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From: TSS ()
Subject: Keep Mad Cow Disease Out of the US Food Supply! Keep the Border Closed! DEHAVEN TO TSS and TSS REPLY
Date: March 31, 2005 at 11:20 am PST

-------- Original Message --------
Subject: Re: Keep Mad Cow Disease Out of the US Food Supply! Keep the Border Closed!
Date: Wed, 30 Mar 2005 16:20:07 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy

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

Hello Dr. Ron Dehaven,

Many thanks for your kind reply.

However, I have some problems with your assessment of the risk factor
and the science to date on TSE/BSE/CJD. I don't wish to debate this
with you, simply show you the science. You did not respond to some of
the serious issues I presented i.e. ;

Why WB was not used to help confirm the final diagnosis of the last
positive, positive, inconclusive, that eventually was announced as
negative, without WB ?

Why the stumbling and staggering Texas cow was rendered without being tested ?

Why USDA et al are abandoning the BSE GBR risk assessments ?

Why were those Vermont atypical TSE sheep mouse bio-assays put off for 2 years ?

Mr Dehaven states ;

>In seeking to establish the possible prevalence of BSE in this country, it is most efficient and effective for us to focus our surveillance resources on the segment of the cattle population where the disease is most likely to be identified if it is present. This includes adult cattle that exhibit some type of clinical sign that could be considered consistent with the diseaseCincluding, among others, nonambulatory cattle, those condemned at slaughter because of signs of central nervous system disorders, and those that die on farms for unexplained reasons.

ODD that the 1st BSE cow in Washington that Dave capped, was a healthy walker, one
that did NOT show signs of a CNS disorder, just capped in the wrong spot ;

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

Mr. Dehaven states ;

> The goal of our enhanced surveillance is to sample as many of the animals in the targeted population as we can during a 12- to 18-month period. We estimate that the targeted population is approximately 446,000 animals, or about 1 percent of the total adult cattle population. So far, from June 1, 2004, to March 20, 2005, we have tested more than 284,200 samples, all of which were confirmed negative for BSE.

BUT, we have had one very suspicious CNS (stumbling and staggering) cow that was
refused testing and sent directly to render head and all to be rendered, and 3
inconclusives that I am aware of that were declared BSE/TSE free WITHOUT Western
Blot confirmation, when the first case of BSE in the USA WAS confirmed with
Western Blot, all this is very suspicious to me (the lay public/consumer).
PLUS, we have the recent GAO report, which was most disturbing, but exactly what
I have been saying for years (see references below)...

Mr. Dehaven states ;

>With regard to BSE testing technology, we assure you that our testing methods are scientifically sound and are comparable to those used in Europe and elsewhere. In selecting rapid screening tests for BSE, officials with the USDA's Center for Veterinary Biologics compare the test kit's sensitivity and specificity-the ability of a test to identify known positive and negative animals-to the immunohistochemistry (IHC) test, the internationally recognized standard.

This is NOT correct Sir !

>We would like to emphasize that the test kits are only used for screening purposes. If any rapid test produces a non?negative result, the sample is forwarded to USDA's National Veterinary Services Laboratories in Ames, Iowa, for confirmatory testing. USDA uses the IHC test to confirm the results.

Q&A Dr. Jean-Philippe Deslys

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

The regime is an initial screening by a high-output test, the Bio-Rad test. If a result raises suspicion, a confirmatory test is conducted with the Western blot test.

2. How long has this been the case?

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

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

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

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

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

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

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

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

This his a very recent phenomenon. I have no opinion on its virulence. We do not know where it comes from. It could be a version of sporadic infection. Western blot caught them, but we would not even know it existed if we weren’t running systematic testing in the EU.

BSE was around for a long time before we caught it and by then, it was everywhere. It had become highly infectious. It probably amplified due to low-temperature rendering. The disease was recycled through the food chain, and was given time to amplify. By the time it was identified, even good cooking couldn’t eliminate it.

I can’t stress enough that systematic testing is necessary. Withdrawing all positives from the food chain is the best way to break the cycle.

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

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

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

snip ...END

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

Q&A Prof. Adriano Aguzzi

Dear Mr. Singeltary

I sympathize with your wish to have the most sensitive assay implemented.
However, the situation is not as simple as one might think. In the case of
homogeneously distributed agent, biochemical detection of PrPSc is indeed
likely to be more sensitive than immunohistochemistry. In the case of
variegated, punctate distribution of the agent, morphological methods may
indeed be an asset.

