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From: TSS ()
Subject: BSE USA INCONCLUSIVE TSS SUBMISSION TO OIG Mon, 02 May 2005
Date: June 14, 2005 at 5:07 am PST

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

Greetings,

a few comments please;

>>>The Inspector General, in reviewing our surveillance system that
we have in place, decided to retest with a second confirmatory test which
is called the Western Blot. We have received test results showing a positive
on one animal for the Western Blot.<<<

>>>The department has not explained why the new tests were ordered. The
inspector general's office, an independent arm of the agency, would not
comment Monday, saying a brief statement would be issued Tuesday.<<<

I happened to write the OIG about this very issue, on several occasions.
THIS is _one_ of several emails i sent the OIG about this issue and
others in the past, and all the data to back it up. ...TSS

-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us


Greetings Honorable Paul Feeney, Keith Arnold, and William Busby
et al at OIG,

My name is Terry S. Singeltary Sr. and on 12/14/97 I lost my
mother to a most hideous disease called ;

Heidenhain Variant Creutzfeldt Jakob Disease (CONFIRMED)

MY MOM AND MANY MORE
were murdered by corporate greed, to say the least.

I have wasted almost 8 years of my life seeking the truth.
I have been searching for answers ever since. I kindly wish
to submit the following data that I have acquired over the last
7+ years. There has indeed been a cover-up of TSE in the USA
bovine. PLEASE remember, there is now more than one strain
of TSE in cattle. Many strains of TSE in other species. The
new TSE in cattle does not resemble BSE in cattle or
nvCJD in humans, but very similar to the sporadic CJD ;


Identification of a second bovine amyloidotic spongiform
encephalopathy: Molecular similarities with sporadic
Creutzfeldt-Jakob disease

Cristina Casalone *{dagger} , Gianluigi Zanusso {dagger} {ddagger} ,
Pierluigi Acutis *, Sergio Ferrari {ddagger} , Lorenzo Capucci § ,
Fabrizio Tagliavini ¶, Salvatore Monaco {ddagger} ||, and Maria Caramelli *

*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto
Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via
Bologna, 148, 10195 Turin, Italy; {ddagger} Department of Neurological
and Visual Science, Section of Clinical Neurology, Policlinico G.B.
Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; § Istituto
Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via
Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico
"Carlo Besta," Via Celoria 11, 20133 Milan, Italy

Edited by Stanley B. Prusiner, University of California, San Francisco,
CA, and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are
mammalian neurodegenerative disorders characterized by a
posttranslational conversion and brain accumulation of an insoluble,
protease-resistant isoform (PrPSc) of the host-encoded cellular prion
protein (PrPC). Human and animal TSE agents exist as different
phenotypes that can be biochemically differentiated on the basis of the
molecular mass of the protease-resistant PrPSc fragments and the degree
of glycosylation. Epidemiological, molecular, and transmission studies
strongly suggest that the single strain of agent responsible for bovine
spongiform encephalopathy (BSE) has infected humans, causing variant
Creutzfeldt-Jakob disease. The unprecedented biological properties of
the BSE agent, which circumvents the so-called "species barrier" between
cattle and humans and adapts to different mammalian species, has raised
considerable concern for human health. To date, it is unknown whether
more than one strain might be responsible for cattle TSE or whether the
BSE agent undergoes phenotypic variation after natural transmission.
Here we provide evidence of a second cattle TSE. The disorder was
pathologically characterized by the presence of PrP-immunopositive
amyloid plaques, as opposed to the lack of amyloid deposition in typical
BSE cases, and by a different pattern of regional distribution and
topology of brain PrPSc accumulation. In addition, Western blot analysis
showed a PrPSc type with predominance of the low molecular mass
glycoform and a protease-resistant fragment of lower molecular mass than
BSE-PrPSc. Strikingly, the molecular signature of this previously
undescribed bovine PrPSc was similar to that encountered in a distinct
subtype of sporadic Creutzfeldt-Jakob disease.

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

ALSO, PLEASE REMEMBER, SCRAPIE IN SHEEP AND
GOATS ARE RAMPANT IN THE USA, SCRAPIE TRANSMITS
TO PRIMATES, AND THERE HAS NEVER BEEN TRANSMISSION STUDIES ON HUMANS ;

1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=6997404&dopt=Abstract


USDA USE TO BE VERY CONCERNED ABOUT THIS AGENT
AND THE POTENTIAL FOR TRANSMISSION TO HUMANS,
what changed there mind?


12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all
countries.

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human
dementias"

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer
grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf

http://www.bseinquiry.gov.uk/files/yb/1976/10/12002001.pdf


SCRAPIE STATUS USA 2005

MONTHLY REPORT

AS of March 31, 2005, there were 70 Scrapie infected source flocks
(Figure 3). There were 11 new infected and source flocks reported
in March (Figure 4) with a total of 51 flocks reported for FY 2005
(Figure 5). The total infected and source flocks that have been released
in FY 2005 are 39 (Figure 6), with 1 flock released in March. The
ratio of infected and source flocks released to newly infected and
source flocks for FY 2005 = 0.76 : 1. In addition, as of March 31,
2005, 225 Scrapie cases have been confirmed and reported by the
National Veterinary Services Laboratories (NVSL), of which
53 were RSSS cases (Figure 7). This includes 57 newly confirmed
cases in March 2005 (Figure 8). Fourteen cases of Scrapie in Goats
have been reported since 1990 (Figure 9). The last goat cases was
reported in January 2005. New infected flocks, source flocks, and
flocks released or put on clean-up plans for FY 2005 are depicted
in Figure 10...

