent was detected from a tissue
different from the Specified Risk Material, or SRM, the review of the
Specified Risk Material, or SRM might be urged on the Japanese Government.
International Symposium of PRION DISEASES for food and drug safety
http://www.knt.co.jp/ec/2004/prion/
national institute of animal health(only in Japanese)
http://niah.naro.affrc.go.jp/index-j.html
The statement of the Ministry of Health, Labour and Welfare
(only in Japanese)
http://www.maff.go.jp/www/press/cont2/20041101press_7.htm
Yomiuri on line (only in Japanese)
http://www.yomiuri.co.jp/science/news/20041102i503.htm
Asahi on line(only in Japanese)
http://www.asahi.com/special/bse/TKY200411010291.html
Mainichi on line(only in Japanese)
http://www.mainichi-msn.co.jp/shakai/jiken/disease/news/20041102ddm041040128000c.html

====================================


EMBO reports AOP Published online: 11 April 2003

Widespread PrPSc
accumulation in muscles of hamsters orally infected with scrapie

Achim
Thomzig, Christine Kratzel, Gudrun Lenz, Dominique Krüger & Michael
Beekes Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, Germany

Received 13 February 2003; Accepted 13 March 2003; Published online 11
April 2003.

Abstract :

Scrapie, bovine spongiform encephalopathy and chronic wasting disease
are orally communicable, transmissible spongiform encephalopathies
(TSEs). As zoonotic transmissions of TSE agents may pose a risk to human
health, the identification of reservoirs for infectivity in animal
tissues and their exclusion from human consumption has become a matter
of great importance for consumer protection. In this study, a variety of
muscles from hamsters that were orally challenged with scrapie was
screened for the presence of a molecular marker for TSE infection, PrPSc
(the pathological isoform of the prion protein PrP). Sensitive western
blotting revealed consistent PrPSc accumulation in skeletal muscles from
forelimb and hindlimb, head, back and shoulder, and in tongue.
Previously, our animal model has provided substantial baseline
information about the peripheral routing of infection in naturally
occurring and orally acquired ruminant TSEs. Therefore, the findings
described here highlight further the necessity to investigate thoroughly
whether muscles of TSE-infected sheep, cattle, elk and deer contain
infectious agents.

http://www.emboreports.org/

some previous data on TSE in muscle;

J69

CVO BSE 1 5

SCRAPIE AGENT IN MUSCLE - PATTISON I A (1990) VETERINARY RECORD, 20
JANUARY 1990, p.68

Background

1 Dr Pattison, a retired but eminent worker on scrapie for many years in
the AFRC, has pointed out that in one of his experimental studies of
scrapie in goats he found scrapie agent in the biceps femoris (rump)
muscle of one animal with clinical disease but not in 2 others with
clinical disease and in none with pre-clinical disease. MAFF have based
their policy on BSE in regard to meat (beef) on the results of studies
of natural scrapie (ie disease occurring under farm conditions) in both
sheep and goats by Hadlow 1979, 80, 81.

Other Infectivity Studies

2. These studies on 52 animals by equally eminent scrapie workers
(Hadlow et al) revealed no evidence whatever of infectivity in skeletal
muscle from these natural cases either in the pre-clinical or even
clinical stages of disease.

It is clear that the pathogenesis of experimental (Pattison) and natural
(Hadlow) scrapie may be different and it was therefore considered wise
to base present policy on knowledge of the natural disease.

3. Pattison exposed his 14 goats to intracerebral inoculation of thrice
passaged scrapie virus (in goats). This may have resulted in strain
selection and/or mutation of the natural agent. In contrast Hadlow's
study involved natural strains (probably multiple) in a flock with a
high incidence of disease in which exposure would almost certainly have
been by the mouth.

4. The fact that Hadlow identified no infectivity in muscle by mouse
inoculation (whereas some other tissues not normally consumed had
detectable infectivifcy) shows that cross contamination of his tissues
did not occur. Pattison's experiments were reported about 20 years
earlier when much less was known about Scrapie. In the intervening
period the knowledge available to Hadlow on the insensitivity of scrapie
agent to heat became available. There is therefore at least the
possibility that Pattison's instruments were not sterilised effectively,
thus possibly giving the false positive result for muscle.

5. Pattison used a more sensitive model for the detection of
infectivifcy, namely goats, whereas Hadlow used mice ie necessitating
crossing the species barrier and possibly reducing the test sensitivity.

90/1.19/9.1

CVO BSE 1 5

6. In regard to the choice of species for agent assay, mice (Hadlow),
these would be guaranteed free of pre-existing Scrapie infection.
Pattison could offer no such guarantee that this was the case in the
animal to which muscle was passaged and disease could have developed
from exposure from a source other than muscle.