There are also issues of feasibility. In my laboratory, we routinely run
phosphotungstic acid precipitation followed by Western blotting. However,
this is an extraordinarily cumbersome procedure. The sensitivity is
increased vastly, but the amount of work needed is also amazing. There is
no way I could see our own procedure implemented for mass screening of
millions of cows - unless one would draft a veritable army of laboratory

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


PNAS | March 1, 2005 | vol. 102 | no. 9 |
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



With the discovery of the prion protein (PrP), immunodiagnostic
procedures were applied to diagnose Creutzfeldt–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 10–24 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...




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).

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


> 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.


> 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.



Date: January 27, 2005 at 7:03 am PST

Risk of oral infection with bovine spongiform encephalopathy agent in

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


[BBC radio 4 FARM news] (audio realplayer LISTEN)


Statement on Texas Cow With Central Nervous System Symptoms

horizonal rule

FDA 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).


What GAO Found
United States Government Accountability Office
Why GAO Did This Study
Accountability Integrity Reliability
To view the full product, including the scope
and methodology, click on the link above.
For more information, contact Robert A.
Robinson at (202) 512-3841 or
Highlights of GAO-05-101, a report to
congressional requesters
February 2005
FDA’s Management of the Feed Ban Has
Improved, but Oversight Weaknesses
Continue to Limit Program Effectiveness
FDA has made needed improvements to its management and oversight of the
feed-ban rule in response to GAO’s 2002 report, but program weaknesses
continue to limit the effectiveness of the ban and place U.S. cattle at risk of
spreading BSE. Improvements made include FDA establishing a uniform
method of conducting compliance inspections and training FDA inspectors,
as well as state inspectors who carry out inspections under agreements with
FDA, on the new method. FDA also implemented new data-entry procedures
that are designed to more reliably track feed-ban inspection results.
Consequently, FDA has a better management tool for overseeing compliance
with the feed-ban rule and a data system that better conforms to standard
database management practices. However, various program weaknesses
continue to undermine the nation’s firewall against BSE. For example:
• FDA acknowledges that there are more feed manufacturers and
transporters, on-farm mixers, and other feed industry businesses that are
subject to the feed ban than the approximately 14,800 firms inspected to
date; however, it has no uniform approach for identifying additional
• FDA has not reinspected approximately 2,800, or about 19 percent, of
those businesses, in 5 or more years; several hundred are potentially
high risk. FDA does not know whether those businesses now use
prohibited material in their feed.
• FDA’s feed-ban inspection guidance does not include instructions to
routinely sample cattle feed to test for potentially prohibited material as
part of the compliance inspection. Instead, it includes guidance for
inspectors to visually examine facilities and equipment and review
invoices and other documents.
• Feed intended for export is not required to carry a caution label “Do not
feed to cattle or other ruminants,” when the label would be required if
the feed were sold domestically. Without that statement, feed containing
prohibited material could be inadvertently or intentionally diverted back
to U.S. cattle or given to foreign cattle.
• FDA has not always alerted USDA and states when it learned that cattle
may have been given feed that contained prohibited material. This lapse
has been occurring even though FDA’s guidance calls for such
• Although research suggests that cattle can get BSE from ingesting even a
small amount of infected material, inspectors do not routinely inspect or
review cleanout procedures for vehicles used to haul cattle feed.
More than 5 million cattle across
Europe have been killed to stop the
spread of bovine spongiform
encephalopathy (BSE), commonly
called mad cow disease. Found in
26 countries, including Canada and
the United States, BSE is believed
to spread through animal feed that
contains protein from BSE-infected
animals. Consuming meat from
infected cattle has also been linked
to the deaths of about 150 people
worldwide. In 1997, the Food and
Drug Administration (FDA) issued
a feed-ban rule prohibiting certain
animal protein (prohibited
material) in feed for cattle and
other ruminant animals. FDA and
38 states inspect firms in the feed
industry to enforce this critical
firewall against BSE. In 2002, GAO
reported a number of weaknesses
in FDA’s enforcement of the feed
ban and recommended corrective
actions. This report looks at FDA’s
efforts since 2002 to ensure
industry compliance with the feed
ban and protect U.S. cattle.
What GAO Recommends
GAO recommends FDA, among
other things, develop procedures
for finding additional firms subject
to the feed-ban and using tests to
augment inspections. FDA said the
study was thorough but disagreed
on four of nine recommendations.
GAO continues to believe that,
given the discovery of BSE in North
America and the oversight gaps
described in the report, the
recommended actions are needed
to protect U.S. cattle from BSE.