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.htm
l


YEARLY REPORT

Infected and Source Flocks

As of September 30, 2004, there were 67 scrapie infected and source
flocks (figure 3
).
There were a total of 100** new infected and source flocks reported for
FY 2004 (figure 4
).
The total infected and source flocks that have been released in FY 2004
are 77 (figure 5
).
The percent of new infected and source flocks cleaned up or on clean up
plans was 96%. In addition, as of September 30, 2004, 368 scrapie cases
have been confirmed and reported by the National Veterinary Services
Laboratories (NVSL) in FY 2004, of which 54 were RSSS cases (figure 6
,
and figure 7
).
Thirteen cases of scrapie in goats have been reported since 1990 (figure
8
).
One new goat case was reported in FY 2004. New infected flocks, source
flocks, and flocks released for FY 2004 are depicted in chart 4
.
One new goat case was reported in FY 2004. Approximately 3,058 animals
were indemnified comprised of 47% non-registered sheep, 44% registered
sheep, 6% non-registered goats and 1% registered goats.

http://www.aphis.usda.gov/vs/nahps/scrapie/yearly_report/yearly-report.html


PLEASE note, the june 2004 BSE enhanced surveillance
was meaningless and ''NOT SCIENTIFIC'' without WB.

just ask the experts ;


-------- Original Message --------
Subject: Q&A Dr. Jean-Philippe Deslys USDA REFUSAL TO USE WB ON TEXAS
COW WITH BSE SYMPTOMS (FULL TEXT)
Date: Fri, 22 Apr 2005 11:53:47 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTS.UNI-KARLSRUHE.DE


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

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?

Its 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?

Its not logical. If you have two consecutive questionable screenings,
you do another test. I can only advise, its managements 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 werent 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 couldnt eliminate it.

I cant 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; its not OUR problem, it is our neighbors 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.

6. USDAs list of specified risk materials excludes some products, like
blood and bone meal, that are banned in the EU and UK. Is our feed
supply safe?

With SRMs, where do you stop? Tests have found prions in meat, nerves
travel through meat, and so on. The main infectivity is in the brain and
the spinal cord. A blood and bone meal ban in animal feed is not really
necessary, because except in cases of highly infective animals, it is
unlikely that they are dangerous in themselves. If you combine
systematic testing and targeted SRM removal, the brain and the spinal
column in cattle over 30 months, you can have a compromise that is both
safer and less costly than expanded feed bans.

Certainly, you can stop the spread of BSE with a total ban on offal. But
it has to be a total ban. It cant be given to sheep or swine or
poultry. It would be very expensive and virtually impossible to
accomplish. You can have farmers using the wrong feed or transportation
errors.

Systematic testing makes far more sense. I think of it as a thermometer.
It not only allows us to catch the disease, it also allows us to monitor
its progress. We can watch the levels of infectivity and if they start
going up instead of down, we can take measures.

To an extent, our environment is contaminated. About 10 percent of wild
animals test positive for TSEs. If you recycle these agents, they can
evolve and get more dangerous. This is probably what happened with
BSE. It wasnt very dangerous until it evolved to the disease we know
today.

People complain that testing is very expensive. It is much more
expensive to kill and test whole herds.

7. In your opinion, is infected feed the sole method of transmission of
BSE, apart from the very rare maternal transmission?

Feed is the main problem. However, we are seeing some other
possibilities, including through fat and greases. Calves are fed milk
extracts, with the cream removed. To make it nutritious, they are using
fat and grease from cattle.

(FOLLOW QUESTION: Would that allow BSE to develop into an infective
level in cattle younger than 30 months, assuming they might be getting
infected at a younger age?)

8. You were involved in a study that tested two primates who were fed
infected brain tissue. One eventually died of TSE; the other survived.
The press reported that the main finding was that it would take
something on the order of 1.5 kilograms of infected matter to create an
infection, but that seems to be an oversimplification. Could you explain
it further?

The findings suggest that as little as five grams is enough to infect.
The 1.5 kilo figure is the amount of infected tissue that would have to
be ingested from an animal that would be below the threshold of
infection, and would test negative. In other words, even though a
younger animal may be developing the disease, it would take a
considerable amount of tissue to transmit the disease.

An animal could be just below the testing level, and not be particularly
dangerous. But that is why you have to keep testing. Once it reaches the
threshold, it can become highly infective.

9. BSE is a pretty horrifying disease, but overall, it has killed less
than 200 humans, and only a handful in recent years. Listeria, by
comparison, kills thousands every year. Overall, how do you rate the
threat from BSE?


The overall risk is not particularly high. Over two million infected
animals went into the food chain in Europe, 400,000 of them before the
SRMs, the brains and spinal column, were removed from the carcass. Less
than 200 died, and less than 4,000 are at risk of developing the
disease. What we know now is that one particle is not going to kill you.
There has to be condensation of the prions to be truly dangerous.

This is not a sterile world. But the danger is that now that the crisis
appears to be over, attention will turn elsewhere and that will allow
the disease to amplify again. Just as we stopped paying attention to
AIDS when medication seemed to control it, then were surprised when a
new and more infectious and aggressive strain appeared, we could be
surprised by a more serious strain of BSE. That is why I support
systematic testing for the long term. The object is to keep levels of
BSE low, and to recognize the danger if it suddenly pops back up. ...END

TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html
##########


-------- Original Message --------
Subject: Re: Q&A Dr. Jean-Philippe Deslys USDA REFUSAL TO USE WB ON
TEXAS COW WITH BSE SYMPTOMS (FULL TEXT)
Date: Fri, 22 Apr 2005 12:14:14 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTS.UNI-KARLSRUHE.DE
References: <42692C1B.7090200@wt.net>


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

IN FACT, i must bring this up again.
IN TEXAS, when they are really worried about a mad cow,
when the cow is clinical and stumbling and staggering, TEXAS
does not bother TESTING the cow at all. nope, they just send
it directly to be rendered head and all to get rid of all evidence.
the june 2004 enhanced bse cover-up was just that. the USA
could test every cow that goes to slaughter, and it would be meaningless
unless properly done with the most sensitive testing to date.
but not in TEXAS or any other state in the USA.............