7. Pattison did not report that his recipient animals, including the one
inoculated with muscle, were examined by histopathology to confirm the
presence of disease. This is a significant deficit. Clinical diagnosis
alone is not acceptable as adequate evidence for the existence of scrapie.

8. Even in Pattison's studies only in 1 out of 14 goats was infectivity
detected in muscle and that was in a CLINICAL case. In BSE all clinical
cases are notified and do not enter any food chain.

9. The last paragraph of Pattison's letter is illogical. Furthermore,
this is no evidence whatsoever that scrapie or BSE is a danger to man.

W A WATSON 19 January 1990

Private Offices Mr K C Meldrum Mrs E Attridge Mr R Lowson Ms L Austin Mr
R Bradley

90/1.19/9.2

http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf

Prions in skeletal muscle

Patrick J. Bosque*,dagger ,Dagger , Chongsuk Ryou*, Glenn Telling*,§,
David Peretz*,dagger , Giuseppe Legname*,dagger , Stephen J.
DeArmond*,dagger ,¶, and Stanley B. Prusiner*,dagger ,||,**

* Institute for Neurodegenerative Diseases and Departments of dagger
Neurology, ¶ Pathology, and || Biochemistry and Biophysics, University
of California, San Francisco, CA 94143

Contributed by Stanley B. Prusiner, December 28, 2001

Considerable evidence argues that consumption of beef products from
cattle infected with bovine spongiform encephalopathy (BSE) prions
causes new variant Creutzfeldt-Jakob disease. In an effort to prevent
new variant Creutzfeldt-Jakob disease, certain "specified offals,"
including neural and lymphatic tissues, thought to contain high titers
of prions have been excluded from foods destined for human consumption
[Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in The BSE
Inquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here we
report that mouse skeletal muscle can propagate prions and accumulate
substantial titers of these pathogens. We found both high prion titers
and the disease-causing isoform of the prion protein (PrPSc) in the
skeletal muscle of wild-type mice inoculated with either the Me7 or
Rocky Mountain Laboratory strain of murine prions. Particular muscles
accumulated distinct levels of PrPSc, with the highest levels observed
in muscle from the hind limb. To determine whether prions are produced
or merely accumulate intramuscularly, we established transgenic mice
expressing either mouse or Syrian hamster PrP exclusively in muscle.
Inoculating these mice intramuscularly with prions resulted in the
formation of high titers of nascent prions in muscle. In contrast,
inoculating mice in which PrP expression was targeted to hepatocytes
resulted in low prion titers. Our data demonstrate that factors in
addition to the amount of PrP expressed determine the tropism of prions
for certain tissues. That some muscles are intrinsically capable of
accumulating substantial titers of prions is of particular concern.
Because significant dietary exposure to prions might occur through the
consumption of meat, even if it is largely free of neural and lymphatic
tissue, a comprehensive effort to map the distribution of prions in the
muscle of infected livestock is needed. Furthermore, muscle may provide
a readily biopsied tissue from which to diagnose prion disease in
asymptomatic animals and even humans. Dagger Present address: Department
of Medicine, Denver Health Medical Center, Denver, CO 80204.

§ Present address: Department of Microbiology and Immunology, University
of Kentucky, Lexington, KY 40536-0230.

** To whom reprint requests should be addressed. E-mail: vann@cgl.ucsf.edu.

www.pnas.org/cgi/doi/10.1073/pnas.052707499

http://www.pnas.org/cgi/content/abstract/99/6/3812maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1024346978866_6016&stored_search=&FIRSTINDEX=0&fdate=1/1/2002


FULL TEXT;

http://www.pnas.org/cgi/content/full/99/6/3812maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&author1=prusiner&author2=prusiner&titleabstract=prions+meat+tissue+mice&fulltext=prions+meat+tissue+mice&searchid=1050249844061_1953&stored_search=&FIRSTINDEX=0&fdate=1/1/2002

Extraneural Pathologic Prion Protein in Sporadic Creutzfeldtâ¬Jakob Disease


Markus Glatzel, M.D., Eugenio Abela, Manuela Maissen, M.S., and Adriano Aguzzi, M.D., Ph.D.


snip...


Conclusions Using sensitive techniques, we identified extraneural deposition
of PrPSc in spleen and muscle samples from approximately one third of patients
who died with sporadic Creutzfeldtâ¬Jakob disease. Extraneural PrPSc appears
to correlate with a long duration of disease.


http://content.nejm.org/cgi/content/short/349/19/1812?query=TOC

The first case of BSE (or “mad cow disease”) in Japan
raised serious public health concerns
because of the possible transmission of
BSE to human, causing a fatal disease
– vCJD (variant Creutzfeldt-Jakob Disease).

