SEARCH VEGSOURCE:

 

 

Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.
  




From: TSS ()
Subject: re--Give USDA control of beef industry ?
Date: April 11, 2005 at 2:42 pm PST

-------- Original Message --------
Subject: re--Give USDA control of beef industry ?
Date: Mon, 11 Apr 2005 16:44:01 -0500
From: "Terry S. Singeltary Sr."
To: elsberry@greeleytrib.com, juliep@windsortribune.com, eruis@greeleytribune.com, nemec@greeleytrib.com, towen@greeleytribune.com, Bovine Spongiform Encephalopathy
CC: john.simons@swiftbrands.com


Give USDA control of beef industry

Guest Commentary
April 10, 2005

John Simons is the president and chief executive officer of Swift & Co.
in Greeley

snip...

> It doesn't involve processing only younger cattle that are
> scientifically proven to be BSE-free

>What science has made very clear in the
>> past two years is: There
>> is no scientific evidence that cattle under 30
>> months old show evidence of
>> mad cow disease.
>

http://www.greeleytrib.com/article/2005104100049

Greetings,

I would kindly like to correct John Simons president and chief executive
officer of Swift & Co. in Greeley. Evidently he is not familiar with
the real science of human and animal TSE (BSE). THE statements
above made by John Simons are simply NOT TRUE!

IF you are going to be the PRESIDENT of a major food retailer that sells
food for human consumption, and to be this oblivious to TSE/BSE science,
this is a frightening thought. BUT, even more frightening, having someone
like me trying to educate these folks ;-).....tss

> younger cattle that are scientifically proven to be BSE-free

>There
>> is no scientific evidence that cattle under 30
>> months old show evidence of
>> mad cow disease
>

FACTS ;

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA

snip...

the youngest age of BSE case to date is 20 months old; As at: 31 May
2003 Year of onset Age youngest case (mnths) Age 2nd youngest case
(mnths) Age 2nd oldest case (yrs.mnths) Age oldest case (yrs.mnths) 1986
30 33 5.03 5.07 1987 30 31 9.09 10.00 1988 24 27 10.02 11.01(2) 1989 21
24(4) 12.00(2) 15.04 1990 24(2) 26 13.03 14.00 1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02 1993 29 30(3) 14.10 18.10 1994 30(2) 31(2) 14.05
16.07 1995 24 32 14.09 15.05 1996 29 30 15.07 17.02 1997 37(7) 38(3)
14.09 15.01 1998 34 36 14.07 15.05 1999 39(2) 41 13.07 13.10 2000 40 42
17.08 19.09 2001 48(2) 56 14.10 14.11 2002 51 52 15.08 15.09(2) 2003 50
62 11.11 14.11

http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html

NEW URL ;

http://www.defra.gov.uk/animalh/bse/statistics/bse/yng-old.html

http://www.defra.gov.uk/animalh/bse/index.html

The implications of the Swiss result for Britain, which has had the most
BSE, are complex. Only cattle aged 30 months or younger are eaten in
Britain, on the assumption, based on feeding trials, that cattle of that
age, even if they were infected as calves, have not yet accumulated
enough prions to be infectious. But the youngest cow to develop BSE on
record in Britain was 20 months old, showing some are fast incubators.
Models predict that 200-300 cattle under 30 months per year are infected
with BSE and enter the food chain currently in Britain. Of these 3-5
could be fast incubators and carrying detectable quantities of prion.

http://www.sare.org/htdocs/hypermail/html-home/28-html/0359.html


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


Docket

>Response: We understand the interest expressed by some commenters
>in testing certain cattle for slaughter. However, no live animal tests
>exist for BSE and the currently available postmortem tests, although
>useful for disease surveillance (i.e., in determining the rate of
>disease in the cattle population), are not appropriate as food safety
>indicators. We know that the earliest point at which current testing
>methods can detect a positive case of BSE is 2 to 3 months before the
>animal begins to demonstrate clinical signs. We also know that the
>incubation period for this diseasethe time between initial infection
>and the manifestation of clinical signsis generally very long, on the
>average of about 5 years. Accordingly, we know there is a long period
>during which, using the current methodology, testing an infected animal
>that has not demonstrated clinical signs of the disease would,
>incorrectly, produce negative results. If, however, the infected animal
>is already exhibiting some type of clinical signs that could be
>consistent with BSE, then the test is not likely to produce false
>negative results. .......see link below.....tss