FDA Statement

FOR IMMEDIATE RELEASE
Statement
May 4, 2004

Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


Statement on Texas Cow With Central Nervous System Symptoms

On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to
a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately
began an investigation. On Friday and throughout the weekend, FDA
investigators inspected the slaughterhouse, the rendering facility, the
farm where the animal came from, and the processor that initially
received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over
the weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known
as "mad cow disease," can exhibit such symptoms. In this case, there is
no way now to test for BSE. But even if the cow had BSE, FDA's animal
feed rule would prohibit the feeding of its rendered protein to other
ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and
informing the firm that FDA will not object to use of this material in
swine feed only. If it is not used in swine feed, this material will be
destroyed. Pigs have been shown not to be susceptible to BSE. If the
firm agrees to use the material for swine feed only, FDA will track the
material all the way through the supply chain from the processor to the
farm to ensure that the feed is properly monitored and used only as feed
for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the
U.K. showed that the disease spreads by feeding infected ruminant
protein to cattle.

Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action
specifying that the material go only into swine feed means also that it
will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates
closely with the U.S. Department of Agriculture on all BSE issues. The
animal feed rule provides crucial protection against the spread of BSE,
but it is only one of several such firewalls. FDA will soon be improving
the animal feed rule, to make this strong system even stronger.

####

http://www.fda.gov/bbs/topics/news/2004/NEW01061.html

TSS


------------------------------------------------------------------------
Date
------------------------------------------------------------------------

APHIS Statement: June 29 Inconclusive BSE Test is Negative
07/02/2004

APHIS Statement: First Inconclusive BSE Test is Negative
06/30/2004

APHIS Statement Regarding Second Inconclusive BSE Test
06/29/2004

APHIS Statement Regarding First Inconclusive BSE Test
06/25/2004

Week 25
(11/1511/21)
7,900
1
Negative
0
7,901

Week 5
(6/287/4)
3,500
1
Negative
0
3,501
Week 4
(6/216/27)
3,254
1
Negative
0
3,255

USDA orders silence on mad cow in Texas

By Steve Mitchell
United Press International
Published 5/11/2004 10:16 PM

WASHINGTON, May 11 (UPI) -- The U.S. Department of Agriculture has
issued an order instructing its inspectors in Texas, where federal mad
cow disease testing policies recently were violated, not to talk about
the cattle disorder with outside parties, United Press International has
learned.

The order, sent May 6 by e-mail from the USDA's Dallas district office,
was issued in the wake of the April 27 case at Lone Star Beef in San
Angelo, in which a cow displaying signs of a brain disorder was not
tested for mad cow disease despite a federal policy to screen all such
animals.

The deadly illness also is known as bovine spongiform encephalopathy.

Both the USDA and its Inspector General -- amid allegations that an
offsite supervisor overruled the opinion of the inspectors onsite and
made the final decision not to test the animal -- have opened up
investigations to determine why agency policy was violated.

The order, which was obtained by UPI, was issued by Ijaz Qazi, circuit
supervisor for the USDA's Food Safety and Inspection Service's Dallas
district, which covers the entire state. It reads: "All BSE inquiries
MUST be directed to Congressional Public Affairs Phone 202-720-9113
attention Rob Larew OR Steve Khon. This is an urgent message. Any
question contact me. Ijaz Qazi."

Although the language might sound innocuous, experienced inspectors
familiar with USDA parlance have taken to referring to the notice as a
"gag order."

The National Joint Council of Food Inspection Locals -- the national
inspectors union -- considers the order a violation of inspectors' free
speech rights and is considering legal action against the USDA for
breaching the labor agreement they have with the agency.

Inspectors alleged the order also suggests the agency is concerned about
its personnel leaking damaging information about either the Texas case
or the USDA's overall mad cow disease surveillance program, which has
come under fire since the discovery of an infected cow in Washington
state last December.

"Anytime the government suppresses an individual's freedom of speech,
that's unconstitutional," Gary Dahl, president of Local 925, the
Colorado inspectors union, told UPI.

Stanley Painter, chairman of the National Joint Council, said the USDA
has sent out notices in the past stating inspectors cannot talk to
reporters.

"It's an intimidation thing," Painter told UPI. Inspectors have the
right to talk to anybody about any subject, as long as they clarify they
are not speaking on behalf of the USDA and they are not doing it on
government time, he said.

USDA spokesman Steven Cohen said he was not familiar with the notice
from the Dallas office. He said he would look into it, but did not
respond by UPI's publication time. In general, Cohen said, "There's an
expectation any statement on behalf of the agency would come from the
office of communications (in Washington.)"

Asked if employees could speak freely as long as they clarified that
their views did not reflect those of the agency, Cohen said, "We'd
rather that agency policy be communicated by those in a position to
speak for the agency."

Qazi told UPI the notice was not issued in conjunction with the Texas
case and it was routine agency practice that outside inquiries be
referred to the Washington office. He said inspectors are free to talk
to outside parties, including reporters, and he did not consider the
e-mail a violation of the labor agreement with the inspectors.

Painter said the USDA's efforts to keep its employees from talking about
mad cow would be better spent "with issues like protecting the consuming
public instead of trying to hide things." He added he would "just about
bet his last nickel" agency management was attempting to suppress
information about the Texas case.

"To keep federal employees from reporting government waste, misuse of
appropriations -- those types of things -- that's not a good thing
either," Dahl said. "If there is something wrong, let's get it out in
the open -- let's get it fixed. We're working for the public, the
American consumers. I think they have the right to know this," he said.

"And believe me there's so many indicators saying that the USDA's mad
cow testing program is broken," Dahl added.

At least one member of Congress, Sen. Tom Harkin, D-Iowa, agrees.

Harkin, a long-time critic of the USDA, sent a letter to Agriculture
Secretary Ann Veneman on Monday, saying the Texas incident "calls into
question the effectiveness and reliability of USDA's current and
proposed surveillance system."

The USDA has proposed testing more than 200,000 cows -- or 10 times its
current rate -- in an expanded program scheduled to begin June 1. Harkin
wrote in the five-page letter, however, that given the realities of the
cattle industry, it is "quite doubtful" the USDA will be able to test
that many cows, particularly because it had difficulty finding 20,000
last year.