Highlights -

GAO-05-51, FOOD SAFETY: USDA and FDA Need to Better Ensure Prompt and Complete Recalls of ...

... Discovery of an Animal in the United States Infected with BSE 39 Beef Recall Was Triggered by a BSE-Positive Sample from One Cow 39 Recall Begun in December ... Actions Related to the Discovery of an Animal Infected with BSE 45 Table 4: USDA and FDA Actions on GAO’s ...

"Controls Can Be Strengthened to Reduce the Risk of Disease Linked to Unsafe Animal Feed" (GAO/RCED-00255).

GAO-02-183: Mad Cow Disease: Improvements in the Animal Feed Ban and Other Regulatory Areas Would Strengthen U.S. Prevention Efforts

GAO-02-183, Mad Cow Disease: Improvements in the Animal Feed Ban and Other Regulatory Areas Would Strengthen U.S. Prevention Efforts

September 2000 FOOD SAFETY
Controls Can Be
Strengthened to
Reduce the Risk of
Disease Linked to
Unsafe Animal Feed


In 1997, FDA issued a regulation to prevent BSE in the United
States. To assess compliance with this regulation, FDA and state inspectors
have visited over 9,100 firms, such as farms that produce their own feed
and rendering plants that process meat scraps for animal feed. Inspectors
found that, among other things, nearly 1,700 firms were not aware of the
regulation and thus could produce or use animal feed that was not in


Page 11 GAO/RCED-00-255 Safety of Animal Feed
BSE Regulation Has Not
Been Fully Implemented by
the Feed Industry
To determine how firms were implementing the June 1997 BSE regulation,
FDA, with the assistance of state officials, inspected over 9,100 firms from
January 1998 through January 2000. Table 1 shows the types and number of
firms inspected.
Table 1: Types of Firms Inspected
a Includes haulers and distributors of feed, and firms or persons who receive prohibited
materials directly from manufacturers.
Source: FDA.
The BSE inspection results revealed that 1,688 of the 9,184 firms were not
aware of the new BSE feed regulation. Furthermore, inspection results of
the 2,481 firms that were identified as handling “prohibited” material—
Type of firm Number of firms inspected
Licensed feed mill 1,029
Nonlicensed feed mill 4,901
Ruminant feeder 1,400
Dairy farm 495
Renderer 211
Protein blender 121
Othera 1,027
Total 9,184
Page 12 GAO/RCED-00-255 Safety of Animal Feed
material that is not allowed to be fed to ruminants—revealed some serious
deficiencies. For example:
• Required cautionary statement not on product label. Of the firms
inspected, 699, or 28 percent, did not label their products with the
required cautionary statement that the feed should not be fed to cattle
or other ruminants.
• Required records not properly maintained. One-hundred and thirtyseven
firms, or about 6 percent, did not properly maintain the name and
address of the consignee of their products, which would make it difficult
to trace sales of contaminated feed.
In addition, of the 1,771 firms that manufacture both prohibited and
nonprohibited material, 361, or 20 percent, did not have a system in place
to prevent commingling and cross-contamination, as required by the
Because renderers and FDA-licensed feed mills are at the greatest risk of
introducing BSE to a wide segment of the animal feed market, the
inspection results for these firms were particularly disturbing. For
• Twenty-three of the 211 renderers inspected, about 11 percent, were not
aware of the BSE regulation.
• Twenty-seven of the 163 renderers that handle prohibited material,
about 17 percent, did not label their products with the required
cautionary statement.
• Ten of the 63 renderers that manufacture both prohibited and
nonprohibited material, about 16 percent, did not have a system in place
to prevent commingling.
The results for the FDA-licensed feed mills were similar. For example,
• Sixty-three of the 1,023 mills, about 6 percent, were not aware of the
• Eighty-five of the 409 mills that handle prohibited material, about 21
percent, did not label their products with the required cautionary
• Thirty-seven of the 300 mills that manufacture both prohibited and
nonprohibited material, about 12 percent, did not have a system in place
to prevent commingling.
FDA told us that as a result of the BSE inspections, two warning letters
have been issued and five firms have voluntarily recalled products. As of
July 2000, however, FDA had not completed its analysis of the inspection
results and had not updated its enforcement strategy for achieving industry
compliance with the BSE regulation. FDA also told us that the next rounds
of BSE inspections will include only those firms that handle prohibited
material. In addition, FDA told us it will direct its efforts towards those
firms or segments of the industry that are not in compliance with the
FDA Has Not Established a
Time Frame for Issuing a
New Regulation to
Strengthen Controls for
Microbial Contamination
FDA is drafting a new regulation to strengthen controls over bacterial and
other contaminants in animal feed but has not established a timetable for
its issuance. FDA told us the new regulation is intended to limit
contamination in feed ingredients and will require manufacturers to (1)
evaluate all hazards associated with their feed ingredients, including but
not limited to microbial hazards; (2) determine which hazards pose a risk
to the safety of the product; and (3) establish controls to minimize these
risks. FDA also told us the new regulation would be modeled after the
hazard analysis and critical control point (HACCP) management practices
currently followed by nearly all firms that handle meat, poultry, and
Recent studies of animal feed demonstrate the need for this new
regulation. For example, several recent studies by USDA and others show
evidence of Salmonella in animal feed and in rendered animal proteins that
often become ingredients in animal feed.
No Regulations Issued to
Safeguard the Transport of
Animal Feed
As of July 2000, the Department of Transportation had not issued
regulations to ensure the safety of food, including animal feed, during
transport by rail vehicles or trucks, as directed by the Sanitary Food
Transportation Act of 1990. Transportation officials pursued a number of. ...

