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From: TSS (
Subject: Re: Atypical Case of Bovine Spongiform Encephalopathy in an East-Flemish Cow in Belgium
Date: February 7, 2005 at 2:54 pm PST

In Reply to: Re: Atypical Case of Bovine Spongiform Encephalopathy in an East-Flemish Cow in Belgium posted by Terry S. Singeltary Sr. on February 4, 2005 at 1:11 pm:

-------- Original Message --------
Subject: Re: Atypical Case of Bovine Spongiform Encephalopathy in an East-Flemish Cow in Belgium
Date: Mon, 7 Feb 2005 15:52:18 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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

hello jim,

>What the hell is wrong with this

>The Belgian cow's results were:
>SAF -
>HP -
>IHC -
>WB +

NOTHING, this is part of june 2004 usda enhanced bse/tse cover-up.
part of the program was to start NOT confirming with WB,
due to the first confirmed finding. same with the other mad cows
in TEXAS i.e. the stumbling and staggering one they refused
to test and rendered;

IF we look at this Belgium atypical cow (and try to forget about those
damn imported belgium sheep that were never confirmed with mouse
bio assay, as we were told they would be, which could very well have
been BSE, i mean there was a declaration of emergency declared for
an ATYPICAL TSE in them), and then look at the #8 and #9 cow of Japan;

8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
No clinical signs WB+, IHC-, HP-

9. 4/11/2003 Holstein Steer 13/1/2002
21 mths No clinical signs WB+, IHC-, HP-

THIS explains very well why the USDA decided to NOT use WB anymore.
damn thing finds things when people don't want it found. simple as that.;f=12;t=000385

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


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
national institute of animal health(only in Japanese)
The statement of the Ministry of Health, Labour and Welfare
(only in Japanese)
Yomiuri on line (only in Japanese)
Asahi on line(only in Japanese)
Mainichi on line(only in Japanese)


Bovine spongiform encephalopathy (BSE) in Japan

Takashi Yokoyama, Kumiko M. Kimura, Morikazu Shinagawa
Prion Disease Research Center, National Institute of Animal Health, Japan

Bovine spongiform encephalopathy (BSE) has become an important problem
not only for animal industry, but
also for public health. In Japan, BSE was first recognized in September
2001 by fallen stock surveillance.
Since October 2001, BSE examination for all cattle slaughtered at
abattoirs has started. In April 2004, all dead
cattle examination (over 24 months) has been conducted at livestock
hygiene service center. Samples positive
in enzyme linked immunosorbent assay (ELISA) are further subjected to
western blot (WB) and
immunohistochemistry (IHC). Thirteen BSE cases have been reported by
September 2004. Twelve cases
were classified as typical BSE, and the remained one was an atypical
BSE. Variant forms of BSE with atypical
histopathological and/or biochemical phenotype were reported in Italy
and France. Further study is required
for BSE prion characteristics.
To characterize BSE prion properties, brain homogenates of Japanese BSE
cases were intracerebrally
inoculated into wild-type mice. The first case (BSE/Chiba) was
successfully transmitted to rodents. The mean
incubation periods (409.0 days) in this experiment was preferably longer
than that of previously reported.
PrPSc distribution, prion titer, mice susceptibility and/or storage
condition of sample might be influenced the
result. Recently, we introduced transgenic mice that overexpress a
bovine PrP gene to overcome the species
barrier problem. These mice are expected to accelerate the transmission
experiment of BSE prion.
Transmission of atypical BSE case is undergoing by using these
transgenic mice.

Research Foundation

Tissue distribution of protease resistant prion protein in variant
Creutzfeldt-Jakob disease using a highly sensitive immunoblotting assay.

Wadsworth JD, Joiner S, Hill AF, Campbell TA, Desbruslais M, Luthert
PJ, Collinge J.

MRC Prion Unit and Department of Neurogenetics, Imperial College
School of Medicine at St Mary's, Norfolk Place, W2 1PG, London, UK.

