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From: TSS ()
Subject: APHIS BSE Ongoing Surveillance Program update October 31, 2006
Date: October 31, 2006 at 12:14 pm PST

BSE Ongoing Surveillance Program
Monthly Test Results

APHIS reports ongoing surveillance totals monthly.

The BSE ongoing surveillance program will sample approximately 40,000 animals each year. Under the program, USDA will continue to collect samples from a variety of sites and from the cattle populations where the disease is most likely to be detected, similar to the enhanced surveillance program procedures.

BSE Ongoing Surveillance Program Cumulative Total
From Sep 1, 2006: 1 ,792

Month Number of Tests
Sep 2006
1,792


http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml

hell at this rate they will not even find the infamous spontaneous BSE/TSE in the USDA bovine.

of course, we know the spontaneous TSE is only wishful thinking
(please see Chesebro et al at bottom on spontaneous TSE).

daaaaa...............problem solved. i can't believe this is happening. ...TSS

Release No. 0255.06
Contact:
Ed Loyd (202) 720-4623
Karen Eggert (202) 690-4755

USDA ANNOUNCES NEW BSE SURVEILLANCE PROGRAM

WASHINGTON, July 20, 2006-Agriculture Secretary Mike Johanns announced today that the U.S. Department of Agriculture will soon begin transitioning to an ongoing Bovine Spongiform Encephalopathy (BSE) surveillance program that corresponds to the extremely low prevalence of the disease in the U.S.

"It's time that our surveillance efforts reflect what we now know is a very, very low level of BSE in the United States," said Johanns. "This ongoing surveillance program will maintain our ability to detect BSE, provide assurance that our interlocking safeguards are successfully preventing BSE, while continuing to exceed science-based international guidelines."

The ongoing BSE surveillance program will sample approximately 40,000 animals each year. Under the program, USDA will continue to collect samples from a variety of sites and from the cattle populations where the disease is most likely to be detected, similar to the enhanced surveillance program procedures.

The new program will not only comply with the science-based international guidelines set forth by the World Animal Health organization (OIE), it will provide testing at a level ten times higher than the OIE recommended level.

USDA has an obligation to provide 30 days notice of the change to contractors who are performing the sampling and testing, so the earliest the new surveillance program would begin is late August. Once the ongoing surveillance program begins, USDA will periodically analyze the surveillance strategy to ensure the program provides the foundation for market confidence in the safety of U.S. cattle.

In April, USDA released an analysis of 7 years of BSE surveillance data. This included data from an enhanced surveillance program, which began in June 2004, as a one-time effort to determine the prevalence of BSE in the United States. The analysis concluded that the prevalence of BSE in the United States is less than 1 case per million adult cattle. The analysis further revealed that the most likely number of cases is between 4 and 7 infected animals out of 42 million adult cattle. The analysis was submitted to a peer review process and a panel of outside experts affirmed the conclusions.

The enhanced surveillance program has been funded using emergency CCC funds totaling $157.8 million since June 2004. Ongoing surveillance will cost approximate $17 million per year using funds appropriated by Congress. The President's FY 2007 budget request includes this level of funding.

BSE surveillance is not a food safety program. Human and animal health is protected by a system of interlocking safeguards, including the removal of specified risk materials - those tissues that studies have demonstrated may contain the BSE agent in infected cattle, along with the U.S. Food and Drug Administration's 1997 ruminant to ruminant feed ban. Scientific studies indicate that the longer a feed ban is in place, the lower the prevalence of BSE will become.

An outline of the ongoing BSE surveillance plan is available at http://www.aphis.usda.gov/newsroom/hot_issues/bse.shtml.


http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2006/07/0255.xml

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006


The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end


http://www.upi.com/

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...


http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm

US SENATOR AND STAN THE MAN SLAM USDA ''DAMNING TESTIMONY''

Senator Michael Machado from California

''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''

Stanley Prusiner

''nobody has ever ask us to comment''

''they don't want us to comment''

''they never ask''

i tried to see Venemon, after Candian cow was discovered with BSE.
went to see lyle. after talking with him... absolute ignorance... then
thought i
should see Venemon... it was clear his entire policy was to get cattle
bonless beef prods
across the border... nothing else mattered...
his aids confirmed this... 5 times i tried to see Venemon, never worked...
eventually met with carl rove the political... he is the one that
arranged meeting
with Venemon... just trying to give you a sense of the distance... healh
public safety...
was never contacted...
yes i believe that prions are bad to eat and you can die from them...END

Dr. Stan bashing Ann Veneman - 3 minutes

*** YOU MUST WATCH THIS! ...TSS

http://maddeer.org/video/embedded/08snip.ram

PAUL BROWN M.D.