"We simply cannot tolerate a BSE testing system that fails to give valid
answers to critical questions for U.S. consumers and foreign customers,"
Harkin said in the letter, which sharply criticizes the agency's failure
to address explicitly how its new surveillance program will be implemented.

"We look forward to receiving (Harkin's) letter and having the
opportunity to review it and respond to him," USDA spokesman Ed Loyd
told UPI. "USDA has acknowledged there was a failure in not testing that
cow in Texas for BSE, so we are all working to ensure that does not
occur again."

Jim Rogers, a spokesman for USDA's Animal and Plant Health Inspection
Service, which oversees the agency's mad cow surveillance program, told
UPI the agency has tested about 15,500 animals since fiscal year 2004
began, on Oct. 1, 2003. However, the agency has refused to identify the
states and facilities from which the cows originated. Rogers said UPI
would have to seek that information through the Freedom of Information Act.

The question is central to the USDA's implementation of its expanded
surveillance program. Downer cows -- those unable to stand or walk --
made up the bulk of the animals the agency tested for mad cow in
previous years, but these were banned from being slaughtered for human
consumption in December. This means the agency inspectors no longer can
obtain brain samples from these cows at slaughterhouses as they could in
the past.

Furthermore, the USDA has not provided any evidence it has worked out
agreements with rendering facilities or ranchers, where downers and dead
cows are now most likely to be found, to obtain the extra animals for
testing.

Loyd said the agency is "working very hard to get animals on the farm
that would never show up in a processing facility," and he was "not
aware of any issues" that would delay the launch of the new program.

However, he was unable to provide the names or locations of the
rendering facilities where the agency will be obtaining cow brains for
BSE testing. He said he would look into it but did not return two
follow-up phone calls from UPI before publication.

--

Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com

Copyright © 2001-2004 United Press International

http://www.upi.com/view.cfm?StoryID=20040511-015527-4917r


USDA did not test possible mad cows

By Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM

WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims it
tested 500 cows with signs of a brain disorder for mad cow disease last
year, but agency documents obtained by United Press International show
the agency tested only half that number.

USDA officials said the difference is made up in animals tested at state
veterinary diagnostic laboratories, but these animals were not tested
using the "gold standard" test employed by the agency for confirming a
case of the deadly disease. Instead, the state labs used a less
sensitive test that experts say could miss mad cow cases.

In addition, the state lab figures were not included in a March 2004
USDA document estimating the number of animals most likely to be
infected among U.S. herds, and apparently were not given to a
congressional committee that had requested agency data on the number of
cows with brain disorder signs that had been tested for the disease.

"This is just adding to the demise of USDA's credibility," said Felicia
Nestor, senior policy adviser to the Government Accountability Project,
a group in Washington, D.C., that works with federal whistleblowers.

"If the USDA is going to exclude from testing the animals most likely to
have the disease, that would seem to have a very negative impact on the
reliability of their conclusion," Nestor told UPI.

Nestor, who has monitored the USDA's mad cow surveillance program
closely for several years, asked, "Are they deliberately avoiding
testing animals that look like they have the disease?"

Concerns about the number of cows in U.S. herds with brain disorder
symptoms have been heightened due to the recent case in Texas, in which
USDA officials failed to test an animal with such symptoms, also known
as central nervous system or CNS signs. This was a violation of USDA
policy, which stipulates all CNS cows should be tested because they are
considered the most likely to be mad cow infected. To date, the
Washington cow that tested positive last December is the only confirmed
case of mad cow disease -- also known as bovine spongiform
encephalopathy -- among U.S. herds.

The Texas incident has alarmed the public and members of Congress
because humans can contract a fatal brain disorder called variant
Creutzfeldt-Jakob disease from consuming meat infected with the mad cow
pathogen. If the USDA's surveillance program is allowing the riskiest
cows to go untested, it raises concerns about the ability of the
monitoring system to detect the disease reliably in U.S. herds, Rep.
Henry Waxman, D-Calif., charged in a May 13 letter to Agriculture
Secretary Ann Veneman.

Dr. Peter Lurie, of the consumer group Public Citizen, said CNS cows
should be the one category that absolutely has to be tested to have a
sound surveillance system.

"CNS animals are far and away the most important animals to test," said
Lurie, who has done several analyses of the USDA's mad cow surveillance
program.

"If there's any category that needs 100 percent testing, that's it,
because they would be the most likely place to find mad cow in America,"
he told UPI. "Any CNS cow that slips into the food supply represents a
major case of malpractice by USDA, and similarly, the failure to test
the brain of that animal to see if it was indeed infected is really a
failure to protect the public."

USDA officials said the agency has no estimate on how many CNS cows
occur in U.S. herds. But spokesman Ed Loyd has told UPI, and at least
one other media outlet, that 500 CNS cows were tested in fiscal year
2003. Yet agency testing records for the first 10 months of FY 2003,
obtained by UPI under the Freedom of Information Act, show only 254
animals that fall under the CNS category -- or about half the number
Loyd cited.

After failing to respond to repeated requests from UPI for clarification
of the apparent discrepancy, Loyd finally offered the explanation that
an additional 45 CNS cows were tested by the USDA during the final two
months of FY 2003. The remainder, he said, was made up by CNS cases
tested at various state veterinary diagnostic laboratories.

"We also include data reported to us from state veterinary diagnostic
laboratories, and all of these are CNS cases that have been tested for
BSE using a histological examination," Loyd said.

"We were not using any other labs during this period, other than (the
USDA lab), to run the IHC tests for BSE, which is the gold standard," he
said. "This (state laboratory) information contributes important data to
our surveillance effort."

However, the state labs did not use the immunohistochemistry test, which
the USDA has called the "gold standard" for diagnosing mad cow disease.
Instead, the labs used a different test called histopathology, which the
USDA itself does not use to confirm a case, opting instead for the more
sensitive IHC test.

The histopathology test, unlike the IHC test, does not detect prions --
misfolded proteins that serve as a marker for infection and can be
spotted early on in the course of the illness. Rather, it screens for
the microscopic holes in the brain that are characteristic of advanced
mad cow disease.

