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From: TSS ()
Subject: WHY WANT JOHANN SPEAK OF THE TEXAS MAD COWS THEY COVER-UP, like he speaks of the 1997 suspect cows ???
Date: April 15, 2005 at 6:24 am PST

-------- Original Message --------
Subject: [Fwd: Release No. 0128.05 Washington, D.C. - April 14, 2005]
Date: Fri, 15 Apr 2005 08:30:51 -0500
From: "Terry S. Singeltary Sr."
To: Gary Burkholder , BillBullard@R-Calfusa.com, mike@nobull.net

-------- Original Message --------
Subject: Release No. 0128.05 Washington, D.C. - April 14, 2005
Date: Fri, 15 Apr 2005 08:28:17 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy

MODERATOR: "Ron Hayes of Clear Channel Agriculture Network in Oklahoma
City will be next with his question. And he'll be followed by Bill Tomson.

"Ron, go ahead."

REPORTER: "Thank you, Larry. Good morning, Mr. Secretary. Greetings from
Oklahoma. A couple questions in regards to BSE. The Canadian media seems
to be all abuzz with some allegations from a former USDA employee in
regards to potentially mishandling some cases really back in the 1990s,
1997. Does this have any bearing or does this give us any problems as
far as assuring our consumers here, assuring our consumers overseas
about the safety of our beef supply?

"And then secondly, related to that are expanded BSE surveillance effort
going on right now here in 2004, 2005 over 314,000 critters have been
tested all negative. How long do we go? In other words, how many more
animals are we going to test in this expanded surveillance effort?"

SEC. JOHANNS: "In reference to your first question, the gentleman that
is making these allegations is really doing so with no proof whatsoever.
There's just no mileage whatsoever in the USDA not being absolutely
transparent. And in fact if we've had any criticism as you know, the
criticism has been along the lines of why are you publishing false
positives? And the whole effort there was to just get the information
out so the claim could not be made that we were trying to cover
something up as this gentleman is claiming. He gets a lot of attention
because he makes baseless claims, and that's really what it comes down
to. There just isn't any accuracy in what he's saying.

"Again there's just no mileage in approaching the testing this way. We
feel very strongly that that testing needs to get out even to the point
of publishing the false positives-- which like I said we've been
criticized about because we've been so transparent there.

"The other thing I would mention in terms of the other question that you
asked, you had a second question there. If you could run that by me again?"

MODERATOR: "The second question related to the effect on the markets."

SEC. JOHANNS: "Oh, Larry, thank you. The effect on the markets? We're
not seeing the effect. We're not seeing anybody buying in to what he's
trying to sell. I think it's getting some media attention in Canada just
simply because they've been so involved with working with us to try to
get the border reopened. But no. My phone is not ringing over this. Like
I said, he just doesn't have any proof, and his baseless claims just
aren't causing my phone to ring on this one."

MODERATOR: "And I'm reminded he did ask about how many more animals
would be tested."

SEC. JOHANNS: "The other piece of your question relative to the number
of animals being tested, we've tested 314,000. As of just a couple days
ago. Fortunately all those tests have been negative. One of things that
we want to make sure of is we've touched the bases, we've hit the areas
of the country that we want to test, and so we're looking at that. We
want to make sure that everything we headed out to do we've done.
Somewhere out here in the next few months we'll take a look at that. As
you point out, it is a surveillance effort; it is not a food safety
effort. Our whole goal is to get an idea of what the herd in the United
States looked like relative to BSE. And we're doing that.

"So in the next few months we'll be making an evaluation as to where we
go here in terms of that increased surveillance and the number of tests
to continue in the future."

snip...