ODD, the 1st mad cow documented in the USA in Washington, the one old
Dave capped, was a healthy walker, was not a CNS cow....TSS

> The cow was not a downer. I killed that cow and I'm telling you it was
> a good walker. A big white cow with no BSE symptoms at all. I killed
> that cow along with the down cows because I was in a hurry and did not
> feel like separating her out. ...
>
> Dave Louthan April 1, 2004


Agriculture Department, Animal and Plant Health Inspection Service,
, Bovine Spongiform Encephalopathy; Minimal-Risk Regions and
Importation of Commodities


General Information


Department: DEPARTMENT OF AGRICULTURE

Agency: Treasury Department


Published: 2005-01-04

SUMMARY: We are amending the regulations regarding the importation of
animals and animal products to establish a category of regions that
present a minimal risk of introducing bovine spongiform encephalopathy
(BSE) into the United States via live ruminants and ruminant products
and byproducts, and we are adding Canada to this category. We are also
establishing conditions for the importation of certain live ruminants
and ruminant products and byproducts from such regions. These actions
will continue to protect against the introduction of BSE into the United
States while removing unnecessary prohibitions on the importation of
certain commodities from minimalrisk regions for BSE, currently only
Canada.

CFR Citation

9 CFR Parts 93, 94, 95, and 96

Docket ID

[Docket No. 03-080-3]

DOCUMENT AGENCY 2

Animal and Plant Health Inspection Service, USDA.

FOR FURTHER INFORMATION CONTACT

For information concerning ruminant
products, contact Dr. Karen JamesPreston, Director, Technical Trade
Services, National Center for Import and Export, VS, APHIS, 4700 River
Road Unit 38, Riverdale, MD 207371231; (301) 7344356.
For information concerning live ruminants, contact Lee Ann Thomas,
Director, Technical Trade Services, Animals, Organisms and Vectors, and
Select Agents, National Center for Import and Export, VS, APHIS, 4700
River Road Unit 38, Riverdale, MD 207371231; (301) 7344356.
For other information concerning this rule, contact Dr. Gary
Colgrove, Director, Sanitary Trade Issues Team, National Center for
Import and Export, VS, APHIS, 4700 River Road Unit 38, Riverdale, MD
207371231; (301) 7344356.

snip...


>Issue: One commenter asked whether APHIS consulted with or sought
>the opinion of leading international scientific experts with regard to
>the proposed mitigation measures and, if so, whether those experts
>considered those risk mitigation measures adequate.
> Response: The risk mitigation measures in this rulemaking are
>equivalent to those measures considered appropriate by the OIE, which
>are guidelines developed by teams of international veterinary and other
>scientific experts. Additionally, following the diagnosis of BSE in
>Canada in May 2003, a review team of international experts evaluated
>the situation and reported favorably on the measures being taken in
>that country with regard to BSE. Those measures are equivalent to those

>set forth in this rulemaking.

IN OTHER WORDS, hell know, GW says, 'bring em on', science means nothing.
PLUS, most every country that went by those same OIE BSE guidelines came
down with BSE. GWs BSE MRR POLICY HAS NOTHING TO DO WITH SCIENCE AND
EVERYTHING TO DO WITH COMMODITIES AND FUTURES $$$ TSS