According to the USDA's Web site, histopathology proves reliable only if
the brain sample is removed soon after the death of the animal. If there
is too much of a delay, the Web site states, it can be "very difficult
to confirm a diagnosis by histopathology" because the brain structures
may have begun to disintegrate.

That is one reason the agency began using the IHC test -- it can confirm
a diagnosis if the brain has begun disintegrating or been frozen for
shipping.

The state labs used histopathology to screen 266 CNS cases in FY 2003,
as well as 257 cases in FY 2002, according to Loyd. He did not explain
why this information was not included in the testing records the agency
provided to UPI and has not responded to requests for the identity of
the state labs.

Linda Detwiler, a former USDA veterinarian who oversaw the agency's mad
cow testing program, told UPI the histopathology test probably is
adequate for screening CNS cows. If they have mad cow disease, she said,
it would likely be an advanced stage that should be obvious.

Other mad cow disease experts, however, said having a back-up test such
as IHC would be advisable, because histopathology tests sometimes can
miss evidence of infection.

The Food and Agriculture Organization of the United Nations offers
similar recommendations in its protocol for conducing a histopathology
test. The protocol states that even if histopathology is negative,
"further sampling should be undertaken" in cases "where clinical signs
have strongly suggested BSE" -- a criteria that includes all of the cows
tested at the state labs.

The USDA seems to agree on the need for a back-up test. Its expanded
surveillance program, which began June 1, calls for using IHC -- or
another test called Western blot -- to confirm any positives found on
rapid tests. The March 15 document that describes the new program does
not mention using histopathology to confirm cases of mad cow disease.

"Subtle changes can be missed on histopathology that would probably not
be as easy to miss using IHC," said Elizabeth Mumford, a veterinarian
and BSE expert at Safe Food Solutions in Bern, Switzerland, a company
that provides advice on reducing mad cow risk to industry and governments.

"Therefore I believe it is valuable to run (histopathology)," Mumford
told UPI.

She noted that in Europe, two tests -- neither one the histopathology
test -- are used to ensure no cases are missed. A rapid test is used
initially for screening, followed by IHC as a confirmatory test.

Markus Moser, a molecular biologist and chief executive officer of the
Swiss firm Prionics, which manufactures tests for detecting mad cow
disease, agrees about the possibility of a case being missed by
histopathology.

"There were cases which were (histopathology) negative but still clearly
positive with the other (testing) methods," Moser said. "BSE testing
based on histology on sub-optimal tissue was probably one of the reasons
why Germany was allegedly BSE-free until our test discovered that they
were not" in 2000, Moser told UPI.

He agreed with Detwiler that histopathology should be suitable for most
cases of CNS cows, but added it still can fail to detect the disease in
some CNS cases -- particularly if the sample is not optimum.

"It is difficult, if not impossible, to distinguish the subtle changes
in a diseased brain from artifacts like ruptures in the tissue due to
tissue damage during the sampling, transport or preparation," he said.

Loyd asserted the additional CNS cases from the state labs actually
yielded a total of 565 such cows the USDA had tested -- 65 more than his
original figure of 500. Whether the USDA considers its total to be 500
or 565, however, either figure would exceed the agency's own estimates
for the total number of such cows that it identifies annually.

According to data the USDA provided to the House Committee on Government
Reform, and numbers the agency included in the March document about its
expanded surveillance plan, only 201 to 249 CNS cows are identified at
slaughterhouses. Approximately 129 additional cases occur on farms
annually. At most, that yields a combined total of 378 CNS cows, or
nearly 200 less than the 565 Loyd claims the agency tested.

The USDA surveillance plan document makes no mention of the number of
CNS animals tested at state veterinary diagnostic labs. The figure also
does not appear to be included in the agency's estimates of the number
of high-risk animals that occur in the United States each year. The
latter number was used to help the USDA calculate the number of animals
it will screen for mad cow disease in its expanded surveillance plan.

USDA officials also did not include the state lab figures in response to
a question from the House Committee on Government Reform, a source close
to the issue told UPI. The committee, on which Waxman is the ranking
Democrat, had requested in a March 8 letter to Veneman that she provide
"the number of BSE tests that were conducted on cattle exhibiting
central nervous system symptoms" for each of the last five years.

Loyd did not respond to a request from UPI asking why agency officials
did not provide that information to the committee or include it in
USDA's explanation of its expanded surveillance plan.

The committee has taken note of the CNS issue and plans to delve into it
further in a hearing slated for sometime in the next few months.

"The committee will explore this and other issues surrounding USDA and
BSE testing at a hearing later this summer," Drew Crockett, spokesman
for the committee, told UPI.

--

Steve Mitchell is UPI's Medical Correspondent. E-mail sciencemail@upi.com

Copyright © 2001-2004 United Press International

http://www.upi.com/view.cfm?StoryID=20040608-014607-3865r

IN FACT, i must bring this up again.
IN TEXAS, when they are really worried about a mad cow,
when the cow is clinical and stumbling and staggering, TEXAS
does not bother TESTING the cow at all. nope, they just send
it directly to be rendered head and all to get rid of all evidence.
the june 2004 enhanced bse cover-up was just that. the USA
could test every cow that goes to slaughter, and it would be meaningless
unless properly done with the most sensitive testing to date.
but not in TEXAS or any other state in the USA.............


FDA Statement

FOR IMMEDIATE RELEASE
Statement
May 4, 2004

Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA


Statement on Texas Cow With Central Nervous System Symptoms

On Friday, April 30 th , the Food and Drug Administration learned that a
cow with central nervous system symptoms had been killed and shipped to
a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately
began an investigation. On Friday and throughout the weekend, FDA
investigators inspected the slaughterhouse, the rendering facility, the
farm where the animal came from, and the processor that initially
received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been
rendered into "meat and bone meal" (a type of protein animal feed). Over
the weekend FDA was able to track down all the implicated material. That
material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest
because cattle with bovine spongiform encephalopathy or BSE, also known
as "mad cow disease," can exhibit such symptoms. In this case, there is
no way now to test for BSE. But even if the cow had BSE, FDA's animal
feed rule would prohibit the feeding of its rendered protein to other
ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and
informing the firm that FDA will not object to use of this material in
swine feed only. If it is not used in swine feed, this material will be
destroyed. Pigs have been shown not to be susceptible to BSE. If the
firm agrees to use the material for swine feed only, FDA will track the
material all the way through the supply chain from the processor to the
farm to ensure that the feed is properly monitored and used only as feed
for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian
protein out of animal feed for cattle and other ruminant animals. FDA
established its animal feed rule in 1997 after the BSE epidemic in the
U.K. showed that the disease spreads by feeding infected ruminant
protein to cattle.