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf


9 December 2005
Division of Dockets Management (RFA-305)

SEROLOGICALS CORPORATION
James J. Kramer, Ph.D.
Vice President, Corporate Operations


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf

Embassy of Japan


http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm

Dockets Entered on December 22, 2005
2005D-0330, Guidance for Industry and FDA Review Staff on Collection of
Platelets
by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ...


http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm


03-025IF 03-025IF-631 Linda A. Detwiler [PDF]
Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4.
Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12.


http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf

03-025IF 03-025IF-634 Linda A. Detwiler [PDF]
Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2.
Page 3. Page 4. Page 5. Page 6. Page 7. Page 8.
http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf


Page 1 of 17 9/13/2005 [PDF]
... 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov Subject: [Docket
No. 03-025IFA]
FSIS Prohibition of the Use of Specified Risk Materials for Human Food ...
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

03-025IFA 03-025IFA-6 Jason Frost [PDF]
... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al
[Docket No. 03-
025IF] Prohibition of the Use of Specified Risk Materials for Human Food and
...
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf

http://www.fsis.usda.gov/Search/Search_Results/Index.asp?q=03-025IF&mode=simple&num=10&as_occt=any&restrict=FSIS_DOCKET_COMMENTS

In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF]
Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone:
732-741-2290
Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...


http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf


Page 1 of 17 9/13/2005 [PDF]
... Page 1 of 17 From: Terry S. Singeltary Sr. [flounder9@verizon.net] Sent:
Thursday,
September 08, 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov
Subject ...
www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


03-025IF 03-025IF-618 Richard L. Crawford [PDF]
Page 1. 03-025IF 03-025IF-618 Richard L. Crawford
Page 2. Page 3. Page 4.
http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-618.pdf

03-038IF 03-038IF-15 Richard L. Crawford [PDF]
Page 1. 03-038IF 03-038IF-15 Richard L. Crawford
Page 2. Page 3. Page 4.
http://www.fsis.usda.gov/OPPDE/Comments/03-038IF/03-038IF-15.pdf

PLEASE NOTE, if spontaneous scrapie or CWD does not occur, then why is it that now only atypical BSE and sproadic CJD are capable of spontaneous mutation $$$ seems the UK study just posted about different strains of UK scrapie cause different strains of TSE when transmitted to UK cattle in the lab would dispute the spontaneous, natural, sporadic, lame duck excuse for any TSE, and how could these few 'unusual cases' _scientifically_ explain 85%+ of all sCJD, of which there are 6 documented phenotypes, or 5, depending whom you believe ? bottom line, they can't......TSS


Science 24 September 2004:
Vol. 305. no. 5692, pp. 1918 - 1921
DOI: 10.1126/science.1103581

Perspectives
BIOMEDICINE:
A Fresh Look at BSE
Bruce Chesebro*
Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle
form of a family of progressive brain diseases. These diseases include
scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and chronic
wasting disease (CWD) in deer and elk. They are also known as either "prion
diseases" because of the association of a misfolded cellular prion protein
in pathogenesis or "transmissible spongiform encephalopathies" (TSEs)
because of the spongelike nature of the damaged brain tissue (1).

The recent discovery of two BSE-infected cows, one in Canada and one in the
United States, has dramatically increased concern in North America among
meat producers and consumers alike over the extent to which BSE poses a
threat to humans as well as to domestic and wild animals. The European BSE
epidemic of the late-1980s seems to have been initiated a decade earlier in
the United Kingdom by changes in the production of meat and bone meal (MBM)
from rendered livestock, which led to contamination of MBM with the BSE
infectious agent. Furthermore, the fact that UK farmers fed this rendered
MBM to younger animals and that this MBM was distributed to many countries
may have contributed to the ensuing BSE epidemic in the United Kingdom and
internationally (2).

