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From: TSS ()
Subject: USDA ANNOUNCES BSE ROUNDTABLE DISCUSSION
Date: May 18, 2005 at 1:40 pm PST

-------- Original Message --------
Subject: USDA ANNOUNCES BSE ROUNDTABLE DISCUSSION
Date: Tue, 17 May 2005 13:55:22 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org


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

Release No. 0168.05

Jim Rogers (202) 690-4755
Jerry Redding (202) 720-6959

USDA ANNOUNCES BSE ROUNDTABLE DISCUSSION


WASHINGTON, May 17, 2005-Agriculture Secretary Mike Johanns today announced that the U.S. Department of Agriculture (USDA) will hold a roundtable discussion on June 9 regarding the safety of North American beef and the changing infrastructure of the industry. Johanns noted that data illustrating the success of USDA's enhanced BSE surveillance program will be part of the roundtable discussion entitled "The Safety of North American Beef and the Economic Effect of BSE on the U.S. Beef Industry."

"It is time to clearly present the science that underlies the safety of North American beef and examine the changing infrastructure of the industry," Johanns said. "It is remarkable that we've not found a single new case of BSE throughout our year-long aggressive search. Now it is time to put into perspective for producers, processors, and decision-makers the facts and the future implications of the course we are following."

The enhanced surveillance program targets the population of animals in which BSE is most likely to be detected, including non-ambulatory or downer animals, animals exhibiting signs of a central nervous system disorder or any other signs that could be consistent with BSE and animals that die from unknown causes. More than 350,000 animals have been tested and all have been negative.

The event will bring together USDA experts, producers, packers, other industry groups and academia to discuss the science of BSE and the economic impacts on the U.S. beef industry.

The roundtable discussion will be open to the public and held on Thursday, June 9, from 9:30-2:30 at the Andrew Boss Laboratory, University of Minnesota, St. Paul campus, St. Paul, MN. Potential participants will receive invitations.

#

USDA News
oc.news@usda.gov
202 720-4623


http://www.usda.gov/2005/05/0168.xml

>USDA ANNOUNCES BSE ROUNDTABLE DISCUSSION


not...


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

TSS

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA

#################### https://lists.aegee.org/bse-l.html ####################


Gerald Wells: Report of the Visit to USA, April-May 1989

snip...

The general opinion of those present was that BSE, as an
overt disease phenomenon, _could exist in the USA, but if it did,
it was very rare. The need for improved and specific surveillance
methods to detect it as recognised...

snip...

It is clear that USDA have little information and _no_ regulatory
responsibility for rendering plants in the US...

snip...

3. Prof. A. Robertson gave a brief account of BSE. The US approach
was to accord it a _very low profile indeed_. Dr. A Thiermann showed
the picture in the ''Independent'' with cattle being incinerated and thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...

snip...

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

To be published in the Proceedings of the
Fourth International Scientific Congress in
Fur Animal Production. Toronto, Canada,
August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

ēDepartment of Veterinary Science, University of Wisconsin-Madison, Madison,
Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT
Epidemiologic investigation of a new incidence of
transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin
suggests that the disease may have resulted from feeding infected
cattle to mink. This observation is supported by the transmission of
a TME-like disease to experimentally inoculated cattle, and by the
recent report of a new bovine spongiform encephalopathy in
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
and Burger who demonstrated that the disease was transmissible with a long incubation
period, and that affected mink had a spongiform encephalopathy similar to that found in
scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965).
Because of the similarity between TME and scrapie, and the subsequent finding that the
two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was
concluded that TME most likely resulted from feeding mink scrapie-infecied sheep.
The experimental transmission of sheep scrapie to mink (Hanson et al., 1971)
confirmed the close association of TME and scrapie, but at the same time provided
evidence that they may be different. Epidemiologic studies on previous incidences of
TME indicated that the incubation periods in field cases were between six months and
one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be
transmitted to mink in less than one year.
To investigate the possibility that TME may be caused by a (particular strain of
scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie
agent, including their sheep or goat sources, were inoculated into a total of 61 mink.
Only one mink developed a progressive neurologic disease after an incubation period of
22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused
by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent
from an unidentified source.

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin
reported that many of his mink were "acting funny", and some had died. At this time, we
visited the farm and found that approximately 10% of all adult mink were showing
typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of
normal habits of cleanliness, deposition of droppings throughout the pen rather than in a
single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over
their _backs like squirrels. These signs were followed by progressive deterioration of
neurologic function beginning with locomoior incoordination, long periods of somnolence
in which the affected mink would stand motionless with its head in the corner of the
cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
practices, we obtained a careful history of feed ingredients used over the past 12-18
months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy
cattle and a few horses. Sheep had never been fed.

Experimental Transmission. The clinical diagnosis of TME was confirmed by
histopaihologic examination and by experimental transmission to mink after incubation
periods of four months. To investigate the possible involvement of cattle in this disease
cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally
with a brain suspension from affected mink. Each developed a fatal spongiform
encephalopathy after incubation periods of 18 and 19 months.

DISCUSSION
These findings suggest that TME may result from feeding mink infected cattle and
we have alerted bovine practitioners that there may exist an as yet unrecognized
scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new
bovine spongiform encephalopathy has recently been reported in England (Wells et al.,
1987), and investigators are presently studying its transmissibility and possible
relationship to scrapie. Because this new bovine disease in England is characterized by
behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be
confused with rabies in the United Stales and not be diagnosed. Presently, brains from
cattle in the United States which are suspected of rabies infection are only tested with
anti-rabies virus antibody and are not examined histopathologically for lesions of
spongiform encephalopathy.
We are presently pursuing additional studies to further examine the possible
involvement of cattle in the epidemiology of TME. One of these is the backpassage of
our experimental bovine encephalopathy to mink. Because (here are as yet no agent-
specific proteins or nucleic acids identified for these transmissible neuropathogens, one
means of distinguishing them is by animal passage and selection of the biotype which
grows best in a particular host. This procedure has been used to separate hamster-
adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral
backpassage of the experimental bovine agent resulted in incubations of only four months
indicating no de-adaptation of the Stetsonville agent for mink after bovine passage.
Mink fed infected bovine brain remain normal after six months. It will be essential to
demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic
association is to be confirmed.

ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences,
University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United
States Department of Agriculture. The authors also wish to acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and
natural transmission. J. Infec. Dis. 115:393-399.
Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson,
D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861.
Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and
clinical observations. 3. Infec. Dis. 115:387-392.
Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the
transmissible mink encephalopathy agent. 3. ViroL 3:176-180.
Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink
encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible
diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460.
Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle?
Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary
Medicine. University of Arizona, pp 20.
Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M.,
Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

TSS



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