Under the current regulation, the material from this Texas cow is not
allowed in feed for cattle or other ruminant animals. FDA's action
specifying that the material go only into swine feed means also that it
will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates
closely with the U.S. Department of Agriculture on all BSE issues. The
animal feed rule provides crucial protection against the spread of BSE,
but it is only one of several such firewalls. FDA will soon be improving
the animal feed rule, to make this strong system even stronger.

####

http://www.fda.gov/bbs/topics/news/2004/NEW01061.html

-------- Original Message --------
Subject: Screening tests for animal TSE: present and future
Date: Sun, 1 May 2005 16:02:16 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org


##################### Bovine Spongiform Encephalopathy
##################### Tests de dépistage des ESST animales : présent et
futur Screening tests for animal TSE: present and future J.P. Deslysa
and J. Grassib , Corresponding Author Contact Information , E-mail The
Corresponding Author aCEA, groupe dinnovation diagnostique et
thérapeutique sur les infections à prions, département de recherche
médicale, CEA/Fontenay aux Roses, France bCEA, service de pharmacologie
et dimmunologie, département de recherche médicale, bâtiment 136,
CEA/Saclay, 91191 Gif sur Yvette cedex, France Received 23 February
2004; accepted 28 July 2004. Available online 21 September 2004. Résumé
En 1999, trois tests rapides (Prionics, Bio-rad et Enfer) ont été
validés par la Commission Européenne pour le diagnostic post-mortem de
l'ESB chez les bovins. Aujourd'hui, ils sont utilisés à grande échelle
sur le territoire européen. Ils reposent tous sur une détection
immunologique de la PrPres. En l'absence d'anticorps reconnaissant
spécifiquement la PrPres dans sa conformation native, la distinction
avec la forme normale de la PrP est obtenue sur la base des propriétés
biochimiques de la forme anormale (résistance à la protéinase K,
agrégation en présence de détergents). Dans tous les cas, ces tests
incluent une étape de dénaturation de la PrPres afin de permettre sa
détection à l'aide d'anticorps. Appliqués sur des populations de bovins
à risques ou sur les animaux abattus pour la consommation humaine, ils
ont permis de préciser l'étendue réelle de l'épizootie et d'éliminer
efficacement de la chaîne alimentaire les animaux présentant un risque
pour l'homme. Depuis 2002, ils sont aussi utilisés pour le diagnostic
post-mortem de la tremblante chez les ovins et les caprins. Cinq
nouveaux tests ont été récemment évalués par la Commission européenne
(ID-Lelystad ; Perkin-elmer, Prionics Check LIA, UCSF, Imperial college)
mais il est trop tôt pour évaluer la place qu'ils tiendront sur le
terrain. Les tests actuels permettent une détection préclinique des
ESSTs, notamment chez les ovins où une détection très précoce est
possible sur les organes lymphoïdes périphériques. Cependant, à ce jour,
aucun test sur animal vivant n'a été véritablement validé. Compte tenu
du nombre d'équipes de recherche maintenant mobilisées sur cet objectif,
il est raisonnable d'attendre des développements spectaculaires dans les
années à venir. Abstract In 1999, three rapid tests (Prionics, Bio-Rad,
Enfer) have been validated by the European Commission for the
post-mortem diagnosis of BSE in cattle. They are now used on a large
scale over the entire Europe. In absence of antibodies specifically
recognizing the native conformation PrPres, its selective determination
is based on the biochemical properties of this abnormal form (PK
resistance, aggregation in presence of detergents). In addition, all
these tests include a denaturation step so that PrP can be detected by
appropriate antibodies. When applied on risk populations or on
healthy animals entering into the human food chain, these rapid tests
have provided a better estimation of the epizootic and allowed an
efficient removal of animals bearing a risk for human consumption. Since
2002, they have also been used for the post-mortem diagnosis of scrapie
in sheep and goat. Five new tests have been recently evaluated
(ID-Lelystad; Perkin-elmer, Prionics Check LIA, UCSF, Imperial college)
but it is too early to know which place they will take in the field.
Current tests allow a preclinical diagnosis of TSE, especially in sheep
and goats for which a very early detection is possible in peripheral
lymphoid tissues. However, to date, no test on living animal has been
validated. Taking into account the important number of research teams
now involved on this topic one may expect spectacular progress in the
forthcoming years. Mots clés: Encéphalopathies spongiformes subaiguës
transmissibles (ESSTs); Encéphalopathie spongiforme bovine; diagnostic
des ESSTs; tests rapides; ELISA; western-blot; anticorps anti-PrP
Keywords: Transmissible spongiform encephalopathies (TSEs); bovine
spongiform encephalopathy; diagnosis of TSEs; rapid tests; ELISA;
western-blot; anti-PrP antibodies Corresponding Author Contact
Information Auteur correspondent.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W8H-4DCD84V-1&_co
verDate=05%2F31%2F2005&_alid=272857000&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi
=6655&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md
5=e550564d4bd0e589e21154c3b67bbc4c
TSS ############ https://www.lists.uni-karlsruhe.de/warc/bse-l.html
############


-------- Original Message --------
Subject: Discriminating BSE from Scrapie in sheep
Date: Sun, 1 May 2005 16:13:10 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org