Despite extensive knowledge about the spread of BSE through contaminated
MBM, the source of BSE in Europe remains an unsolved mystery (2). It has
been proposed that BSE could be derived from a cross-species infection,
perhaps through contamination of MBM by scrapie-infected sheep tissues (see
the figure). Alternatively, BSE may have been an endemic disease in cattle
that went unnoticed because of its low level of horizontal transmission.
Lastly, BSE might have originated by "spontaneous" misfolding of the normal
cellular prion protein into the disease-associated abnormal isoform (3),
which is postulated to be the infectious agent or "prion."

Five possible sources of BSE in North American cattle. Sheep, deer, and elk
could spread prion diseases (TSEs) to cattle through direct animal contact
or contamination of pastures. Endemic BSE has not been proven to exist
anywhere in the world, but it is difficult to exclude this possibility
because of the inefficient spread of BSE infectivity between individual
animals (2). BSE caused by spontaneous misfolding of the prion protein has
not been proven.
CREDIT: KATHARINE SUTLIFF/SCIENCE

Spontaneous protein misfolding is not a new phenomenon as proteins are known
to sometimes misfold after synthesis. Cells in turn have devised ingenious
ways to deal with this problem. These include molecular chaperone proteins
that bind to misfolded proteins and help them to unfold, and organelles
called proteosomes that degrade misfolded or unwanted proteins. However,
although misfolded prion proteins have been generated in test tubes as well
as in cultured cells, it has been difficult to demonstrate that such
misfolded abnormal prion proteins are infectious (4, 5). Even the most
recent data do not prove conclusively that infectivity has been generated in
vitro because misfolded synthetic prion proteins were not able to transfer
disease directly to wild-type mice (6). To obtain infectivity and subsequent
prion disease, the misfolded proteins had to be inoculated and incubated for
1 to 2 years in transgenic mice that overexpressed a mutant version of the
prion protein. Previous data from this group showed that transgenic mice
expressing high amounts of prion protein developed neurological disease
without inoculation of misfolded prion protein (7). Thus, at the biochemical
level, the critical attributes of the misfolded prion protein required for
infectivity are not known, and misfolding of prion protein alone may not be
sufficient to generate an infectious agent (.
Nevertheless, the idea that BSE might originate due to the spontaneous
misfolding of prion proteins has received renewed interest in the wake of
reports suggesting the occurrence of atypical BSE (9-11). These results
imply that new strains of cattle BSE might have originated separately from
the main UK outbreak. Where and how might such strains have originated?
Although such rare events cannot be studied directly, any number of sources
of the original BSE strain could also explain the discovery of additional
BSE strains in cattle (see the figure). However, it would be worrisome if
spontaneous BSE were really a valid etiology because such a mechanism would
be impossible to prevent--unlike other possible scenarios that could be
controlled by large-scale eradication of TSE-positive animals.

Another way to look at this problem is to examine evidence for possible
spontaneous TSE disease in other animals besides cattle. Spontaneous BSE
would be extremely difficult to detect in cattle, where horizontal spread is
minimal. However, in the case of the sheep TSE disease, scrapie, which
spreads from ewes to lambs at birth as well as between adults, spontaneous
disease should be detectable as new foci of clinical infection. In the early
1950s scrapie was eradicated in both Australia and New Zealand, and the
mainland of both these countries has remained scrapie-free ever since. This
scrapie-free status is not the result of selection of sheep resistant to
scrapie because sheep from New Zealand are as susceptible as their UK
counterparts to experimental scrapie infection (12). These experiments of
man and nature appear to indicate that spontaneous clinical scrapie does not
occur in sheep. Similarly, because CWD is known to spread horizontally, the
lack of CWD in the deer or elk of eastern North America but its presence in
western regions would also argue against a spontaneous disease mechanism.
This is particularly noteworthy in New Zealand, where there are large
numbers of deer and elk farms and yet no evidence of spontaneous CWD. If
spontaneous scrapie does not occur in sheep or deer, this would suggest that
spontaneous forms of BSE and sporadic Creutzfeldt-Jakob disease (sCJD) are
unlikely to be found in cattle or humans. The main caveat to this notion is
that spontaneous disease may arise in some animal species but not others. In
humans, sCJD--which is considered by some researchers to begin by
spontaneous misfolding of the prion protein--usually takes more than 50
years to appear. Thus, in animals with a shorter life-span, such as sheep,
deer, and cattle, an analogous disease mechanism might not have time to
develop.