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/04/0128.xml

> we've tested 314,000. As of just a couple days ago. Fortunately all
> those tests have been negative


IF you consider the pos. pos. incl. negs, WITHOUT WB,
and the mad cow in Texas they rendered without testing
at all, IT is my opinion that the USA has documented
4 mad cows besides the one dave capped. UNTIL the USDA
comes forward about these cows and produce evidence
(RETEST WITH WB), they are simply not telling the truth.
I could care less about these cows in 97. I want the ones they
cover-up in 2003-4-5. WHY want the USDA comment on
these like they are on the ones in 1997? because they know
i am correct, and they simply refuse to go there. WHY then
after all these years of using WB for confirmation, why then
did they decide not to continue using WB?


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.... snip ...END Dr.
Jean-Philippe Deslys, Head, Prions Research Group, Atomic Energy
Commission, France Q&A Prof. Adriano Aguzzi Dear Mr. Singeltary I
sympathize with your wish to have the most sensitive assay implemented.
However, the situation is not as simple as one might think. In the case
of homogeneously distributed agent, biochemical detection of PrPSc is
indeed likely to be more sensitive than immunohistochemistry. In the
case of variegated, punctate distribution of the agent, morphological
methods may indeed be an asset. There are also issues of feasibility. In
my laboratory, we routinely run phosphotungstic acid precipitation
followed by Western blotting. However, this is an extraordinarily
cumbersome procedure. The sensitivity is increased vastly, but the
amount of work needed is also amazing. There is no way I could see our
own procedure implemented for mass screening of millions of cows -
unless one would draft a veritable army of laboratory technicians. For
all these reasons, while I see all your points, I feel unable to offer a
strong public opinion in favor or against any specific methods. The
final decision needs to take into account a variety of complex factors,
and that is why I believe that it is best left to a panel of experts
rather than to a public discussion. Best regards Adriano Aguzzi
____________________________ Prof. Adriano Aguzzi (MD PhD hc FRCP
FRCPath) Institute of Neuropathology, University Hospital of Zürich
Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland Tel. ++41-1-255 2107
Tel. (direct line): 2869 Fax: ++41-1-255 4402, cellular: +41-79-320 1516
http://www.unizh.ch/pathol/neuropathologie/
=========================================== PNAS | March 1, 2005 | vol.
102 | no. 9 | 3501-3506 NEUROSCIENCE Diagnosis of human prion disease
Jiri G. Safar *, , Michael D. Geschwind , Camille Deering *, Svetlana
Didorenko *, Mamta Sattavat ¶, Henry Sanchez ¶, Ana Serban *, Martin
Vey ||, Henry Baron **, Kurt Giles *, , Bruce L. Miller , Stephen J.
DeArmond *, ¶ and Stanley B. Prusiner * *Institute for
Neurodegenerative Diseases, Memory and Aging Center, and Departments of
Neurology, ¶Pathology, and Biochemistry and Biophysics, University of
California, San Francisco, CA 94143; ||ZLB Behring, 35041 Marburg,
Germany; and **ZLB Behring, 75601 Paris, France Contributed by Stanley
B. Prusiner, December 22, 2004 AB Abstract With the discovery of the
prion protein (PrP), immunodiagnostic procedures were applied to
diagnose Creutzfeldtâ¬Jakob disease (CJD). Before development of the
conformation-dependent immunoassay (CDI), all immunoassays for the
disease-causing PrP isoform (PrPSc) used limited proteolysis to digest
the precursor cellular PrP (PrPC). Because the CDI is the only
immunoassay that measures both the protease-resistant and
protease-sensitive forms of PrPSc, we used the CDI to diagnose human
prion disease. The CDI gave a positive signal for PrPSc in all 10â¬24
brain regions (100%) examined from 28 CJD patients. A subset of 18 brain
regions from 8 patients with sporadic CJD (sCJD) was examined by
histology, immunohistochemistry (IHC), and the CDI. Three of the 18
regions (17%) were consistently positive by histology and 4 of 18 (22%)
by IHC for the 8 sCJD patients. In contrast, the CDI was positive in all
18 regions (100%) for all 8 sCJD patients. In both gray and white
matter, 90% of the total PrPSc was protease-sensitive and, thus, would
have been degraded by procedures using proteases to eliminate PrPC. Our