>Issue: APHIS proposed to limit live cattle imported from a BSE
>minimalrisk region to those that would be less than 30 months of age
>at slaughter. A number of commenters expressed concerns regarding that
>maximum age. The commenters stated that, because there have been
>multiple detections of BSE in cattle less than 30 months of age in
>Europe and Japan, APHIS should decrease the maximum age for imports.
>Recommended maximums ranged from 18 to 28 months of age. Several
>commenters requested that APHIS more comprehensively state and validate
>the scientific basis for determining that cattle in the 20 to 30 month
>age range do not present a risk of BSE. Another commenter cited
>evidence from Britain that the commenter said indicates some cattle may
>be fast incubators of the disease and, therefore, have the potential to
>introduce detectable levels of BSE into the food chain. One commenter
>expressed concern that, because bulls are routinely slaughtered at 19
>to 22 months old, they may be too young to test positive for the
>disease, even though those animals may be infected with BSE. One
>commenter stated that with prion diseases, the incubation time tends to
>become shorter the longer a specific prion has been circulating within
>a species.
> Response: As discussed in our proposal, pathogenesis studieswhere
>tissues obtained from orally infected calves were assayed for
>infectivityhave illustrated that levels of infectious BSE agent in
>certain tissues vary with the age of an animal. Infectivity was not
>detected in most tissues in cattle until at least 32 months post
>exposure. The exception to this is the distal ileum (a part of the
>intestines), where infectivity was confirmed in the experimentally
>infected cattle as early as 6 months postexposure, and the tonsils,
>where infectivity was confirmed at 10 months postexposure.
> Research demonstrates that the incubation period for BSE in cattle
>is linked to the infectious dose receivedi.e., the larger the
>infectious dose received, the shorter the incubation period. While some
>cases of BSE have been found in cattle less than 30 months of age,
>these are relatively few and have occurred in countries with
>significant levels of circulating infectivity (i.e., where infected
>ruminants are used for feed for other ruminants, which in turn become
>infected).
> In our proposal, we set out a list of standards we will use to
>evaluate the BSE risk from a region and determine whether it is
>appropriate to classify that region as a region of minimalrisk for
>BSE. We stated that we would use these standards as a combined and
>integrated evaluation tool, basing a BSE minimalrisk classification on
>the overall effectiveness of control mechanisms in place (e.g.,
>surveillance, import controls, and a ban on the feeding of ruminant
>protein to ruminants). Given the low level of circulating infectivity
>in minimalrisk regions, we proposed a 30month age limit for cattle
>and proposed that the intestines be removed from those imported cattle.
>As discussed already, following the detection of a BSEpositive cow in
>Washington State in December 2003, FSIS implemented additional measures
>to protect the human food supply in the United Statesincluding a
>requirement that SRMs be removed from all cattleand prohibited the
>use of SRMs in human food.
> Under these circumstances, we continue to consider 30 months of age
>to be the appropriate age threshold for removal of most SRMs. We are
>evaluating whether cattle over 30 months of age could be safely
>imported into the United States from a BSE minimalrisk region under
>the same conditions as younger cattle, since SRM removal is now
>standard operating procedure for all cattle 30 months of age and older
>that go to slaughter in the United States. However, we are not making a
>change with regard to live cattle over 30 months of age in this final
>rule, because, as stated in our March 8, 2004, notice, we are currently
>evaluating the appropriate approach regarding live cattle other than
>those specified in our proposal and intend to address that issue in a
>supplemental rulemaking proposal in the Federal Register.


http://thefederalregister.com/d.p/2005-01-04-04-28593

EVEN THE CANADIAN CATTLE INDUSTRY ITSELF SAID THERE
OWN GOVERNMENT FAILED THEM TERRIBLY, and have sued ;


> Federal Government's Gross Negligence Was The Cause Of Canada's
> Mad Cow Outbreak
>
> TORONTO, April 11 /CNW/ - The BSE crisis, the closing of the U.S. border
> to Canadian cattle and beef, and the loss of billions of dollars by the
> Canadian cattle industry, was the result of gross incompetence and
> negligence
> on the part of the Canadian Government, says a group of lawyers
> representing
> cattle producers from across Canada who have launched what could
> become the
> largest class action in Canadian legal history.
> The cattle producers, represented by Clint Docken, Q.C. of Calgary,
> Reynold Robertson of Saskatoon, Gilles Gareau of Montreal and Cameron
> Pallett
> of Toronto, claim that Agriculture Canada failed to consider safety
> issues
> when compiling a list of permitted animal feed ingredients in
> 1988-1990 and
> lost track of 80 cattle that had been imported from the UK and Ireland,
> allowing them to be ground up into cattle feed. As a consequence, BSE
> infected
> a number of Canadian cattle, which in turn led to devastating
> consequences for
> the Canadian cattle industry.