snip... full text ;

suppressed peer review of Harvard study October 31, 2002

Dr. Dehaven,

All in all Sir, the BSE triple firewalls that the USDA/APHIS/FDA
spoke about all these years never existed.

The science behind the BSE MRR (Minimal Risk Region) was based
on anything BUT science.

The myth of cattle not being infectious or infected at ages
under 30 months is not true ;


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

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


The myth of the BSE/nvCJD only theory is simply not true Sir ;

cover-up 4th farmer from cjd

Government experts hold secret inquiry as fourth farmer with
infected cattle falls victim to deadly brain disease


should there be any further press enquiries specifically about the diagnosis
in this case, I therfore suggest that we say that the diagnosis has been
confirmed but that there is nothing to add to SEACs earlier advice.


10. Dr. Will presented information on CJD in farmers in other
European countries - three cases in France in 1992 and 1993,
two of which were dairy farmers, and two cases in dairy farmers
in Germany since October 1993.

IF this new strain of TSE in cattle aBSE or BaSE is in older cattle.

IF this new strain of TSE in cattle looks IDENTICAL to sporadic CJD.

WHY is it so hard to believe that these sporadic CJD deaths in farmers

we not related to this Base or BaSE?...TSS

Medical Sciences

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.


{dagger} C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.


BSE prions propagate as either variant CJD-like or sporadic CJD-like

prion strains in transgenic mice expressing human prion protein

Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan
Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah
E. Lloyd, Jonathan D.F. Wadsworth and John Collinge1

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology, University College, Queen Square, London WC1N 3BG, UK 1
Corresponding author e-mail:

Received August 1, 2002; revised September 24, 2002; accepted October
17, 2002


Variant CreutzfeldtJakob disease (vCJD) has been recognized to date
only in individuals homozygous for methionine at PRNP codon 129. Here we
show that transgenic mice expressing human PrP methionine 129,
inoculated with either bovine spongiform encephalopathy (BSE) or variant
CJD prions, may develop the neuropathological and molecular phenotype of
vCJD, consistent with these diseases being caused by the same prion
strain. Surprisingly, however, BSE transmission to these transgenic
mice, in addition to producing a vCJD-like phenotype, can also result in
a distinct molecular phenotype that is indistinguishable from that of
sporadic CJD with PrPSc type 2. These data suggest that more than one
BSE-derived prion strain might infect humans; it is therefore possible
that some patients with a phenotype consistent with sporadic CJD may
have a disease arising from BSE exposure...

S. E. Lloyd, J. M. Linehan, M. Desbruslais, S. Joiner, J. Buckell, S.
Brandner, J. D. F. Wadsworth, and J. Collinge

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

J. Gen. Virol., August 1, 2004; 85(8): 2471 - 2478.

[Full Text]

Published online before print March 20, 2001, 10.1073/pnas.041490898

Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

Corinne Ida Lasmézas*,dagger
, Jean-Guy
Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François
Lamoury*, Nicolas KoppDagger , Jean-Jacques Hauw§, James Ironside¶,
Moira Bruce|| , Dominique Dormont*, and Jean-Philippe Deslys*