Many Japanese consumers stopped eating beef
because of the concerns.


- The following month (October 2001), per capita beef consumption dropped to 42% of the previous year’s level. (Data from Japanese Government)
Some backgrounds of this consumers’ reaction include the terrifying nature of the disease …
- Even though the possibility of having vCJD is low, we could be infected just by eating.
And we can’t prevent it by heat or other measures.

- We do not know whether we get actually infected until several years later.

-Then one day, brain and central nervous systems could be attacked. And once we are attacked, this disease is incurable and leads to death.

… and generally High Expectations of Japanese consumers for food safety.
- While the annual death toll from foodborne diseases is 5,000 in US (estimate),
it is only 18 in Japan (2002) ! (Data from CDC, MHLW )

After the first BSE case in the country,
Japan introduced a comprehensive beef safety system.


BSE Preventive Measures Since October 2001

(*) SRM (specific risk materials) include, among others, brain, spinal cord and eyeballs, as well as the distal part of the ileum, of every cattle regardless of the age.
With the 100% cattle testing under this new system,
Japan has found another 10 BSE cases
(as of April 2004).

BSE Cases in Japan


Date of Confirmation
Age
Condition

1
September 10, 2001
65 months
Anastasia (non-ambulatory)

2
November 21, 2001
67 months
No Clinical Signs

3
December 2, 2001
68 months
No Clinical Signs

4
May 13, 2002
73 months
Muscular split of forelimb (non-ambulatory)

5
August 23, 2002
80 months
Hip joint dislocation (non-ambulatory)

6
January 20, 2003
83 months
Dystaxia (non-ambulatory)

7
January 23, 2003
81 months
No Clinical Signs

8
October 7, 2003
23 months
No Clinical Signs

9
November 4, 2003
21 months
No Clinical Signs

10
February 22, 2004
95 months
Hip joint dislocation (non-ambulatory)

*11
March 9, 2004
94 months
Hip joint dislocation (non-ambulatory)

* This case was found by all fallen stock testing on the farm, while other cases were found by all cattle testing at the slaughterhouses
Some Findings from Japan’s Cases
- Many of the BSE cases were with old cows, but there were 2 cases with much younger cattle – 21 and 23 months of age ( one of them was atypical BSE).

- None of the cows showed any clinical signs of BSE. The cattle in 5 cases were not even non-ambulatory.

At the same time, Japan introduced a new scheme that requires the government to base its food safety policy on science and to enhance risk communication.
Basic Principles of Japan’s Food Safety Policy, as stipulated in Food Safety Basic Law : May 23, 2003
- “The Protection of the Health of the People shall be a top priority.”

- “The Necessary Policy Measures shall be taken at each stage of the Food Supply Process.”

- “These Policy Measures shall be taken on the basis of Scientific Knowledge and in consideration of International Trends and the People’s Opinions.”

Food Safety Agencies in Japanese Government (Since July 2003)


While pursuing food safety and ensuring consumer’s confidence, Japan also cooperates with other countries to acquire more scientific knowledge of BSE, …
BSE was found only about 20 years ago, and there is still much we do not know about this disease. Accordingly, the OIE code is not solid and is reviewed for revision year by year.
… to prevent and ultimately eliminate BSE, and to make early resumption of beef trade possible.

Japan appreciates the ongoing efforts of the US government to improve its BSE measures, although these measures are not regarded as being equivalent to those in Japan.
Japan also appreciates some private sector efforts trying to meet the customers’request, although the support from the US government would be still necessary for these initiatives.
Japan hopes that the current US-Japan consultation on the BSE issue, including the discussions in the working group, will lead to the conclusions satisfactory to all the parties concerned.


Embassy of Japan
2520 Massachusetts Avenue NW, Washington D.C. 20008
Tel: 202.238.6700 fax: 202.328.2187

©2003 Embassy of Japan. All Rights Reserved.


http://www.us.emb-japan.go.jp/english/html/fafacts/bse/bse.htm


IF one looks at Japan BSE # 8 and # 9 BSE case ;

8. 6/10/2003 Holstein Steer 13/1/2001 23 mths
NO CLINICAL SIGNS WB+, IHC-, HP-


9. 4/11/1003 Holstein Steer 13/1/2002 21 mths
NO CLINICAL SIGNS WB+, IHC-, HP-


TSS





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