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

Discriminating
BSE from scrapie
in sheep

A DISCRIMINATORY diagnostic kit to
distinguish between scrapie and BSE in
sheep has recently been launched by the
Veterinary Laboratories Agency (VLA).
DEFRA notes that EU legislation
requires that, from 2005, all samples
from small ruminants that are positive
for a TSE on rapid testing should be further
screened using an approved discriminatory
method. A small number
of methods have been evaluated and
approved. The method developed by
the VLA uses protein extraction and
Western blotting techniques to differentiate
between scrapie and BSE. The
new kit is a modified version of the
Prionics-Check technique and DEFRA
says it provides a cleaner, more defined
signal of the abnormal prion protein
profile for analysis.

http://veterinaryrecord.bvapublications.com/cgi/reprint/156/17/527-a

TSS

############ https://www.lists.uni-karlsruhe.de/warc/bse-l.html ############


WHY ELSE IS THE NIH NOW DESTROYING OUR LOVED
ONES BRAINS THAT WE STRAINED TO DONATE FOR SCIENCE? I will tell you why,
they know we are very very close
to strain typing and finding route and source of agent;

NIH sends mixed signals on CJD brains


By Steve Mitchell
Medical Correspondent

Washington, DC, Apr. 7 (UPI) --

Terry Singeltary, whose mother passed away from a type of CJD in 1997,
said the NIH should use the samples for scientific research, not just
store them in freezers.

Both Singeltary and Ewanitz said they would feel more reassured if Major
verified in writing the collection will not be destroyed.

"I would go further and ask Major what he plans to do with them,"
Singeltary said. "If the samples are just going to sit up there and go
bad, then they should give them out to researchers looking for cause and
cure."

snip...

http://washingtontimes.com/upi-breaking/20050407-110535-2570r.htm

United Press International: French woman may have had vCJD in 1971
... collection," said Terry Singeltary, who is associated with several
CJD patient
... died of a type of CJD called Heidenhain variant in 1997, told UPI. ...
www.upi.com/view.cfm?StoryID=20050323-061733-6847r - 11k - Cached
- Similar pages


United Press International: NIH may destroy human brain collection
... Terry Singeltary, whose mother died of a type of CJD called
Heidenhain ...
a lot of trouble to get these brain samples to the NIH," Singeltary
told UPI. ...
www.upi.com/view.cfm?StoryID=20050323-053919-8481r - 14k - Cached
- Similar pages


Groups seek to save NIH brain collection
... The NIH, as UPI reported last week, may destroy its collection of
brains and
... them is an outrage," Terry Singeltary, whose mom died of CJD in
1997, ...
www.sciencedaily.com/upi/index.php?feed=Science&
article=UPI-1-20050401-16375100-bc-us-nihbrains.xml - 44k - Cached
- Similar pages

Groups seek to save NIH brain collection - (United Press ...
... Singeltary's mother died of a type of CJD called Heidenhain variant
in 1997.
Hutchinson's office did not return a call from UPI. ...
washingtontimes.com/upi-breaking/ 20050401-033307-7296r.htm - 54k - Apr
11, 2005 - Cached
- Similar pages


French re-testing 1971 case for vCJD - (United Press International)
... Allied Countries Collaborative Study Group of CJD, wrote in an
e-mail to UPI.
... Singeltary, whose mother died of a type of CJD called the Heidenhain
...
www.washtimes.com/upi-breaking/ 20050331-095613-8807r.htm - 51k - Cached
- Similar pages


SouthAsiaNews.com - US health body to discard brain collection
... find a cure for the brain-wasting illness Creutzfeldt Jakob, reports
UPI. ...
Terry Singeltary, whose mother died of a type of CJD called Heidenhain ...
www.southasianews.com/showNews.asp?nid=1264 - 30k - Cached
- Similar pages


Mad Cow: Linked to thousands of CJD cases?


By Steve Mitchell
United Press International
Published 12/29/2003 9:50 AM

The U.S. government's monitoring system for cases of Creutzfeldt-Jakob
disease, a fatal human brain illness, could be missing tens of thousands
of victims, scientists and consumer advocates have told United Press
International. ...

http://www.upi.com/view.cfm?StoryID=20030721-102924-4786r


USDA vets question agency's mad cow lab

By Steve Mitchell
United Press International
Published 2/9/2004 7:06 PM

WASHINGTON, Feb. 9 (UPI) -- The federal laboratory in Ames, Iowa, that
conducts all of the nation's tests for mad cow disease has a history of
producing ambiguous and conflicting results -- to the point where many
federal meat inspectors have lost confidence in it, Department of
Agriculture veterinarians and a deer rancher told United Press
International.

The veterinarians also claim the facility -- part of the USDA and known
as the National Veterinary Services Laboratories -- has refused to
release testing results to them and has been so secretive some suspect
it is covering up additional mad cow cases. ...

http://www.upi.com/view.cfm?StoryID=20040209-061848-3665r


UPI Exclusive: No mad cow tests in Wash.

By Steve Mitchell
United Press International
Published 1/15/2004 2:46 PM

WASHINGTON, Jan. 15 (UPI) -- Federal agriculture officials did not test
any commercial cattle for mad cow disease through the first seven months
of 2003 in Washington state -- where the first U.S. case of the disease
was detected last month -- according to records obtained by United Press
International.

The U.S. Department of Agriculture's records of mad cow screenings,
conducted on 35,000 animals between 2001 to 2003, also reveal no animals
were tested for the past two years at Vern's Moses Lake Meats, the
Washington slaughterhouse where the mad cow case was first detected.

In addition, no mad cow tests were conducted during the two-year period
at any of the six federally registered slaughterhouses in Washington
state. This includes Washington's biggest slaughterhouse, Washington
Beef in Toppeni$h -- the 17th largest in the country, which slaughters
290,000 head per year -- and two facilities in Pasco that belong to
Tyson, the largest beef slaughtering company in the United States.

In 2002, nearly every test conducted in Washington was on animals from
Midway Meats in Centralia, the packing plant where Vern's Moses sent the
infected cow carcass. The meat was distributed to several states where
some people apparently consumed it, raising concerns about the
possibility of contracting the human equivalent of mad cow, an always
fatal, brain-wasting condition known as variant Creutzfeldt-Jakob
disease. ...

http://www.upi.com/view.cfm?StoryID=20040114-041124-1470r


Mad Cow: Prion research misguided?