* Commissariat à l'Energie Atomique, Service de Neurovirologie,
Direction des Sciences du Vivant/Département de Recherche Medicale,
Centre de Recherches du Service de Santé des Armées 60-68, Avenue du
Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Dagger
Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003 Lyon,
France; § Laboratoire de Neuropathologie, Hôpital de la Salpêtrière, 83,
Boulevard de l'Hôpital, 75013 Paris, France; ¶ Creutzfeldt-Jakob Disease
Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4
2XU, United Kingdom; and || Institute for Animal Health,
Neuropathogenesis Unit, West Mains Road, Edinburgh EH9 3JF, United Kingdom

Edited by D. Carleton Gajdusek, Centre National de la Recherche
Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000
(received for review October 16, 2000)


There is substantial scientific evidence to support the notion that
bovine spongiform encephalopathy (BSE) has contaminated human beings,
causing variant Creutzfeldt-Jakob disease (vCJD). This disease has
raised concerns about the possibility of an iatrogenic secondary
transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be
transmitted from primate to primate by intravenous route in 25 months,
and (ii) an iatrogenic transmission of vCJD to humans could be readily
recognized pathologically, whether it occurs by the central or
peripheral route. Strain typing in mice demonstrates that the BSE agent
adapts to macaques in the same way as it does to humans and confirms
that the BSE agent is responsible for vCJD not only in the United
Kingdom but also in France. 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. These data will be key in identifying the origin of
human cases of prion disease, including accidental vCJD transmission,
and could provide bases for vCJD risk assessment.


Characterization of the CJD and Scrapie Strains. Controls were set up by
transmitting one French and one U.S. scrapie isolate from ruminants as
well as French sCJD and iCJD cases from humans. None of these revealed a
lesion profile or transmission characteristics similar or close to those
of BSE or vCJD, respectively, thus extending to the present French
scrapie isolate the previous observation that the BSE agent was
different from all known natural scrapie strains (4
, 24

The lesion profiles of sCJD and iCJD differed only slightly in severity
of the lesions, but not in shape of the profile, revealing the identity
of the causative agents. One of us reported the absence of similarity
between sCJD (six cases) and U.K. scrapie (eight cases) in transmission
characteristics in mice (4
). Herein, we made
the striking observation that the French natural scrapie strain (but not
the U.S. scrapie strain) has the same lesion profile and transmission
times in C57BL/6 mice as do the two human TSE strains studied. This
strain "affiliation" was confirmed biochemically. There is no
epidemiological evidence for a link between sheep scrapie and the
occurrence of CJD in humans (25
). However, such a
link, if it is not a general rule, would be extremely difficult to
establish because of the very low incidence of CJD as well as the
existence of different isolates in humans and multiple strains in
scrapie. Moreover, scrapie is transmissible to nonhuman primates (26
). Thus, there is
still a possibility that in some instances TSE strains infecting humans
do share a common origin with scrapie, as pointed out by our findings.

Atypical Case of Bovine Spongiform Encephalopathy
in an East-Flemish Cow in Belgium

H. De Bosschere, DVM, PhD

S. Roels, DVM, PhD

E. Vanopdenbosch, DVM, Lic

Veterinary and Agrochemical Research Centre (CODA/CERVA)

National Reference Laboratorium for Veterinary TSEs

Groeselenberg 99, B-1180

Ukkel (Brussels), Belgium

KEY WORDS: Bovine spongiform encephalopathy, BSE, Western blot, atypical


For many years, researchers believed that only one bovine spongiform
encephalopathy (BSE) strain existed, in contrast to the many different
scrapie strains found. However, only very recently reports emerged about
unconventional BSE strains seen in Italy, France, and Japan. The present
case describes an atypical strain of BSE in Belgium in a 64-month-old
East-Flemish cow with an electrophoretic profile and other features
similar to those described in Japan. ...



For many years, researchers assumed that only one BSE strain
existed.7–10 Only in the past months, reports of atypical BSE cases were
announced.11–13 The Japanese case11 describes a very young bull (23
months) characterized by the absence of spongiform changes and PrPsc
deposits immunohistochemically. The WB analysis revealed an
electrophoretic profile different from that of typical BSE,
characterized by low content of the di-glycosylated molecular form of
PrPsc and a faster migration of the nonglycosylated form of PrPsc. In
Italy,12 two BSE affected cattle with a previously unrecognized
neuropathologic profile and PrPsc type were seen. These cases were
determined using a different staining pattern on immunohistochemistry, a
difference in size and glycoform ratio of PrPsc on immunoblot and a
difference in regional distribution of lesions. The two cases in
France13 showed variant molecular features with a different PrPsc
electrophoretic profile from other BSE cases, mainly characterized by a
higher molecular mass of the nonglycosylated PrPsc. The present case
shows the most similarities (ie, identical electrophoretic profile, only
ELISA and WB positive and histopathology and immunohistochemistry
negative) with the Japanese case,11 although the cow in the Japanese
case was only 23 months old, and the cow in this case was 64 months old.