What can we conclude so far about BSE in North America? Is the BSE detected
in two North American cows sporadic or spontaneous or both? "Sporadic"
pertains to the rarity of disease occurrence. "Spontaneous" pertains to a
possible mechanism of origin of the disease. These are not equivalent terms.
The rarity of BSE in North America qualifies it as a sporadic disease, but
this low incidence does not provide information about cause. For the two
reported North American BSE cases, exposure to contaminated MBM remains the
most likely culprit. However, other mechanisms are still possible, including
cross-infection by sheep with scrapie or cervids with CWD, horizontal
transmission from cattle with endemic BSE, and spontaneous disease in
individual cattle. Based on our understanding of other TSEs, the spontaneous
mechanism is probably the least likely. Thus, "idiopathic" BSE--that is, BSE
of unknown etiology--might be a better term to describe the origin of this
malady.

What does all this imply about testing cattle for BSE in North America?
Current testing in the United States indicates that BSE is rare (one
positive result in 40,000 cattle tested). However, additional testing of
200,000 head of slaughtered cattle over the next 1 to 2 years, as recently
proposed by the U.S. Department of Agriculture (USDA), should tell us the
incidence more precisely. Nevertheless, if any rare cases are detected, we
may still not know their origin. If evidence arises of a focal occurrence of
BSE, we might gain important insight into unexpected sources of
contamination. However, because current tests do not seem to be able to
detect BSE in infected animals less than 30 months of age, even more
extensive testing will not completely guarantee the negative status of
younger animals in the food chain. Therefore, the alternative option of
testing all slaughtered cattle, as implemented in some countries such as
Japan, would appear to provide little additional benefit. This fact has been
acknowledged as the basis for a new agreement between the United States and
Japan aimed at reestablishing the beef trade between the two countries.

One problem with the current U.S. testing program was the announcement a few
months ago of unconfirmed positive BSE tests in two additional North
American animals that were subsequently found to be negative when tested
with the more accurate method of Western blotting. The public release of
information about unconfirmed positive tests detected by the rapid test used
for mass screening may be a good idea in the interest of openness, but it ha
s the potential to create unwarranted anxiety. If unconfirmed positives are
a frequent occurrence, it would seem reasonable to follow a more cautious
approach and wait until confirmatory testing is complete before publicly
announcing the details.

Based on the experience of many European countries, the mainstays of
controlling BSE in cattle and avoiding spread to humans are threefold:
first, eliminate feeding of ruminant tissues to ruminants; second, remove
high-risk cattle tissues from human food; and third, continue to test for
BSE in cattle in order to monitor progress with the elimination of the
disease on a local and national basis. In the next 12 months, after
extensive USDA test results are available, the extent of any possible BSE
spread in the United States will be better documented. But, in fact, the
United States and Canada have already instituted the most important steps to
prevent the spread of cattle BSE in advance of the results--that is, a ban
on feeding ruminant MBM to other ruminants and removal of high-risk tissues
from meat for human consumption. It is hoped that the new data will not
deviate enough from previous predictions to require further measures for
management of this problem. The most important line of defense against any
possible spread of BSE will be to maintain strict vigilance in the
implementation of the current regulations.

References


S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998) [Medline].
P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline].
C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997) [Medline].
A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline].
R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline].
G. Legname et al., Science 305, 673 (2004).
D. Westaway et al., Cell 76, 117 (1994) [Medline].
B. Chesebro, Science 279, 42 (1998).
A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline].
Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline].
C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004)
[Medline].
E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].

http://www.sciencemag.org/cgi/content/full/305/5692/1918


Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518






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