BACKGROUND: Variant Creutzfeldt-Jakob disease (vCJD) has a
pathogenesis distinct from other forms of human prion disease:
disease-related prion protein (PrP(Sc)) is readily detectable in
lymphoreticular tissues. Quantitation of risk of secondary
transmission, and targeting of risk reduction strategies, is limited
by lack of knowledge about relative prion titres in these and other
peripheral tissues, the unknown prevalence of preclinical vCJD, and
a transmission barrier which limits the sensitivity of bioassay. We
aimed to improve immunoblotting methods for high sensitivity
detection of PrP(Sc) to investigate the distribution of PrP(Sc) in a
range of vCJD tissues. METHODS: We obtained tissues at necropsy from
four patients with neuropathologically confirmed vCJD and from
individuals without neurological disease. Tissues were analysed by
sodium phosphotungstic acid precipitation of PrP(Sc) and western
blotting using high sensitivity enhanced chemiluminescence.
FINDINGS: We could reliably detect PrP(Sc) in the equivalent of 50
nL 10% vCJD brain homogenate, with a maximum limit of detection
equivalent to 5 nl. PrP(Sc) could be detected in tissue homogenates
when present at concentrations 10(4)-10(5) fold lower than those
reported in brain. Tonsil, spleen, and lymph node were uniformly
positive for PrP(Sc) at concentrations in the range of 0.1-15% of
those found in brain: the highest concentrations were consistently
seen in tonsil. PrP(Sc) was readily detected in the retina and
proximal optic nerve of vCJD eye at levels of 2.5 and 25%,
respectively of those found in brain. Other peripheral tissues
studied were negative for PrP(Sc) with the exception of low
concentrations in rectum, adrenal gland, and thymus from a single
patient with vCJD. vCJD appendix and blood (Buffy coat fraction)
were negative for PrP(Sc) at this level of assay sensitivity.
INTERPRETATION: We have developed a highly sensitive immunoblot
method for detection of PrP(Sc) in vCJD tissues that can be used to
provide an upper limit on PrP(Sc) concentrations in peripheral
tissues, including blood, to inform risk assessment models. Rectal
and other gastrointestinal tissues should be further investigated to
assess risk of iatrogenic transmission via biopsy instruments.
Ophthalmic surgical instruments used in procedures involving optic
nerve and the posterior segment of the eye, in particular the
retina, might represent a potential risk for iatrogenic transmission
of vCJD. Tonsil is the tissue of choice for diagnostic biopsy and
for population screening of surgical tissues to assess prevalence of
preclinical vCJD infection within the UK and other populations.

PMID: 11476832 [PubMed - indexed for MEDLINE]

Creutzfeldt-Jakob disease and inclusion body myositis: Abundant
disease-associated prion protein in muscle
Gabor G. Kovacs, MD PhD 1 2, Elisabeth Lindeck-Pozza, MD 1, Leila
Chimelli, MD, PhD 3, Abelardo Q. C. Araújo, MD, PhD 4, Alberto A.
Gabbai, MD, PhD 5, Thomas Ströbel, PhD 1, Markus Glatzel, MD 6, Adriano
Aguzzi, MD, PhD 6, Herbert Budka, MD 1 *
1Institute of Neurology, University of Vienna, and Austrian Reference
Centre for Human Prion Diseases, Vienna, Austria
2National Institute of Psychiatry and Neurology, Budapest, Hungary
3Department of Pathology, School of Medicine, Federal University of Rio
de Janeiro
4Department of Neurology, School of Medicine, Federal University of Rio
de Janeiro
5Department of Neurology, School of Medicine, Federal University of Sao
Paulo, Brazil
6Institute of Neuropathology, University Hospital of Zürich, Zürich,
email: Herbert Budka (

*Correspondence to Herbert Budka, Institute of Neurology, AKH 4J,
Wühringer Gürtel 18-20, POB 48, A-1097 Vienna, Austria

Funded by:
European Union (EU) Project; Grant Number: TSELAB QLK2-CT-2002-81523
EU Concerted Action PRIONET; Grant Number: QLK2-2000-CT-00837


Pathologicalprion protein (PrPSc) is the hallmark of prion diseases
affecting primarily the central nervous system. Using
immunohistochemistry, paraffin-embedded tissue blot, and Western blot,
we demonstrated abundant PrPSc in the muscle of a patient with sporadic
Creutzfeldt-Jakob disease and inclusion body myositis. Extraneural
PrPC-PrPSc conversion in Creutzfeldt-Jakob disease appears to become
prominent when PrPC is abundantly available as substrate, as in
inclusion body myositis muscle.