By Steve Mitchell
United Press International
Published 12/29/2003 9:30 AM

http://www.upi.com/view.cfm?StoryID=20030701-094458-6348r


There will be several more emails of my research to follow.

I respectfully request a full inquiry into the cover-up of TSEs
in the United States of America over the past 30 years. I
would be happy to testify...

Thank you,
I am sincerely,

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
281-559-3131


Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW
BSE SAFEGUARDS (comment submission)

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08
d?OpenDocument

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


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


Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html


PART 2


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html


PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...


http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf


Asante/Collinge et al, that BSE transmission to the 129-methionine

genotype can lead to an alternate phenotype that is indistinguishable

from type 2 PrPSc, the commonest _sporadic_ CJD;


http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice
in Manufacturing, Packing, or Holding Dietary Ingredients a
Comment Number: EC -2
Accepted - Volume 7

http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm


[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML
Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of
those who provided comments in response to Docket No. ...
Meager 8/18/01 Terry S. Singeltary Sr ...


www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food
Facilities, Section 305
Comment Number: EC-254 [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm


Dockets Entered On October 2, 2003 Table of Contents, Docket #,
Title, 1978N-0301,

OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr.
Vol #: 1, ...

www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm


Daily Dockets Entered on 02/05/03

DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2.
... Vol#: 1.

03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...


www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm


Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html


Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003
- Cached


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 1
Terry S. Singeltary Sr.
Vol #:
1

http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm


2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1

2003D-0186
Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 7
Terry S. Singeltary Sr.
Vol #:
1


http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm

Send Post-Publication Peer Review to journal:


Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States


Email Terry S. Singeltary:


flounder@wt.net


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


http://www.neurology.org/cgi/eletters/60/2/176#535


LANCET INFECTIOUS DISEASE JOURNAL


Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost

my mom to hvCJD (Heidenhain variant CJD) and have been searching for

answers ever since. What I have found is that we have not been told the

truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained

largely unsatisfied after being told that a close relative died from a

rapidly progressive dementia compatible with spontaneous

Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of

documents on transmissible spongiform encephalopathies (TSE) and

realised that if Britons could get variant CJD from bovine spongiform

encephalopathy (BSE), Americans might get a similar disorder from

chronic wasting disease (CWD)the relative of mad cow disease seen among

deer and elk in the USA. Although his feverish search did not lead him

to the smoking gun linking CWD to a similar disease in North American

people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the

occurrence of CJD and CWD in the USA. Only a few states have made CJD

reportable. Human and animal TSEs should be reportable nationwide and

internationally, he complained in a letter to the Journal of the

American Medical Association (JAMA 2003; 285: 733). I hope that the CDC

does not continue to expect us to still believe that the 85% plus of all

CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small

region in Colorado. But since early 2002, it has been reported in other

areas, including Wisconsin, South Dakota, and the Canadian province of

Saskatchewan. Indeed, the occurrence of CWD in states that were not

endemic previously increased concern about a widespread outbreak and

possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be

transmitted to cattle by intracerebral inoculation and that it can cross

the mucous membranes of the digestive tract to initiate infection in

lymphoid tissue before invasion of the central nervous system. Yet the

plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD

is only reported in those areas known to be endemic foci of CWD.

Moreover, US authorities have been criticised for not having performed

enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration

issued a directive to state public-health and agriculture officials

prohibiting material from CWD-positive animals from being used as an

ingredient in feed for any animal species, epidemiological control and

research in the USA has been quite different from the situation in the

UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling

teeth, Singeltary argues. You get it when they want you to have it,

and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the

University of Michigan (Ann Arbor, MI, USA), says that current

surveillance of prion disease in people in the USA is inadequate to

detect whether CWD is occurring in human beings; adding that, the

cases that we know about are reassuring, because they do not suggest the

appearance of a new variant of CJD in the USA or atypical features in

patients that might be exposed to CWD. However, until we establish a

system that identifies and analyses a high proportion of suspected prion

disease cases we will not know for sure. The USA should develop a

system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently

reported the cases of three hunterstwo of whom were friendswho died

from pathologically confirmed CJD, says that at present there are

insufficient data to claim transmission of CWD into humans; adding that

[only] by asking [the questions of venison consumption and deer/elk

hunting] in every case can we collect suspect cases and look into the

plausibility of transmission further. Samii argues that by making both

doctors and hunters more aware of the possibility of prions spreading

through eating venison, doctors treating hunters with dementia can

consider a possible prion disease, and doctors treating CJD patients

will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating

the [Samii] cases because there is no evidence that the men ate

CWD-infected meat. He notes that although the likelihood of CWD

jumping the species barrier to infect humans cannot be ruled out 100%

and that [we] cannot be 100% sure that CWD does not exist in humans&

the data seeking evidence of CWD transmission to humans have been very

limited.

http://infection.thelancet.com/journal/journal.isa

he complained in a letter to the Journal of the American Medical


Association (JAMA 2003; 285: 733). I hope that the CDC does not

continue to expect us to still believe that the 85% plus of all CJD

cases which are sporadic are all spontaneous, without route or source.<<<


actually, that quote was from a more recent article in the Journal of

Neurology (see below), not the JAMA article...


Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=
10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&
searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama


BRITISH MEDICAL JOURNAL


SOMETHING TO CHEW ON


BMJ


http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2


BMJ


http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1


THE PATHOLOGICAL PROTEIN

BY Philip Yam

Yam Philip Yam News Editor Scientific American www.sciam.com
http://www.thepathologicalprotein.com/

IN light of Asante/Collinge et al findings that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'flounder@wt.net'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.


I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.


Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


AND 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


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

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

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


ALL animals for human/animal consumption must be tested for TSE.

ALL human TSE must be made reportable Nationally and Internationally,
of ALL AGES...TSS


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
281-xxx-xxxx





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