findings argue that the CDI should be used to establish or rule out the
diagnosis of prion disease when a small number of samples is available
as is the case with brain biopsy. Moreover, IHC should not be used as
the standard against which all other immunodiagnostic techniques are
compared because an immunoassay, such as the CDI, is substantially more
sensitive... snip... Discussion snip... The studies reported here are
likely to change profoundly the approach to the diagnosis of prion
disease in both humans and livestock (31 33). The superior performance
of the CDI in diagnosing prion disease compared to routine
neuropathologic examination and IHC demands that the CDI be used in
future diagnostic evaluations of prion disease. Prion disease can no
longer be ruled out by routine histology or IHC. Moreover, the use of
IHC to confirm cases of bovine spongiform encephalopathy after detection
of bovine PrPSc by the CDI (10) seems an untenable approach in the
future. Clearly, the CDI for HuPrPSc is as sensitive or more sensitive
than bioassays in Tg(MHu2M) mice (Fig. 1). Our results suggest that
using the CDI to test large numbers of samples for human prions might
alter the epidemiology of prion diseases. At present, there is limited
data on the frequency of subclinical variant CJD infections in the U.K.
population (34). Because appendixes and tonsils were evaluated only by
IHC, many cases might have escaped detection (Tables 1 and 2). Equally
important may be the use of CDI-like tests to diagnose other
neurodegenerative disorders, such as Alzheimer's disease, Parkinson's
disease, and the frontotemporal dementias. Whether IHC underestimates
the incidence of one or more of these common degenerative diseases is
unknown. Moreover, CDI-like tests may help determine the frequency with
which these disorders and the prion diseases occurs concomitantly in a
single patient (35, 36).
http://www.pnas.org/cgi/content/abstract/102/9/3501 Dr. Dehaven, this
brings me back to those other TEXAS cows, those at the Purina Gonzales
feed mill. FDA stated ; > FOR IMMEDIATE RELEASE P01-05 January 30, 2001
snip... > FDA has determined that each animal could have consumed, at
most and > in total, five-and-one-half grams - approximately a quarter
ounce -- > of prohibited material. These animals weigh approximately 600
pounds. > snip... > It is important to note that the prohibited material
was domestic in > origin (therefore not likely to contain infected
material because > there is no evidence of BSE in U.S. cattle), fed at a
very low level, > and fed only once. The potential risk of BSE to such
cattle is > therefore exceedingly low, even if the feed were
contaminated. > snip...
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html Subject: 1 in 2
CHANCE OF GETTING BSE AKA MAD COW BY THE ORAL ROUTE (PRIMATE STUDY)
Date: January 27, 2005 at 7:03 am PST Risk of oral infection with bovine
spongiform encephalopathy agent in primates Corinne Ida Lasmézas,
Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm
Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray,
Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The
uncertain extent of human exposure to bovine spongiform encephalopathy
(BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is
compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain
homogenate from a BSE-infected cow. One macaque developed vCJD-like
neurological disease 60 months after exposure, whereas the other
remained free of disease at 76 months. On the basis of these findings
and data from other studies, we made a preliminary estimate of the food
exposure risk for man, which provides additional assurance that existing
public health measures can prevent transmission of BSE to man. Published
online January 27, 2005 http://www.thelancet.com/journal/journal.isa or
BSE/TSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts [BBC
radio 4 FARM news] (audio realplayer LISTEN)
http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram THE ONE THAT GOT
AWAY Statement on Texas Cow With Central Nervous System Symptoms
horizonal rule 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). snip...
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html What GAO Found
United States Government Accountability Office Why GAO Did This Study
Highlights Accountability Integrity Reliability
www.gao.gov/cgi-bin/getrpt?GAO-05-101.

TSS






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