The fact that these strains were detected worldwide and in several
breeds suggest that there is no local or breed-dependent feature
involved. It could be that the WB techniques have become more specific
within the past year in the detection of minor differences in di-,
mono-, and nonglycosylated molecular forms of PrPsc. Infection of cattle
by scrapie could also be considered since scrapie can be transmitted by
direct contact between animals or through environmental contamination.13

In conclusion, this Belgian case should be added to the list of atypical
BSE strains only very recently detected worldwide and may contribute to
further research studies about epidemiologic significance. Current
continued research on BSE would appear to reveal different BSE strains
in analogy with the different scrapie strains.

Full Text ;

Dr. Dehaven,

THIS brings me back to those Atypical TSE sheep from
Vermont that were imported from Belgium, the new
aytpical TSE cattle in Belgium could have been fed
same infectious type feed (cheese, milk and other
products of the mad river valley atypical TSE that
went for human consumption), just pondering here?

BUT I still would like to know why those mouse
bio-assays were put off for 2 years after we were
told they would start immediately, due to the
importance of risk of it being BSE?

Dr. Dehaven states ;

>We believe, however, that it is essential to understand above all that USDA's BSE testing is for the purpose of surveillance, and is not a food safety measure, nor is it a preventive measure in safeguarding public and animal health against BSE.

IT may not, but it is the ONLY thing we have due to the fact the 8/4/97 feed ban
was nothing more than words on a piece of paper, it was a feed ban never adhered too,
nothing more than a voluntary act. IT was never enforceable, thus, decades of TSE
infected material was fed to ruminants for human and animal consumption. What makes
North America very unique, is the fact that the TSE recipe here may just be more
virolent, once all stains are determined, due to the many different species that
have been documented with TSE in North America, all of which have been rendered for
feed for human animal consumption. THIS is what makes the BSE MRR policy so dangerous.
IT will make the legal trading of ALL STRAINS of TSEs go global. A monumental mistake,
well, I would call it another blunder, you knew better.

Finally Sir, while we wait for the fight between R-Calf and the USDA to be over,
win or loose, if this BSE MRR policy goes into effect, everyone will loose,
except those that are trying to decieve ;



To minimise the risk of farmers' claims for compensation from feed

To minimise the potential damage to compound feed markets through
adverse publicity.

To maximise freedom of action for feed compounders, notably by
maintaining the availability of meat and bone meal as a raw
material in animal feeds, and ensuring time is available to make any
changes which may be required.




MAFF remains under pressure in Brussels and is not skilled at
handling potentially explosive issues.

5. Tests _may_ show that ruminant feeds have been sold which
contain illegal traces of ruminant protein. More likely, a few positive
test results will turn up but proof that a particular feed mill knowingly
supplied it to a particular farm will be difficult if not impossible.

6. The threat remains real and it will be some years before feed
compounders are free of it. The longer we can avoid any direct
linkage between feed milling _practices_ and actual BSE cases,
the more likely it is that serious damage can be avoided. ...

SEE full text ;

Dr. Dehaven,

IT'S been about nothing but commodities and futures all along!
THE US has mirrored the mistakes the UK and others made,
that being, ''denial''. Except the US has become more deceptive,
and better at it.

YOU can change this Sir ;

1. TEST all cattle for human and animal consumption for 5 years,
the world will have there answer then.

2. REMOVE all animal protein from animal food, the SRM list is growing.

3. SOMEONE please make ALL HUMAN TSE reportable Nationally of ALL AGES,
the medical and surgical arena will play a crutial role in the spreading
of this agent.