Received: 16 June 2003; Revised: 11 September 2003; Accepted: 11
September 2003
Digital Object Identifier (DOI)

10.1002/ana.10813 About DOI

NINDS Inclusion Body Myositis Information Page

AS Professor Aguzzi kindly put it most recently ;

Vet Pathol 42:107 108 (2005)
Letters to the 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
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,


THE SAD part of all this, is the USDA et al know's all this.
THEY are not this stupid. THUS the June 2004 'ENHANCED'
USA BSE/TSE cover-up continues, more people exposed, more
people die, but it's all sporadic/spontaneous without any sort of
route and source here in the USA and there precious commodity
survives to breath another day. THEY are only fooling themselves
with this so called 'enhanced' surveillence. AT the rate they have been
going, they could test all cows and have them come up incl/neg and
the world would not believe them. open up the borders and fire
up the pits, everything is o.k. in North America, cause GW and
his new Bovine Spongiform Encephalopathy; Minimal Risk Regions
said so, which has absolutely nothing to do what so ever with SCIENCE
and everything to do with just what the title insinuates, importing TSEs;

Bovine Spongiform Encephalopathy; Minimal Risk Regions and Importation
of Commodities; Availability of an Environmental Assessment With
Corrections and Extension of Comment Period

HOW in the hell in the same year can you have a report or reports

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk
(GBR) of the United States of America (USA)
Publication date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)

* 167 kB Report

* 105 kB Summary

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working
Group on the Assessment of the Geographical Bovine Spongiform
Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United
States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in
USA. This scientific report addresses the GBR of USA as assessed in 2004
based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached
domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early nineties. It is
possible that imported meat and bone meal (MBM) into the USA reached
domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle
imports from BSE risk countries were slaughtered or died and were
processed (partly) into feed, together with some imports of MBM. This
risk continued to exist, and grew significantly in the mid 90s when
domestic cattle, infected by imported MBM, reached processing. Given the
low stability of the system, the risk increased over the years with
continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is
likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as there are no
significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently




BUT yet the President of the UNITED STATES refuses to adhere to it.
IN FACT, he rules that North America is now a Minimal Risk Region
for his Commodities market, ignoring every bit of scientific data that
shows otherwise. WHAT GW has done is worse than what Britain
did early on when they were exporting there poison around the Globe.
THEY played stupid, GW has the science now, but ignores it and the
world, and then changes the rules. YOU could call this criminal homicide
with INTENT. I don't think the world will buy his BSe...


TO Karin, or anyone on the list that might have ;

Chris Bostock has said in private correspondence on 17 July 1997 that:

"Scientists at IAH's NPU have completed the neuropathological
examination of post mortem material taken from the Norwegian dog
with a suspected TSE with which they were supplied, but they were
unable to confirm positively a diagnosis of a TSE. There is no
further work ongoing - eg mouse bioassay."

Would there be a neuropathological examination of post
mortem material taken from the Norwegian dog that i could
possible have a copy of (text or PDF) OR of Gov literature?

IF anyone has further info on this, please pass through list
or to my email.....thanks...tss

thank you,
kind regards,

Jim Woodward wrote:

>##################### Bovine Spongiform Encephalopathy #####################
>So let me get this straight. EC regs call for ELISA+
>samples to be confirmed by SAF, histopathology, IHC, and WB
>(all four). The Belgian cow's results were:
>SAF -
>HP -
>IHC -
>WB +
>Conclusion: atypical BSE
>In the US, cattle, deer, and elk with positive ELISA tests
>are confirmed by IHC only. What the hell is wrong with this
>picture? How many US ruminants with atypical BSE/CWD are
>slipping through the cracks?
>>-----Original Message-----
>>From: Bovine Spongiform Encephalopathy
>>Behalf Of Terry S.
>>Singeltary Sr.
>>Sent: Friday, February 04, 2005 10:00 AM
>>Subject: [BSE-L] Atypical Case of Bovine
>>Spongiform Encephalopathy in an
>>East-Flemish Cow in Belgium
>>##################### Bovine Spongiform
>>Encephalopathy #####################
>> Atypical Case of Bovine Spongiform
>>Encephalopathy in an East-Flemish
>> Cow in Belgium
>>H. De Bosschere, DVM, PhD
>>S. Roels, DVM, PhD
>>E. Vanopdenbosch, DVM, Lic
>>Veterinary and Agrochemical Research Centre (CODA/CERVA)
>>National Reference Laboratorium for Veterinary TSEs
>>Groeselenberg 99, B-1180
>>Ukkel (Brussels), Belgium
>>KEY WORDS: Bovine spongiform encephalopathy, BSE,
>>Western blot, atypical
>>For many years, researchers believed that only
>>one bovine spongiform
>>encephalopathy (BSE) strain existed, in contrast
>>to the many different
>>scrapie strains found. However, only very
>>recently reports emerged about
>>unconventional BSE strains seen in Italy, France,
>>and Japan. The present
>>case describes an atypical strain of BSE in
>>Belgium in a 64-month-old
>>East-Flemish cow with an electrophoretic profile
>>and other features
>>similar to those described in Japan.



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