> "By the
> government's own admission one or more of those 80 cattle are the most
> likely
> source of BSE in Canada," said Mr. Pallett. "Where was the monitoring?
> Where
> was the government's concern for the health of Canadians? Why did the
> Government fail so badly in the exercise of its regulatory
> responsibilities?"


http://www.newswire.ca/en/releases/archive/April2005/11/c3704.html


WHY? because the cattle producers in canada fought every attempt at
tracking,
testing, monitoring, and regulation every step of the way.

THE height of hypocracy for cattlemen to be suing the govt for doing
what they asked for.


>
> An Alberta livestock feed mill - taken to court at the height of the
> mad cow probe after firing a worker for wrongly mixing feed
> ingredients - has been ordered to compensate the man for wrongful
> dismissal. A Court of Queen's Bench justice said the company had
> tolerated such conduct by the man in the past and the incident he was
> fired over was not unusual.

http://www.canoe.ca/NewsStand/EdmontonSun/News/2005/04/10/990433-sun.html


EFSA Scientific Report on the Assessment of the Geographical BSE-Risk
(GBR) of Canada
Last updated: 08 September 2004

Adopted July 2004 (Question Nį EFSA-Q-2003-083)

* 165 kB Report


* 108 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 to provide an up-to-date
scientific report on the GBR in Canada, i.e. the likelihood of the
presence of one or more cattle being infected with BSE, pre-clinically
as well as clinically, in Canada. This scientific report addresses the
GBR of Canada as assessed in 2004 based on data covering the period
1980-2003.

The BSE agent was probably imported into the country middle of the
eighties and could have reached domestic cattle in the early nineties.
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 90s. It is possible that imported meat and bone meal (MBM) into
Canada reached domestic cattle and led to an internal challenge in the
early 90s.

A certain risk that BSE-infected cattle entered processing in Canada,
and were at least partly rendered for feed, occurred in the early 1990s
when cattle imported from UK in the mid 80s could have been slaughtered.
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 Canada is III, i.e. it is
confirmed at a lower level that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as the system
remains unstable, it is expected that the GBR continues to grow, even if
no additional external challenges occur.


Publication date: 20 August 2004


http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/564_en.html


COMMENTS FROM TOP TSE/PRION SCIENTIST ;


Q&A Dr. Jean-Philippe Deslys


1. What is the standard regime for testing of suspect animals in the EU?

The regime is an initial screening by a high-output test, the Bio-Rad
test. If a result raises suspicion, a confirmatory test is conducted
with the Western blot test.
2. How long has this been the case?

It‚¨"s a fairly recent development. Only recently has the Western blot
test become sensitive enough, with the addition of phospohtungstic acid
precipitation step. The Bio-Rad test (which Deslys helped develop) is
extremely sensitive, and the standard Western blot is extremely reliable
with high-signal test results. However, it had to be made more sensitive
for low-signal (samples with low density of malformed prions) samples.
It has been made more sensitive.

Reproducibility is the problem with the IHC test. It is not
standardized; depending on the lab and its protocols, or even on the
technician involved in the test, one can get conflicting results.

3. Is there a way to measure the three tests in sensitivity, accuracy
and objectivity?


Historically, yes. The IHC was the gold standard at one point, but we
have shifted to the Western blot. It requires less work, it is more
sensitive and its results are reproducible. IHC relies on localization.
If you have a weak signal case, you may get lucky and test a spot with a
high concentration of prions. But the opposite it true too; you can miss
an infection by testing a sample with low concentrations. Western blot
is much better for low signal situations.

4. The USDA in 2003 used the Western blot to confirm the BSE case in
Washington state, and it sent samples to the U.K. for independent
testing. In the case this November, which it announced was negative, it
instead used the IHC test and did not send samples to the U.K. Is this
good science?