4. STOP the lies. You could test 1 million cattle annually for 5 years
and I would not believe you from the past blunders I have documented above.
Take the bull by the horns and do the right thing, the public deserves
more. Human Health is at risk here, this is proven science, something
the BSE MRR policy was NOT based on ;


EFSA Scientific
Report on the Assessment of the Geographical BSE-Risk (GBR) of the United
States of America (USA)

Publication date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)

* 167 kB Report

* 105 kB Summary

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working
Group on the Assessment of the Geographical Bovine Spongiform
Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United
States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in
USA. This scientific report addresses the GBR of USA as assessed in 2004
based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached
domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early nineties. It is
possible that imported meat and bone meal (MBM) into the USA reached
domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle
imports from BSE risk countries were slaughtered or died and were
processed (partly) into feed, together with some imports of MBM. This
risk continued to exist, and grew significantly in the mid 90’s when
domestic cattle, infected by imported MBM, reached processing. Given the
low stability of the system, the risk increased over the years with
continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is
likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as there are no
significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)

of Canada Adopted July 2004 (Question N° EFSA-Q-2003-083) [20 August 2004]

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR)

of Mexico Adopted July 2004 (Question N° EFSA-Q-2003-083) [20 August 2004]

From: Terry S. Singeltary Sr. []

Sent: Tuesday, July 29, 2003 1:03 PM



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

TO DOCKET 2003N-0312]

Greetings FDA,


PLUS, if the USA continues to flagrantly ignore the _documented_ science
to date about the known TSEs in the USA (let alone the undocumented TSEs
in cattle), it is my opinion, every other Country that is dealing with BSE/TSE
should boycott the USA and demand that the SSC reclassify the USA BSE GBR
II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_
any longer on this issue, should also be regarded with great suspicion as
well. NOT to leave out the OIE and it's terribly flawed system of disease
surveillance. the OIE should make a move on CWD in the USA, and make a risk
assessment on this as a threat to human health. the OIE should also change
the mathematical formula for testing of disease. this (in my opinion and
others) is terribly flawed as well. to think that a sample survey of 400
or so cattle in a population of 100 million, to think this will find anything,
especially after seeing how many TSE tests it took Italy and other Countries
to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to
find 102 BSE cases), should be proof enough to make drastic changes of this
system. the OIE criteria for BSE Country classification and it's interpretation
is very problematic. a text that is suppose to give guidelines, but is not
understandable, cannot be considered satisfactory. the OIE told me 2 years
ago that they were concerned with CWD, but said any changes might take years.
well, two years have come and gone, and no change in relations with CWD
as a human health risk. if we wait for politics and science to finally make
this connection, we very well may die before any decisions

or changes are made. this is not acceptable. we must take the politics and
the industry out of any final decisions of the Scientific community. this
has been the problem from day one with this environmental man made death
sentence. some of you may think i am exaggerating, but you only have to
see it once, you only have to watch a loved one die from this one time,
and you will never forget, OR forgive...yes, i am still very angry... but
the transmission studies DO NOT lie, only the politicians and the industry
do... and they are still lying to this day...TSS

Docket No, 04-047-1 Regulatory Identification No. (RIN)

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

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


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;

File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [] Monday, January 08,200l 3:03 PM freas ...

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

[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 ...

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

# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
TSS 1/27/03 (0)

Docket Management

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

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, ...

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. ...

Docket Management

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

Comment Number: EC -1

Accepted - Volume 1

Daily Dockets - 04/10/03

... 00D-1662 Use of Xenotransplantation Products in Humans.
EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... - 05-20-2003
- Cached

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

Terry S. Singeltary Sr.
Vol #:

Thank You,
I am sincerely,

Terry S. Singeltary SR.
P.O. Box 42
Bacliff, Texas USA 77518

-------- Original Message --------

Subject: RE: Keep Mad Cow Disease Out of the US Food Supply! Keep the
Border Closed!
Date: Tue, 29 Mar 2005 20:09:48 -0500 (EST)
From: ""
To: "''"

Thank you for your e-mail to Secretary Johanns concerning the U.S. Department of Agriculture's (USDA) policies and testing protocols for bovine spongiform encephalopathy (BSE).

We appreciate the opportunity to respond to your concerns. With regard to imports of Canadian cattle, we are aware of the complexities surrounding USDA's final rule, "Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities," published on January 4, 2005. As you may know, there are legal proceedings underway concerning USDA's final rule, and Congress is also looking at this issue. Because developments concerning this matter are occurring so frequently, we encourage you to visit our Agency's Web site to keep abreast of the latest information. You can find BSE information under our "Hot Issues" link at

We must emphasize that USDA published the final rule only after first conducting a thorough risk assessment, an economic analysis, an environmental assessment, and a lengthy rulemaking process. We remain confident that the animal and public health measures in place in the United States and Canada, in combination with the additional safeguards announced as part of USDA's BSE minimal-risk rule, provide the utmost protection to U.S. consumers and livestock. The safeguards in place in both countries include comparable and effective import restrictions, slaughter restrictions, rendering processes, and feed restrictions. Given these safeguards, and the fact that BSE can be transmitted only under very specific conditions and not through casual contact between animals-the risk of BSE introduction into the United States from Canada remains extremely low.

