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From: TSS ()
Subject: Re: Feds skipped key mad cow disease test in 2004 case USDA changes its protocols after animal initially had been cleared
Date: June 17, 2005 at 1:10 pm PST

In Reply to: Re: Feds skipped key mad cow disease test in 2004 case USDA changes its protocols after animal initially had been cleared posted by TSS on June 17, 2005 at 12:55 pm:

-------- Original Message --------
Subject: Re: re-U.S. cattle growers rightly ask Japan: where's the beef?
Date: Sun, 10 Apr 2005 10:18:00 -0500
From: "Terry S. Singeltary Sr."
References: <>

-------- 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."
To:, 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
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
=========================================== 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). 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... Subject: 1 in 2
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 or
radio 4 FARM news] (audio realplayer LISTEN) 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... What GAO Found
United States Government Accountability Office Why GAO Did This Study
Highlights 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 MAD COW DISEASE FDAs 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 GAOs 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
nations 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 firms. " 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. "
FDAs 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 FDAs guidance calls
for such communication. " 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 FDAs enforcement
of the feed ban and recommended corrective actions. This report looks at
FDAs 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 GAOs ... "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 snip... 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 compliance.
snip... 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 B-285212 Page 12 GAO/RCED-00-255 Safety of
Animal Feed material that is not allowed to be fed to ruminantsrevealed
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 regulation. 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 example, " 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
regulation. " Eighty-five of the 409 mills that handle prohibited
material, about 21 percent, did not label their products with the
required cautionary statement. " 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. B-285212
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 regulation. 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 seafood.6 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 ;
IMPORTS FROM CANADA 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. snip...
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 FOURTH FARMER
CONFIRMED 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. IT WAS ALSO
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. E-mail: . 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 Abstract 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. [Abstract] [Full Text] [PDF] Published online before print March
20, 2001, 10.1073/pnas.041490898 Neurobiology 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) Abstract 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. snip... 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 BSE. ABSTRACT 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. ... snip... DISCUSSION For many years, researchers
assumed that only one BSE strain existed.710 Only in the past months,
reports of atypical BSE cases were announced.1113 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 ;
the risk of farmers' claims for compensation from feed compounders. 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. snip... THE FUTURE 4.......... 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 ; USA BSE GBR
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 90s 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 To: Cc:;; BSE-L Subject: Docket No. 2003N-0312 Animal Feed
Safety System [TSS SUBMISSION TO DOCKET 2003N-0312] Greetings FDA,
snip... 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) 0910-AF46 NEW
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; PDF]Freas,
William TSS SUBMISSION 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
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 2003D-0186 Guidance for Industry: Use of Material From Deer and
Elk In Animal Feed EMC 1 Terry S. Singeltary Sr. Vol #: 1
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed EMC 7 Terry S. Singeltary Sr. Vol #: 1 2003D-0186 Guidance
for Industry: Use of Material From Deer and Elk In Animal Feed EMC 7
Terry S. Singeltary Sr. Vol #: 1 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. Sincerely, W. Ron DeHaven Administrator
Animal and Plant Health Inspection Service

Terry S. Singeltary Sr. wrote:

> Hello Mr. Hines,
> My name is Terry S. Singeltary Sr. and I read your article in the
> Houston Chronicle this morning ;
>> re-U.S. cattle growers rightly ask Japan: where's the beef?
> I kindly wish to submit crucial data that dispute ;
>> and no subsequent diseased animals have turned up in the United States
>> over-the-top requirements in place in Japan is individual testing of
>> each head of cattle for BSE
>> dubious science
>> the United States Has addressed all science and safety concerns.
> PLEASE take the time to study the following scientific studies (recent
> and old), some confidential
> documents. I have wasted almost 8 years of my life, daily, trying to
> find the truth. I have it for
> you IF you only take the time to read and study all of it. I lost my
> mother to the ;
> I am no doctor, I have no PhDs, and I am President and or CEO of nothing,
> I have researched in both the U.K. and the USA and other Countries Human
> and animal TSEs for 8 years.
> WHAT this the President and USDA et al plan to do by implementing the ;
> BSE Minimal Risk Region (MRR) will undermine 25 years of trying to
> eradicate
> this hideous disease and will do nothing more than legalize the
> trading of ALL
> strains of TSEs in cattle. THERE are now 2 strains of TSE in cattle.
> One being
> BSE and the other BaSE. THE BaSE being more similar to the sporadic CJDs
> in humans. ALL of this I have documented in a reply to Dr. Dehaven. He
> had
> addressed a few concerns of mine, and I simply returned with more recent
> studies. The USDA et al are living in old days and they are indeed hiding
> cases of TSE in cattle. I have documented all this. Hell, NIH are now
> destroying
> valuable TSE/CJD tissue samples DONATED over decades for research,
> simply due to new more sensitive TSE testing coming out that just
> might start
> STRAIN TYPING, where we would be able to document route and source
> of agent. They know this. I wish to send all this to you, I only hope
> you take
> the time to read. I don't care if you print it or not, the Houston
> chronicle has
> not been very helpful in the past to get the truth out, only when my
> mothers
> death was a story, did they write. they have ignored time and time
> again the
> most recent data I have sent. BUT for if only you read and understand for
> the next time, I will be still grateful....................
> thank you for your time,
> I am sincerely,
> Terry S. Singeltary Sr.
> P.O. Box 42
> Bacliff, Texas USA 77518
> P.S. I can also send you what I am dealing with in NY and the CWD
> Feast that
> they simply will not tell the truth about. I dont wish to overwhelm
> you with data
> and disinterest you, some folks say I do this, but I want you to know
> all of it.
> I have wasted almost 8 years of my life, for what?
> and i am not anti-beef per say, they just have to get it right.
> the incubation period is whats fooling everyone.
> it will catch up.
> google me if you like;
> UPI CJD Singeltary or just CJD TSS or mad cow TSS or endoscopy CJD TSS or
> cjd alzheimer's tss or federal dockets singeltary cjd bse, etc. etc.
> ........MORE TO FOLLOW...END

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