It‚¨"s not logical. If you have two consecutive questionable screenings,
you do another test. I can only advise, it‚¨"s management‚¨"s duty at
USDA to make the decisions. But when you have a discrepancy between the
rapid test and the IHC, it is only logical to confirm it with another test.


5. We are hearing now about a new strain of BSE, atypical BSE or aBSE.
Or BaSE. We have heard that IHC, the so-called gold standard, cannot
detect the variant. Is this true?

Yes. There have been a few cases, one in Italy, one in Belgium, one here
in France. It seems to only affect very old animals. The distribution in
the brain is very different than we see with BSE, it looks very
different. The IHC test will come back negative.

This his a very recent phenomenon. I have no opinion on its virulence.
We do not know where it comes from. It could be a version of sporadic
infection. Western blot caught them, but we would not even know it
existed if we weren‚¨"t running systematic testing in the EU.
BSE was around for a long time before we caught it and by then, it was
everywhere. It had become highly infectious. It probably amplified due
to low-temperature rendering. The disease was recycled through the food
chain, and was given time to amplify. By the time it was identified,
even good cooking couldn‚¨"t eliminate it.
I can‚¨"t stress enough that systematic testing is necessary.
Withdrawing all positives from the food chain is the best way to break
the cycle.

What can happen with testing of only cattle that are clearly at risk is
that several can remain undetected. Canada has tested about 30,000 head
of cattle and has three positives. That would indicate that there are
probably undiscovered cases. And what happens then is that the disease
is allowed to amplify. You have to maintain testing.

When people choose to protect their economic interests over public
health, it can have a boomerang effect. It happened all through Europe.
They always deny; it‚¨"s not OUR problem, it is our neighbor‚¨"s
problem. And then a single case is discovered and the public reacts. The
economic results are devastating. It would be better to just assume BSE
is present and use systematic testing as protection. That way, the
public is reassured that it is not entering the food supply.

By systematic testing, I mean doing as we do in the EU, which is to test
every animal over 30 months of age when it is slaughtered. In Europe,
three times as many cases of BSE have been caught by systematic testing
as by clinical testing (of clearly sick animals). In 2004, eight
clinical cases were discovered, 29 were discovered at rendering plants,
and 17 at slaughter. We should be using these tests as a weapon to
protect the public and to give them assurance that the food supply is
being protected....
snip ...END

Dr. Jean-Philippe Deslys, Head, Prions Research Group, Atomic Energy
Commission, France


Q&A Prof. Adriano Aguzzi

Dear Mr. Singeltary

I sympathize with your wish to have the most sensitive assay implemented.
However, the situation is not as simple as one might think. In the case of
homogeneously distributed agent, biochemical detection of PrPSc is indeed
likely to be more sensitive than immunohistochemistry. In the case of
variegated, punctate distribution of the agent, morphological methods may
indeed be an asset.
There are also issues of feasibility. In my laboratory, we routinely run
phosphotungstic acid precipitation followed by Western blotting. However,
this is an extraordinarily cumbersome procedure. The sensitivity is
increased vastly, but the amount of work needed is also amazing. There is
no way I could see our own procedure implemented for mass screening of
millions of cows - unless one would draft a veritable army of laboratory
technicians.
For all these reasons, while I see all your points, I feel unable to
offer a
strong public opinion in favor or against any specific methods. The final
decision needs to take into account a variety of complex factors, and that
is why I believe that it is best left to a panel of experts rather than
to a
public discussion.
Best regards Adriano Aguzzi
____________________________
Prof. Adriano Aguzzi (MD PhD hc FRCP FRCPath)
Institute of Neuropathology, University Hospital of Z√ľrich
Schmelzbergstrasse 12, CH-8091 Z√ľrich, Switzerland
Tel. ++41-1-255 2107
Tel. (direct line): 2869
Fax: ++41-1-255 4402, cellular: +41-79-320 1516
http://www.unizh.ch/pathol/neuropathologie/