With regard to USDA's testing protocols for BSE, we agree that USDA's BSE safeguarding efforts are very important. We believe, however, that it is essential to understand above all that USDA's BSE testing is for the purpose of surveillance, and is not a food safety measure, nor is it a preventive measure in safeguarding public and animal health against BSE. Because of the nature of the disease and the limitations of current BSE testing technology, it is not accurate to assume that testing every animal, or all animals within a certain age category presented at slaughter would be an effective means of increasing food safety. We know that the earliest point at which current testing methods can detect a positive case of BSE is 2 to 3 months before the animal begins to demonstrate clinical signs. We also know that the incubation period for this disease-the time between initial infection and the manifestation of clinical signs-is generally very long, on average about 5 years. As a result, we know that there is a long period during which testing an infected animal with the current methodology would not be able to detect the disease and; therefore, testing would not be effective. This is especially likely if the animal is both young and clinically normal at the time samples are obtained for testing. We must note that most cattle that go to slaughter in the United States are both young and clinically normal.

Our surveillance program is intended to help identify whether BSE is present in the U.S. cattle population, and if it is present, to help us ascertain at what level. This will help determine the risk level for the disease in the United States and whether current risk mitigation measures are appropriate. USDA has placed a very high priority on the BSE surveillance program, and we have committed significant expertise and resources to ensuring that it is conceptualized and conducted correctly. Given our objectives, we have established a surveillance program that, in its methodology and target numbers, is rigorous, statistically sound, and takes into account recommendations made by an international panel of experts, including the panel's recommendation to focus testing activities on a targeted population of animals.

The United States has an extremely large adult cattle population (approximately 45 million) and a recognized low risk of BSE infectivity. In seeking to establish the possible prevalence of BSE in this country, it is most efficient and effective for us to focus our surveillance resources on the segment of the cattle population where the disease is most likely to be identified if it is present. This includes adult cattle that exhibit some type of clinical sign that could be considered consistent with the diseaseCincluding, among others, nonambulatory cattle, those condemned at slaughter because of signs of central nervous system disorders, and those that die on farms for unexplained reasons. This targeted approach requires fewer samples to reach similar conclusions, as it is based on the assumption that if you cannot find disease in the targeted, or most likely, population (i.e., animals with some type of clinical signs), it will be even more unlikely to be found in the non-targeted population (i.e., clinically normal animals). Since our approach is targeted at the population where we are most likely to find disease if it is present, it is misleading to use the total number of cattle slaughtered annually as a basis for comparison. The goal of our enhanced surveillance is to sample as many of the animals in the targeted population as we can during a 12- to 18-month period. We estimate that the targeted population is approximately 446,000 animals, or about 1 percent of the total adult cattle population. So far, from June 1, 2004, to March 20, 2005, we have tested more than 284,200 samples, all of which were confirmed negative for BSE.

We are confident that the statistical data obtained in this effort will enable us to better determine the estimated prevalence of BSE in the United States, and it will assist us in determining the efficacy of our risk management policies and whether these policies need adjustment. There is no evidence to suggest that testing a larger number of cattle would increase the efficacy of our surveillance efforts.

With regard to BSE testing technology, we assure you that our testing methods are scientifically sound and are comparable to those used in Europe and elsewhere. In selecting rapid screening tests for BSE, officials with the USDA's Center for Veterinary Biologics compare the test kit's sensitivity and specificity-the ability of a test to identify known positive and negative animals-to the immunohistochemistry (IHC) test, the internationally recognized standard. USDA has issued licenses or permits for a number of BSE test kits. All of these tests are now eligible for use as part of USDA's expanded BSE surveillance program.

We would like to emphasize that the test kits are only used for screening purposes. If any rapid test produces a non?negative result, the sample is forwarded to USDA's National Veterinary Services Laboratories in Ames, Iowa, for confirmatory testing. USDA uses the IHC test to confirm the results.

Thank you again for writing. We hope this information is helpful. We assure you that USDA remains committed to the protection of U.S. agricultural and public health.


W. Ron DeHaven
Animal and Plant Health Inspection Service

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