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

PNAS | March 1, 2005 | vol. 102 | no. 9 | 3501-3506
NEUROSCIENCE
Diagnosis of human prion disease
Jiri G. Safar *, , Michael D. Geschwind , Camille Deering *, Svetlana
Didorenko *, Mamta Sattavat √¬∂, Henry Sanchez √¬∂, Ana Serban *,
Martin Vey ||, Henry Baron **, Kurt Giles *, , Bruce L. Miller , Stephen
J. DeArmond *, √¬∂ and Stanley B. Prusiner *

*Institute for Neurodegenerative Diseases, Memory and Aging Center, and
Departments of Neurology, √¬∂Pathology, and Biochemistry and
Biophysics, University of California, San Francisco, CA 94143; ||ZLB
Behring, 35041 Marburg, Germany; and **ZLB Behring, 75601 Paris, France

Contributed by Stanley B. Prusiner, December 22, 2004


AB

Abstract
With the discovery of the prion protein (PrP), immunodiagnostic
procedures were applied to diagnose Creutzfeldt√Ę‚¨‚¨SJakob disease
(CJD). Before development of the conformation-dependent immunoassay
(CDI), all immunoassays for the disease-causing PrP isoform (PrPSc) used
limited proteolysis to digest the precursor cellular PrP (PrPC). Because
the CDI is the only immunoassay that measures both the
protease-resistant and protease-sensitive forms of PrPSc, we used the
CDI to diagnose human prion disease. The CDI gave a positive signal for
PrPSc in all 10√Ę‚¨‚¨S24 brain regions (100%) examined from 28 CJD
patients. A subset of 18 brain regions from 8 patients with sporadic CJD
(sCJD) was examined by histology, immunohistochemistry (IHC), and the
CDI. Three of the 18 regions (17%) were consistently positive by
histology and 4 of 18 (22%) by IHC for the 8 sCJD patients. In contrast,
the CDI was positive in all 18 regions (100%) for all 8 sCJD patients.
In both gray and white matter, 90% of the total PrPSc was
protease-sensitive and, thus, would have been degraded by procedures
using proteases to eliminate PrPC. Our findings argue that the CDI
should be used to establish or rule out the diagnosis of prion disease
when a small number of samples is available as is the case with brain
biopsy. Moreover, IHC should not be used as the standard against which
all other immunodiagnostic techniques are compared because an
immunoassay, such as the CDI, is substantially more sensitive...

snip...

Discussion

snip...


The studies reported here are likely to change profoundly the approach
to the diagnosis of prion disease in both humans and livestock (31 33).
The superior performance of the CDI in diagnosing prion disease compared
to routine neuropathologic examination and IHC demands that the CDI be
used in future diagnostic evaluations of prion disease. Prion disease
can no longer be ruled out by routine histology or IHC. Moreover, the
use of IHC to confirm cases of bovine spongiform encephalopathy after
detection of bovine PrPSc by the CDI (10) seems an untenable approach in
the future. Clearly, the CDI for HuPrPSc is as sensitive or more
sensitive than bioassays in Tg(MHu2M) mice (Fig. 1).

Our results suggest that using the CDI to test large numbers of samples
for human prions might alter the epidemiology of prion diseases. At
present, there is limited data on the frequency of subclinical variant
CJD infections in the U.K. population (34). Because appendixes and
tonsils were evaluated only by IHC, many cases might have escaped
detection (Tables 1 and 2). Equally important may be the use of CDI-like
tests to diagnose other neurodegenerative disorders, such as Alzheimer's
disease, Parkinson's disease, and the frontotemporal dementias. Whether
IHC underestimates the incidence of one or more of these common
degenerative diseases is unknown. Moreover, CDI-like tests may help
determine the frequency with which these disorders and the prion
diseases occurs concomitantly in a single patient (35, 36).

http://www.pnas.org/cgi/content/abstract/102/9/3501


107
Vet Pathol 42:107108 (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 (41:7881, 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):18121820, 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):
121125, 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 358:171180,
2001...

TSS





Follow Ups:



Post a Followup

Name:
E-mail: (optional)
Subject:

Comments:

Optional Link URL:
Link Title:
Optional Image URL: