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From: TSS ()
Subject: R-CALF VS USDA BSE MINIMAL RISK REGION (MRR or legal trading of all phenotypes of TSEs for short)
Date: March 2, 2005 at 2:00 pm PST

-------- Original Message --------
Subject: R-CALF VS USDA BSE MINIMAL RISK REGION (MRR or legal trading of all phenotypes of TSEs for short)
Date: Wed, 2 Mar 2005 15:01:13 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

R-CALF VS USDA

-------- Original Message --------
Subject: Your posts to me this week /3rd week of Feb to date
Date: Fri, 18 Feb 2005 23:25:26 -0800 (PST)
From: Gary Burkholder
To: "Terry S. Singeltary Sr."

Dear Terry:

Well, I am a humbled man...and damn proud of it.

You've already provided us, in the span of a few days,
so much important and relevant information, that is
not arguable.

Great internet research, Terry. Really, really
great.

Whether you realize it or not....it's already had an
impact....


snip...END

-------- Original Message --------
Subject: Fwd: Our PR Campaign is now official! Please distribute
Date: Tue, 22 Feb 2005 13:55:08 -0800 (PST)
From: Gary Burkholder
To: flounder@wt.net

Dear Terry: This press release is a partial result
of contributions you have made to me in the past 10
days. Don't ever think there aren't those in the
cattle industry that don't care. Some of the people
on this list are those that have received the
information you've shared with me, so far, that can be
effective WHEN ACCURATE INFORMATION IS PROVIDED THEM!
Many of the people on this list are "grass-roots"
cattle producers in the United States. They strive to
produce top-quality "safe" beef. And they are usually
pretty open-minded people.

Please realize one thing: You are so far ahead of
these people with your own research, that they might
have a hard time comprehending the information we
"feed" to them. They, too, have been conditioned to
believe the same sad lies that USDA has been telling
everyone. It takes time to absorb things.
These are usually very conservative people....so we
need to keep the politics out of it.

I think we've done a fantastic job of working
together, so far, and I really want that to continue.

All the Best,

Gary "Burkie" Burkholder in Kansas

P.S.

snip...END


-------- Original Message --------
Subject: TESTIMONY OF THE HONORABLE MIKE JOHANNS USDA BEFORE THE U.S.
SENATE COMMITTEE ON AGRICULTURE, NUTRITION & FORESTRY FEBRUARY 3, 2005
Date: Wed, 23 Feb 2005 02:55:08 -0800 (PST)
From: Gary Burkholder
To: mike@nobull.net
CC: BillBullard@R-Calfusa.com, Kathleen Kelley ,
Leesa Zalesky , mdaw@st-tel.net,
cowsrus@st-tel.net, Tom F Spencer

Dear R-Calf Friends: I understand today is the first
Big Day of opening statements regarding R-Calf's
efforts to maintain the Canadian Border
closure/re-opening issue.

Good Luck!

I've just received the following information,
yesterday, so am getting it to you now, as fast as I
can.

Yes, this has the Hon. Secy. of Agriculture's
comments, but also below that is a compendium of
information which, I am sure, might add to your
argument that the Canadian border remain closed.

If you take the time to read it, I am sure anyone,
with any sense of reason or allayed fears regarding
the administration of implementing food safety laws by
the USDA, would come to the conclusion, that
re-opening the Canadian live cattle trade is not safe
and not warranted at this time.

Further to that statement, it is apparent that USDA
and NAHEMS DO NOT yet have their procedures nailed
down, DO NOT monitor border crossings as they say they
have, ARE NOT prepared to do so, and ONLY RELUCTANTLY
ADMIT their inabilities to do so.

There will be more information to come, but for now, I
trust that this information could prove helpful to the
R-CALF cause.

Respectfully,

Gary "Burkie" Burkholder
Abilene, Kansas

------------------------------------------------------

TESTIMONY OF THE HONORABLE MIKE JOHANNS
UNITED STATES DEPARTMENT OF AGRICULTURE
BEFORE THE U.S. SENATE
COMMITTEE ON AGRICULTURE, NUTRITION & FORESTRY
FEBRUARY 3, 2005


Chairman Chambliss, Mr. Harkin, Members of the
Committee, thank you for
holding this important hearing today and for the
opportunity to testify
before you. Accompanying me today are Dr. Keith
Collins, USDAs Chief
Economist and Dr. Ron DeHaven, Administrator of USDAs
Animal and Plant
Health Inspection Service (APHIS). They will be
available to assist in
answering any questions you might have.

Before I begin, I want to thank you all for the
professionalism and
courtesy extended to Stephanie and me during my recent
confirmation
process. I appreciate the close, positive working
relationships that we
have begun forging, and thanks to the diligence of
this Committee, it
was an honor and privilege for me to be the first
Cabinet member
confirmed during President Bushs second term. It is,
therefore, a
pleasure to return for my first hearing as Secretary.

I have said frequently that addressing Bovine
Spongiform Encephalopathy
(BSE) issues, particularly as they relate to trade
disruptions, would
be
my top priority as Secretary. I have also heard from
this Committee
quite clearly on this topic, and I believe very
strongly that we are
all
on the side of American agriculture. The Committee and
your
constituents
have also posed some useful and valid questions that
deserve thorough
examination, which this hearing will help provide.

The actions that the U.S. Department of Agriculture
and the federal
government are taking in regard to BSE are potentially

precedent-setting
and could affect international trade patterns for
years to come, with
important economic implications for our cattle
producers and the entire
beef industry. Therefore, our actions must be
undertaken with the
utmost
deliberation, using science as the basis. In the
absence of that
science, sanitary and phytosanitary (SPS) restrictions
will be used
arbitrarily by many nations, without any basis of
protecting human or
animal health.

Accordingly, this hearing could not be timelier. I
want to be very
clear
that while protecting human and animal health must
remain our top
priorities, I am confident that we can seek to return
to normal
patterns
of international commerce by continuing to use science
as the basis for
decision making by U.S. regulatory authorities and our
trading
partners.

Almost exactly one year ago, Secretary Veneman
appeared before this
Committee to discuss BSE. In the time since then, much
has transpired:

On March 8, 2004, USDA published a notice reopening
the comment period
on a rule to establish minimal-risk regions for BSE
(the minimal-risk
rule).

On March 15, 2004, consistent with the recommendations
of an
International Review Team (IRT) of scientific
advisers, USDA announced
that beginning June 1 it would implement an enhanced
BSE surveillance
program to test as many high risk animals as possible
over a 12-18
month
period. We wanted once and for all to clearly
ascertain whether we had
BSE in our cattle herd and, if so, how prevalent it
might be. USDA
began
the work of setting up the infrastructure required,
including
laboratory
equipment and certification, staff training, outreach
efforts, and
licensing and approval of rapid tests. The plan was
reviewed by the
IRT,
which characterized it as comprehensive,
scientifically based and
address[ing] the most important points regarding BSE
surveillance in
animals.

On June 1, 2004, the enhanced surveillance program
began. Our goal is
to
test as many high- risk cattle as possible in 12-18
months. If we test
268, 500 we will be able to detect the presence of as
few as five
targeted, high-risk cattle with BSE at a 99 percent
confidence level.
At
the time, USDA officials consistently stated that the
surveillance plan
might uncover additional BSE-positive animals. To
date, some eight
months later, more than 200,000 animals have been
tested, all of which
have been negative.

In order to help raise awareness about potential BSE
cases among
animal-health professionals and livestock producers,
education and
outreach have also been critical components of these
efforts. These
activities have included advertisements in industry
publications, media
articles, presentations at trade shows, and other
materials. The role
of
producers, renderers and others in helping obtain
samples of high-risk
animals has been indispensable to the success of our
surveillance
program, and the cooperation we have received has been
outstanding.

On December 29, 2004, USDA announced the final
minimal-risk rule, which
designated Canada as the first minimal-risk region for
BSE, and which
will become effective on March 7, 2005.

On January 2, 2005, Canada confirmed its second
domestic case of BSE in
a cow that was born in October of 1996 (the first
since May 20, 2003).
It was followed nine days later by a third case, an
81-month-old cow.

On January 24, 2005, USDA dispatched a technical team
to Canada. We
sent
the team to investigate the efficacy of Canadas
ruminant to ruminant
feed ban because the animal was born shortly after the
implementation
of
that ban and to determine if there are any potential
links among the
positive animals. We have appreciated Canadas
willingness to cooperate
and assist us in these efforts.

The technical team is focusing both on the efficacy of
Canadas feed
ban
and its epidemiological investigation of the new BSE
cases. The team is
composed of experts from APHIS in the areas of
epidemiology,
transmissible spongiform encephalopathies (the family
of diseases to
which BSE belongs), and official documentation.

An auditor from USDAs Agricultural Marketing Service
(AMS) is also
part
of the team, which will also be joined by
representatives of USDAs
Foreign Agricultural Service (FAS) stationed in
Canada. Technical
experts from the Department of Health and Human
Services Food and Drug
Administration are accompanying the team in an
advisory capacity.

We have been receiving regular updates from the team.
We expect a final
report on feed ban issues in mid-February and the
epidemiological
report
by the end of March. These reports will be critical as
we consider
whether any adjustments to current policies are
warranted.

The Minimal-Risk Rule

As you are aware, USDAs minimal-risk rule has come
under legal
challenge. I will address the process of promulgating
the rule, which
was transparent, deliberative and science-based.

Two rounds of public comment were conducted on the
rule, with more than
3,300 comments received.

The final rule establishes criteria for geographic
regions to be
recognized as presenting minimal risk of introducing
BSE into the
United
States. It places Canada in the minimal-risk category,
and defines the
requirements that must be met for the import of
certain ruminants and
ruminant products from Canada. A minimal-risk region
can include a
region in which BSE-infected animals have been
diagnosed, but where
sufficient risk-mitigation measures have been put in
place to make the
introduction of BSE into the United States unlikely.

Because the rule permits the import of live cattle
under 30 months of
age and ruminant products from older animals, it is
useful to note the
risk mitigation measures. These include: proper animal
identification;
accompanying animal health certification that includes
information on
individual animal identification, age, origin,
destination, and
responsible parties; the movement of the cattle to
feedlots or
slaughter
facilities in sealed containers; the prohibition on
cattle moving to
more than one feedlot in the United States; and the
removal of
specified
risk materials (SRMs) from cattle slaughtered in the
United States.

For live sheep and goats under 12 months of age, all
of the same
mitigation measures apply, except for the requirement
that SRMs be
removed from the animal at slaughter.

We remain very confident that the combination of all
of these
requirements, in addition to the animal and public
health measures that
Canada has in place to prevent the spread of BSE,
along with the
extensive U.S. regulatory food-safety and
animal-health systems,
provide
the utmost protection to U.S. consumers and livestock.

USDA continues to undertake several steps to ensure
Canadas compliance
with its BSE regulations. In addition to the
investigation that I
already discussed, USDAs Food Safety and Inspection
Service in
December
2004 conducted an intensive audit of Canadas
compliance with the BSE
requirements of the United States, with particular
attention to SRM
removal. FSIS visited several facilities that
slaughter only cattle
under 30 months of age and determined that they are
effectively
implementing the BSE regulations.

This month, FSIS will conduct a similar BSE audit of
Canadian plants
that slaughter cattle 30 months and older. Canada
currently has only
seven such plants that are certified to export meat to
the United
States.

I am aware of concerns with the portion of USDAs
minimal-risk rule
that
would allow meat from animals over 30 months of age to
be imported from
Canada, but continue the prohibition on the
importation of live animals
of the same age for processing in the United States.
Some have
suggested
that going forward with this rule will change the
historical
beef-trading patterns in North America to the
detriment of U.S.
packers.

As Secretary of Agriculture, I believe that the
marketplace should
determine cross-border trading patterns. We must make
every effort to
avoid policies that favor one group of packers over
another. Decisions,
however, related to sanitary and phytosanitary
measures must be based
on
science.

I can assure you that I will be reviewing this issue
very carefully in
the days ahead as we move closer to the March 7
implementation date.

The Role of Science

I simply cannot emphasize strongly enough the central
role of science
in
this entire process, particularly with regard to the
rigorous
evaluation
of risk.

Since the discovery of the first case of BSE in Great
Britain in 1986,
we have learned a tremendous amount about this
disease. That knowledge
has greatly informed our regulatory systems and
response efforts.

We have learned that the single most important thing
we can do to
protect human health regarding BSE is the removal of
SRMs from the food
supply. Likewise, the most significant step we can
take to prevent the
spread of BSE and bring about its complete eradication
is the ruminant
to ruminant feed ban. It is because of the strong
systems the United
States has put in place, especially these two
essential firewalls, that
we can be confident of the safety of our beef supply
and that the
spread
of BSE has been prevented in this nation.

After Canada reported its first case of BSE in May
2003, USDA conducted
a comprehensive risk analysis to review the potential
threat it posed.
The initial analysis followed the recommended
structure of the World
Organization for Animal Health, or OIE, and drew on
findings from the
Harvard-Tuskegee BSE risk assessment, findings from
the epidemiological
investigation of BSE in Canada, and information on
Canadian BSE
surveillance and feed ban, and history of imports of
cattle and meat
and
bone meal from countries known to have BSE.

The results of that analysis, available on the USDA
Website, confirmed
that Canada has the necessary safeguards in place to
protect U.S.
consumers and livestock against BSE. These mitigation
measures include
the removal of SRMs from the food chain supply, a
ruminant-to-ruminant
feed ban, a national surveillance program and import
restrictions. The
extensive risk assessment conducted as part of USDAs
rulemaking
process
also took into careful consideration the possibility
that Canada could
experience additional cases of BSE.

In the risk analysis update for the final rule, USDA
also considered
the
additional risk protection from new slaughter
procedures, such as the
prohibition on the use of downer animals for food.

The public commented on the risk assessment that
accompanied the
proposed rule and the Explanatory Note released
following the finding
of
BSE in a cow in Washington State. Over a period of
months, USDA
carefully considered these comments, and responses
were published with
the final rule. The comments were beneficial to the
final risk
analysis.
The risk analysis was reviewed internally at USDA and
by Dr. William
Hueston, an international expert on BSE and a member
of the
International Review Team.

The OIE recommends the use of risk assessment to
manage human and
animal
health risks of BSE. OIE guidelines, based on current
scientific
understanding, recognize that there are different
levels of risk in
countries or regions, and suggest how trade may safely
occur according
to the levels of risk. USDA used OIE as a basis in
developing our
regulations defining Canada as a minimal risk country.

Cattle and Beef Trade Impacts

While SPS regulations protecting human and animal
health are the
foremost concern, USDA also has examined the potential
economic impacts
of the minimal-risk rule and related BSE trade issues,
as required by
Executive Order 12866.

For more than three months following the May 20, 2003,
BSE discovery in
Canada, all imports of Canadian ruminants and ruminant
products were
barred. Then, certain Canadian ruminant products for
which there is
inherently lower risk were allowed to enter under
permit beginning
September 2003.

For all of 2003, the United States imported 336,000
metric tons of beef
from Canada. Imports increased to an estimated 476,000
metric tons in
2004, up nearly 42 percent and back to about the level
that prevailed
in
years prior to 2003. The cost-benefit analysis
conducted as part of the
final rule indicates that U.S. beef imports from
Canada are projected
to
actually decrease slightly in 2005 (about 4 percent),
as Canada shifts
its slaughter capacity to lower-yielding older cattle
not eligible for
export to the United States.

At the same time since the border has been closed to
live cattle since
May 2003, imports of fed and feeder cattle under 30
months are expected
to increase in 2005, which is expected to drive up
U.S. beef
production,
reduce beef prices slightly and, consequently, reduce
cattle prices.
Our
most recent forecast for all of 2005 is that fed
cattle prices are
expected to average $82 per cwt, assuming the Canadian
border opens on
March 7, 2005, and that Asian markets do not open to
our beef during
2005.
The precise economic effects will depend on the timing
and volume of
cattle and beef imports from Canada. If USDAs price
forecast turns out
to be correct, that would be the third-highest annual
fed cattle price
on record. Cattle futures prices may be less affected
than indicated by
our forecast, as market prices have likely already
reflected some
probability of the border opening. In addition, to the
extent that we
can continue to open markets that are currently closed
to our beef,
U.S.
cattle price prospects will strengthen.

U.S. market-maintenance activities have been critical
in helping
restore
our beef export markets. In 2003, the total export
value of U.S. beef
and ruminant products was $7.5 billion. After December
23, 2003, 64
percent of that market was immediately closed. Today,
we have recovered
well over a third of that, so that 41 percent of that
market ($3.1
billion) remains closed. Two countries  Japan ($1.5
billion) and Korea
($800 million)  account for nearly three-quarters of
the existing
closures.

Opening the Japanese Market

As a leader in the critical Asian markets, Japan is a
vital market to
reopen to U.S. beef exports. We are aware that the
decision to resume
trade in this market will set an important precedent
for trade
resumption in many other markets. Therefore we have
endeavored to use
science in our ongoing efforts. Efforts to re-open
this market have
drawn on resources across the federal government and
at the highest
political levels. As I have previously said, this
issue has occupied
much of my first few days as Secretary. Just last
week, I met with
Ambassador Kato and also wrote to my counterpart,
Minister Shimamura,
on
the importance of this issue. At the same time,
Ambassador Baker
continues to press this issue with Government of Japan
officials in
Tokyo, and other U.S. Government officials continue to
contact their
counterparts.

These efforts are just the latest in many policy
discussions and
technical exchanges over the past 13 months. Indeed,
the issue has been
a major focus of direct discussions between President
Bush and Japanese
Prime Minister Koizumi.

On October 23, 2004, Japan and the United States
developed a framework
to allow the resumption of bilateral beef trade
following the
conclusion
of regulatory processes in both countries. As a step
toward the
resumption of normal trade, the agreement establishes
an interim
special
marketing program, known as the Beef Export
Verification (BEV) Program,
to allow the United States to sell beef and beef
products to Japanese
importers from animals 20 months of age and under.
Animal age will be
determined through a combination of production records
and
physiological
(grading) means. We are now working with Japanese
officials to gain
approval of the BEV under their regulatory process.

While we are focusing on Japan because of our
important trading
relationship and its leadership role in the region, we
are also
pursuing
efforts to reopen all of the markets that have been
closed to us. We
are
actively engaged with Korea, Hong Kong, Taiwan, China,
Egypt, and
Russia
and have specific actions underway in each market to
get trade resumed.
I would be pleased to provide Members upon request
additional detail on
these and other secondary markets. While the progress
that has been
made
has taken far longer than we had hoped, progress is
indeed being made.
And, I have stated that USDA, and indeed the entire
U.S. Government,
will exert every effort to resolve the matter at the
earliest possible
time.

Conclusion

As traditional trade barriers such as tariffs are
lowered, our focus to
eliminate unjustified non-tariff barriers such as
non-science based SPS
regulatory measures become all the more important to
maintain the flow
of mutually beneficial trade. For USDA, a common
touchstone across
these
issues is the need to maintain consistency and
predictability, to base
our domestic regulations on science and to encourage
the use of
science-based solutions within the international
community. The United
States has long been a leader in this regard,
including negotiating the
World Trade Organization Agreement on the Application
of Sanitary and
Phytosanitary Measures during the Uruguay Round.

Even before the discovery of a single case of BSE in
the United States,
USDA had begun talking with other countries about the
need for
international trade standards to keep pace with the
science, and we
will
redouble our efforts in this regard.

It is also critical that domestic trade rules reflect
the current state
of knowledge regarding BSE, and here the United States
is leading, as
well. We are confident that trade can be resumed with
countries where
BSE has been discovered, contingent upon strong
protections within
those
countries, as well as the robust and effective
regulatory system those
imports are subject to when they enter the United
States. These facts
are reflected in the minimal-risk rule.

At the same time, we will continue to work with our
trading partners to
ensure the ongoing strength of their own BSE
protection systems,
especially the removal of SRMs and implementation of
the feed ban.
While
trade opportunities are multiplying in an increasingly
global
marketplace, we must always remain mindful of our
paramount
responsibility to protect the public health and animal
health.

In summary, I am confident that we are continuing to
keep the
protection
of public and animal health foremost in our concerns.
It is critical
that we continue to use science as a basis for our
decisions and
regulations, and that the United States maintain its
leadership role in
advancing our scientific understanding of these kinds
of SPS-related
issues and appropriate science-based responses.

Mr. Chairman, thank you once again for holding this
important hearing.
I
would now be pleased to take any questions you or
other members may
have.

###

http://www.usda.gov/agency/ocr/download/Johanns.BSE.020305.doc

July 14
Ann Veneman
,
Secretary of Agriculture Joint Hearing: House
Committee on Agriculture
and House Committee on Government Reform Ongoing
activities related to
Bovine Spongiform Encephalopathy (BSE)


http://www.usda.gov/agency/ocr/download/Veneman.BSE.071404.doc

February 24
The Honorable Elsa Murano
,
Under Secretary for Food Safety; Dr. Ron DeHaven
,
Deputy Administrator for
Veterinary Services
Animal and Plant Health Inspection Service; Dr. Keith
Collins,

Chief
Economist
Senate Appropriations Committee
BSE


http://www.usda.gov/agency/ocr/download/Murano.22404.doc

http://www.usda.gov/agency/ocr/download/Dehaven.22404.doc

http://www.usda.gov/agency/ocr/download/KeithCollins.22404.doc

January 2004
January 27
The Honorable Ann M. Veneman,


Secretary, USDA

Senate Agriculture

Committee

BSE-positive cow found in Washington State and USDA's
response
January 21
The Honorable Ann M. Veneman,


Secretary, USDA

House Agriculture

Committee

BSE-positive cow found in Washington State and USDA's
response


http://www.usda.gov/agency/ocr/download/BSE.Veneman.012704.doc

http://www.usda.gov/agency/ocr/download/BSE.Veneman.012104.doc

June 19
Bobby Accord, Administrator, APHIS
House Resources Subcommittee on Fisheries,
Conservation, Wildlife &
Oceans Chronic Wasting Disease; palentological
resources


NO LINK

May 16
Dr. Jim Butler
,

Duputy
Under Secretary for Marketing & Regulatory Programs
House Committee of Resources - Subcommittees on Forest
and Forest
Health
,

and Fishery Conservation, Wildlife and Oceans Chronic
Wasting Disease


http://www.usda.gov/agency/ocr/download/MRP-Butler-5.16.02.pdf

http://resourcescommittee.house.gov/107cong/forests/2002may16/agenda.htm

ARCHIVES FROM 2001

NOT

http://www.usda.gov/agency/ocr/testimony2001.htm

???

MORE on that OTHER LITTLE OLD MAD COW FROM TEXAS (real
player)

Assigned vet wanted it tested.

Gov. insp. over rided and decided not to test.

SYSTEM broken around the Country.

PROBLEMS NATION WIDE!

APHIS inspectors do not follow through.

http://www.npr.org/dmg/dmg.php?prgCode=ME&showDate=07-May2004&segNum=8&mediaPref=RM

May 13, 2004

Failure To Test Staggering Cow May Reflect Wider
Problems
Rep. Waxman raises concerns that the recent failure of
USDA to test an
impaired cow for BSE may not be an isolated incident,
citing the
failure
of USDA to monitor whether cows condemned for central
nervous system
symptoms are actually tested for mad cow disease.

- Letter to USDA

http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf

http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf

===============================================

THAT ONE TEXAS MAD COW IS ONLY TIP OF ICE BURG;

No mad cow results for nearly 500 cows

By Steve Mitchell
United Press International
Published 8/11/2004 11:23 AM


WASHINGTON, Aug. 11 (UPI) -- The U.S. Department of
Agriculture failed
to test for mad cow disease or collect the correct
portion of the brain
on nearly 500 suspect cows over the past two years --
including some in
categories considered most likely to be infected --
according to agency
records obtained by United Press International.

The testing problems mean it may never be known with
certainty whether
these animals were infected with the deadly disease.
Department
officials said these animals were not included in the
agency's final
tally of mad cow tests, but the records, obtained by
UPI under the
Freedom of Information Act, indicate at least some of
them were
counted...

snip...

--

Steve Mitchell is UPI's Medical Correspondent. E-mail
sciencemail@upi.com
Copyright © 2001-2004 United Press International


http://www.upi.com/view.cfm?StoryID=20040810-042935-2066r


FDA Statement

FOR IMMEDIATE RELEASE
Statement
May 4, 2004

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


Statement on Texas Cow With Central Nervous System
Symptoms

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

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

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

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

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

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

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

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

####

rule

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

LATEST DATA shows .1 gram of infectious material is
lethal to many
cows...TSS

FOR IMMEDIATE RELEASE
P01-05
January 30, 2001
Print Media: 301-827-6242
Consumer Inquiries: 888-INFO-FDA

------------------------------------------------------------------------

Note: On Dec. 23, 2003, the U.S. Department of
Agriculture reported

that a
cow
in Washington state had tested positive for bovine
spongiform
encephalopathy (BSE, or mad cow disease). As a result,
information on
this Web page stating that no BSE cases had been found
in the United
States is now incorrect. However, because other
information on this
page
continues to have value, the page will remain
available for viewing.

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the
results of tests
taken on feed used at a Texas feedlot that was
suspected of containing
meat and bone meal from other domestic cattle -- a
violation of FDA's
1997 prohibition on using ruminant material in feed
for other
ruminants.
Results indicate that a very low level of prohibited
material was found
in the feed fed to cattle.

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.

According to Dr. Bernard Schwetz, FDA's Acting
Principal Deputy
Commissioner, "The challenge to regulators and
industry is to keep this
disease out of the United States. One important
defense is to prohibit
the use of any ruminant animal materials in feed for
other ruminant
animals. Combined with other steps, like U.S.
Department of
Agriculture's (USDA) ban on the importation of live
ruminant animals
from affected countries, these steps represent a
series of protections,
to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is
nonetheless
announcing that it is voluntarily purchasing all 1,222
of the animals
held in Texas and mistakenly fed the animal feed
containing the
prohibited material. Therefore, meat from those
animals will not enter
the human food supply. FDA believes any cattle that
did not consume
feed
containing the prohibited material are unaffected by
this incident, and
should be handled in the beef supply clearance process
as usual.

FDA believes that Purina Mills has behaved responsibly
by first
reporting the human error that resulted in the
misformulation of the
animal feed supplement and then by working closely
with State and
Federal authorities.

This episode indicates that the multi-layered
safeguard system put into
place is essential for protecting the food supply and
that continued
vigilance needs to be taken, by all concerned, to
ensure these rules
are
followed routinely.

FDA will continue working with USDA as well as State
and local
officials
to ensure that companies and individuals comply with
all laws and
regulations designed to protect the U.S. food supply.

------------------------------------------------------------------------
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html


Chapter 5


Center for Veterinary Medicine

Last Update: August 07, 2003


Animal Feeds


Warning Letters Issued for CGMP Violations

* On March 8, 2001, the FDAs New Orleans District
Office issued a
Warning Letter to Prestage Farms, Inc., West
Point, Mississippi.
The firm manufactures medicated and
non-medicated feeds for its
own integrated swine enterprise. An FDA
inspection of the
facility
on February 21 - 22, 2001, disclosed significant
deviations from
the Current Good Manufacturing Practice (CGMP)
requirements for
Medicated Feeds. These deviations included:
failure to perform
assays for the active drug ingredient in one
product since 1999;
failure to perform appropriate investigations
and/or corrective
actions for out of limit assays; and failure to
have master
production records.
* The FDAs Dallas District Office issued a
Warning Letter to
Purina
Mills, St. Louis, Missouri, on March 23, 2001.
The Warning Letter
followed the an FDA inspection of Purina Mills,
Oklahoma City,
Oklahoma, on February 2-6, and 13-14, 2001. The
firm failed to
follow Purina's SOP for Drug Sequencing
Requirements. The SOP
provides for sequencing production (without
flushing the mixer)
of
animal feeds for a species for which a drug
component of a prior
medicated feed is not approved. Additionally,
the firm had
distributed bagged medicated feeds since June
2000, with faulty
tagging equipment and no control to ensure that
all bagged feeds
were completely labeled.


Bovine Spongiform Encephalopathy (BSE)

To help prevent the establishment and amplification of
BSE in the
Unites
States, FDA implemented a final rule that prohibits
the use of most
mammaliam protein in feeds for ruminant animals. This
rule, Title 21
Part 589.2000 of the Code of Federal Regulations,
became effective on
August 4, 1997.

On August 23, 2001, Department of Health and Human
Services (DHHS)
Secretary Tommy Thompson unveiled a department-wide
action plan
outlining new steps to improve scientific
understanding of BSE,
commonly
known as "mad cow disease," and related diseases known
as TSEs. The
plan
incorporates a comprehensive approach to further
strengthen
surveillance, increase research resources, and expand
existing
inspection efforts to prevent BSE and TSEs from
entering or taking hold
in the U.S.


Warning Letters for BSE Violations


FDA Inspection Finds Numerous Violations of
BSE Regulations

* On August 8, 2001, the FDAs Seattle District
Office issued a
Warning Letter to the owner of an animal feed
manufacturing
facility located in Tualatin, Oregon. FDA
investigators conducted
an inspection on July 12, 2001, which disclosed
violations of the
bovine feed ingredient regulations. The
inspection revealed that
the firm failed to separate the receipt,
processing, and storage
of products containing prohibited material from
non-prohibited
material; failed to establish a written system,
including
clean-out and flushing procedures, to avoid
commingling and
cross-contamination of equipment; and failed to
maintain records
sufficient to track the materials. In addition,
the firm failed
to
label products with the required cautionary
statement, Do Not
Feed to Cattle or Other Ruminants.


Gamecock Feedmill Found Violating BSE
Regulations

* On July 12, 2001, the FDAs Cincinnati District
Office issued a
Warning Letter to the Carrollton Farmers
Exchange, Carrollton,
Ohio, a feed mill. FDA investigators conducted
an inspection on
June 25, 2001, which found the firm was
manufacturing gamecock
feed containing prohibited proteins. The firm
was not labeling
the
gamecock feed with the cautionary statement, Do
not Feed to
Cattle or Other Ruminants; was not flushing or
sequencing after
manufacturing the feed, and was not maintaining
distribution
information.


Warning Issued for Lack of Required BSE
Cautionary Statement

* The FDAs New Orleans District Office issued a
Warning Letter to
Shields Feed and Supply, Coffeeville, Alabama,
on March 7, 2001.
An inspection conducted on February 1, 2001, of
Shields animal
feed operation showed the finished product label
lacked the
required ruminant cautionary statement. In
addition, mixing and
distribution records were not maintained; no
written procedures
were established for mixer cleaning; and the
corn used for the
mixer cleaning was not labeled and quarantined.


Firm Warned for No Measures to Avoid
Commingling of Feed

* On May 3, 2001, the FDAs Minneapolis District
Office issued a
Warning Letter to Adrian Elevator, Inc., a
Butterfield,
Minnesota,
a manufacturer of animal feeds. On March 16,
2001, an inspection
conducted by the State of Minnesota (on behalf
of FDA) found
significant deviations from the BSE regulations.
The firm failed
to provide adequate measures to avoid
commingling or
cross-contamination and failed to maintain
adequate records to
assure that prohibited animal proteins were not
incorporated into
feeds that may be used for ruminants. For
example, there was no
documentation to verify that the amount of
"flush" being used was
sufficient, and there were no procedures or
documentation to
verify that production was properly sequenced
and that flushes
were performed.


Warned Issued for Failure to Take Adequate
Steps to Prevent
BSE

* The FDAs Seattle District Office issued a
Warning Letter on May
14, 2001, to Wallowa County Grain Growers, Inc.,
Enterprise,
Oregon, for violations FDA regulations regarding
Animal Proteins
Prohibited in Ruminant Feed. An inspection of
the firm on April
11
- 12, 2001, disclosed that the firm was not
taking adequate steps
to prevent the establishment and amplification
of Bovine
Spongiform Encephalopathy (BSE) in that they
failed to separate
the receipt, processing, and storage of the
product containing
prohibited materials from non-prohibited
material; failed to
establish a written system, including clean-out,
and flushing
procedures to avoid commingling and
cross-contamination of common
equipment; and failed to maintain records
sufficient to track the
materials throughout the receipt, processing,
and distribution of
product.


Contract Feed Manufacturer Found Violating
BSE Regulations

On May 1, 2001, the FDAs Chicago District Office
issued a Warning
Letter to Material Resources, a contract feed
manufacturer in
Washington
Park, Illinois. An inspection of the firm in March
2001, disclosed
several deviations from the BSE regulation. These
included failure to
maintain written procedures and provide adequate means
to prevent
commingling between feeds containing prohibited
protein and all other
protein products. The firm also lacked adequate
records to track
products that contained prohibited protein throughout
their receipt and
processing.


Firm Warned for Lack of Written Procedures
for Clean-Out to
Prevent Commingling

* On June 6, 2001, the FDAs Seattle District
issued a Warning
Letter to Superior Feeds, Chester, Montana. The
firm is an animal
feed manufacturing operation. An inspection of
this firm on April
25, 2001, revealed that the firm failed to label
their product
with the required statement, Do Not Feed to
Cattle or other
Ruminants. In addition, the facility failed to
maintain written
procedures specifying the clean-out or
sequencing procedures used
to prevent commingling or cross-contamination of
ruminant and
non-ruminant containing feeds.


FDA Inspection Discloses Hog Feed Lacks BSE
Statement

* The FDAs Minneapolis District Office issued a
Warning Letter on
May 30, 2001, to Round Lake Farmers Coop, Round
Lake, Minnesota.
The firm manufacturers animal feeds. An
inspection by the State
of
Minnesota (on behalf of FDA) on March 30, 2001,
found significant
deviations from the requirements for Animal
Proteins Prohibited
in
Animal Feed. The firm failed to label a hog feed
with the
required
BSE caution statement. In addition, they failed
to establish and
implement procedures for handling prohibited
animal proteins and
failed to maintain records sufficient to track
the receipt of
products containing prohibited animal proteins.


Import Detentions


Possible Contamination of Fish Food Leads to
Detention

The week of March 7, 2001, the FDAs New York District
Upstate Import
Operations Branch detained three entries of fish food
under Import
Alert
99-25 (Detention Without Physical Examination of
Animal Feed, Animal
Feed Ingredients And Other Products For Animal Use
Consisting Or
Containing Ingredients of Animal Origin) due to
possible contamination
with the infectious agent for BSE. The country of
origin for the fish
food was the Federal Republic of Germany. The local
USDA/Philadelphia/PPQ Office was notified.


Vitamin Supplement for Pets Detained

* The week of February 14, 2001, the FDAs Atlanta
District
reported
the detention of 8,777 cartons of vitamin
supplements for cats,
kittens, puppies, and older dogs. The detention
included both dog
and cat treats. The detention was based on
Import Alert 99-25
(BSE). The products were manufactured by
Beaphar, Raalte,
Netherlands, and were valued at approximately
$63,000.


Calf Ration Detained

The FDAs New York District Office reported that
during the week of
March 21, 2001, FDA investigators detained an entry of
Calf Starter
Ration and Calf Finisher Ration under Import Alert
99-25, since some of
the ingredients originated from France and The
Netherlands (both of
which are listed on IA 99-25 as BSE susceptible
countries). The
manufacturer of the feed was Grober Inc., Cambridge,
Ontario, Canada,
and the consignee was Majestic View Farms in Milan,
Pennsylvania. The
USDA/APHIS/PPQ Buffalo, New York office was contacted.


Recall of Various Animal Feed Products

* The FDAs Cincinnati District Office reported
that The Hyland
Company, Coalton, Kentucky, conducted a recall
of various animal
feed products, including Ultra Bloom and
Endurance Plus horse
feeds, due to cross-contamination with
prohibited bovine
material.
The firm's corrective action involved the
application of a
sticker-label that contained the required BSE
warning statement
on
the labels of their affected products. The firm
initiated the
recall by telephone on July 25, 201, and letters
on July 31,
2001.
* During an FDA inspection by the Cincinnati
District Office
investigators determined that Central Farm
Supply of Kentucky,
Inc., Louisville, Kentucky, had received poultry
feed
manufactured
by Burkmann Mills, Bowling Green, Kentucky, that
contained
prohibited protein, but lacked the required
caution statement. On
May 3, 2001, the district and the University of
Kentucky
Regulatory Services Division met with the
responsible parties of
the mill's parent firm, Burkmann Mills London,
London, Kentucky.
During the meeting the firm volunteered to
recall all feed
products manufactured at the Bowling Green mill
due to the lack
of
the required caution statement.


FDA Announces Animal Feed Recall

On January 30, 2001, FDA issued a Press Release
announcing the results
of tests taken on feed used at a Texas feedlot that
was suspected of
containing meat and bone meal from other domestic
cattle -- a violation
of FDA's 1997 prohibition on using ruminant material
in feed for other
ruminants. The results indicated that a very low level
of prohibited
material was found in the feed fed to cattle.

FDA 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 was
therefore
exceedingly
low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting
Principal Deputy
Commissioner, "The challenge to regulators and
industry is to keep this
disease out of the United States. One important
defense is to prohibit
the use of any ruminant animal materials in feed for
other ruminant
animals. Combined with other steps, like U.S.
Department of
Agriculture's (USDA) ban on the importation of live
ruminant animals
from affected countries, these steps represent a
series of protections,
to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc.,
nonetheless announced
that it was voluntarily purchasing all 1,222 of the
animals held in
Texas and mistakenly fed the animal feed containing
the prohibited
material. Therefore, meat from those animals would not
enter the human
food supply. FDA believes any cattle that did not
consume feed
containing the prohibited material was unaffected by
this incident, and
should be handled in the beef supply clearance process
as usual.

FDA believes that Purina Mills acted responsibly by
first reporting the
human error that resulted in the misformulation of the
animal feed
supplement and then by working closely with State and
Federal
authorities. This episode indicates that the
multi-layered safeguard
system put into place is essential for protecting the
food supply and
that continued vigilance needs to be taken, by all
concerned, to ensure
these rules are followed routinely. FDA continues to
work with USDA as
well as State and local officials to ensure that
companies and
individuals comply with all laws and regulations
designed to protect
the
U.S. food supply.


Drug Residues


Warning Letters Issued for Illegal Drug
Residues

Gentamicin

* The FDAs New England District Office issued a
Warning Letter on
February 1, 2001, to D & K Farm, Middlefield,
Connecticut, for
selling a dairy cow for slaughter as human food
which had the
presence of Gentamicin. Gentamicin is not
approved for use in
cattle. An FDA inspection of this dairy
operation located in
Wallingford, Connecticut, disclosed that in
November 2000, the
owner sold a dairy cow for slaughter as human to
a livestock
dealer. USDA analysis of tissue samples
collected from that
animal
identified the presence of Gentamicin in the
animals kidney at a
level of 4.74 ppm. The Warning Letter also noted
that the owner
holds animals under conditions which are so
inadequate that
diseased animals and/or medicated animals
bearing potentially
harmful drug residues are likely to enter the
food supply.

Penicillin

* On January 31, 2001, the FDAs New York District
Office issued a
Warning Letter to Jay N. Martin, a producer and
the owner of Jay
N. Martin, a.k.a. Horizon Dairy, in Clyde, New
York. An FDA
inspection of the firm on November 20-22, and
27, 2000, confirmed
that the firm offered two dairy cows for
slaughter with drug
residues. A USDA sample analyses indicated the
presence of
penicillin at illegal levels in the kidneys of
both slaughtered
cows, and streptomycin, for which there is no
published
tolerance.
* The FDAs Minneapolis District Office issued a
Warning Letter on
August 28, 2001, to Paskewitz Cattle Company of
Vesta,Minnesota.
The Warning Letter cited adulteration of two
animals (a dairy cow
and a steer) with residues of penicillin that
were above
tolerance. The investigation conducted by the
Minnesota
Department
of Agriculture found that Paskewitz Cattle did
not keep adequate
records of their own drug treatment, and they
did not have an
adequate system for handling purchased animals
that may have been
treated with drugs.
* The FDAs Denver District Office issued a
Warning Letter to
DeJong
Dairy, Greeley, Colorado, on February 23, 2001,
citing
adulteration charges due to the presence of
penicillin residue in
a cow offered for slaughter. An FDA inspection
of this dairy farm
on February 7 and 9, 2001, confirmed that the
owner offered an
animal for slaughter in violation of the FD&C
Act. Specifically,
on October 27, 2000, Mr. DeJong offered a cow
for slaughter as
human food. USDA analysis of tissue samples
collected from this
cow identified the presence of penicillin
residues at 0.89 ppm in
the kidney. A tolerance of 0.05 ppm has been
established for
residues of penicillin in the edible tissue of
cows. The analysis
also identified the presence of gentamicin
residue at 13.31 ppm
in
the kidney. The Warning Letter also addressed
poor animal
husbandry practices which lead to the residue.
USDA condemned
this
cow which was also diagnosed with septicemia,
pneumonia,
pleuritis, peritonitis, hepatitis, nephritis,
and lymphedenitis.
* The FDAs San Francisco District Office issued a
Warning Letter
to
Parreiro-Pinheiro & Sons Dairy, Tipton, CA. The
dairy consigned
for sale for human food a cow that had
penicillin residue in the
liver and kidney that were in excess of the
allowable tolerance.
The FDAs San Francisco District Offices
inspection found that
the dairy was not keeping complete medication
records and lacked
an adequate drug inventory system. In addition,
The FDAs San
Francisco District Offices investigation found
that the dairy
was
adulterated the drug, in that it was not being
used in
conformance
with its labeled instructions.

Sulfadimethoxine

* On June 15, 2001, the FDAs Denver District
Office issued a
Warning Letter to North Point Dairy, Clovis, New
Mexico, citing
adulteration charges due to the presence of
sulfadimethoxine
residue in a cow offered for slaughter. An FDA
inspection of this
dairy farm on April 17, 2001, confirmed that a
cow was offered
for
sale for slaughter as food in violation of the
FD&C Act. USDA
analysis of tissues samples collected from this
cow identified
the
presence of sulfadimethoxine residue of 0.36 ppm
in the liver and
0.34 ppm in the muscle. A tolerance of 0.10 ppm
has been
established for residues of sulfadimethoxine in
the edible
tissues
of beef cows. The Warning Letter also addressed
poor animal
husbandry practices, which led to the residue.

Neomycin

* The FDAs Florida District Office issued a
tissue residue Warning
Letter on April 30, 2001, to Larson's Dairy,
Inc., Okeechobee,
Florida. The FDA conducted an inspection of the
diary farm on
March 27 and 28, 2001, which confirmed that the
firm offered an
adulterated animal for sale or slaughter as
food. USDA analysis
of
the dairy calf confirmed the presence of
Neomycin in the kidney
at
the level of 153.12 ppm, more than 21 times the
established
tolerance of 7.2 ppm. The FDAs Florida District
Office's
investigation found the calf was fed medicated
milk containing
Neomycin and Aureomycin.
* On June 22, 2001, the FDAs Baltimore District
Office issued a
Warning Letter to Richard Edwards, owner of
Oakland View Farm,
Ridgely, Maryland. Mr. Edwards sold veal calves
for slaughter as
human food that were treated with Neomycin, a
drug that is
unapproved for this use. In addition, an FDA
inspection on May 30
- 31, 2001, revealed that Mr. Edwards did not
maintain treatment
records showing the dosage rate, the date the
drug was
administered, or the time period to withhold
treated animals from
sale.

Streptomycin

* The FDAs New Jersey District Office issued a
Warning Letter on
March 8, 2001, to Frank Carper, Cranbury, New
Jersey. An FDA
inspection of this facility on October 24 and
27, 2000, confirmed
that a horse purchased and sold by Mr. Carper
for use as human
food was adulterated due to the presence of
streptomycin above
tolerance levels. USDA analysis of tissues from
the equine
revealed that streptomycin in the kidney tissue
at 0.38 ppm. The
tolerance level for streptomycin in the edible
tissue of equines
is 0.0 ppm. Any animals shipped to USDA
slaughter facilities are
considered to be for human consumption.


Consent Decree of Permanent Injunction Filed
Against Joe
Sozinho Dairies


Firm Enjoined for Continuing to Sell Cattle
With Violative
Drug Residue

On July 30, 2001, a Consent Decree of Permanent
Injunction was filed in
the Eastern District of California against Joe Sozinho
Sr., Danny
Sozinho, Dimas Sozinho, individuals d/b/a Joe Sozinho
Dairy #1 and Joe
Sozinho Dairy #2. The FDAs San Francisco District
Office conducted six
inspections in response to violative drug residues
reported by
USDA/FSIS
of Joe Sozinho Dairies resulting in two Warning
Letters sent to the
firm. Despite repeated warnings during the FDA
inspections, as well as
nine USDA/FSIS warning letters for illegal drug
residues, the Sozinho's
failed to take adequate corrective action. Voluntary
approaches were
not
successful in correcting the animal husbandry and drug
adulteration
problems by the Sozinho's.

The Consent Decree permanently restrains and enjoins
the Sozinho's from
selling cattle for human food until all of the
specifications of the
Decree are met which include an animal identification
system,
medication
record keeping system, drug inventory system, drug use
system,
quarantine system, and animal sales certification
system. In addition,
the Sozinho's reimbursed FDA's costs in the amount of
$12,314.38 for
investigational expenses incurred subsequent to the
1994 inspection and
Warning Letter.

On February 1, 2002, the Sozinho Dairies and the
United States filed a
stipulation settling a dispute concerning the Dairies'
activities while
they were under an order of injunction. Under the
Stipulation, the
Sozinhos admitted to continued violations of the law.
They also
admitted
delivering "at least 56 animals intended for use as
food during a
thirty-six day period beginning on July 31, and ending
on September 4,
2001." The United States had alleged in its motion for
contempt that,
under the injunction, such deliveries were prohibited
until FDA
inspected and cleared the Dairies to resume.

The Dairies were not cleared for such sales until
December 2001. The
Injunction entered by the Court in July 2001 continues
in effect. The
defendants have paid the U.S. Treasury fines in the
amount of $140,000.


Ridge View Farms Consent Decree of Permanent
Injunction


Consent Decree Provides FDA With Future
Shutdown Authority

United States v. Ridge View Farms, Inc., Carol A.
Castine, and Daniel
A.
Castine (N.D.N.Y.) On August 7, 2001, the U.S.
District Court for the
Northern District of New York entered a Consent Decree
of Permanent
Injunction that prohibits the defendants from
introducing any
food-producing animal into interstate commerce until
they have
established a system for drug administration and
record-keeping to
prevent the distribution of any animal containing
illegal drug residues
in its edible tissues.

The Decree also requires the defendants to provide a
copy of the Decree
to all persons to whom they have delivered cattle in
the past year and
to any person to whom they deliver cattle in the
future. In addition,
the Decree provides the government with the authority
to require future
shutdown of operations and to impose fines in the
event of further
violations.


Consent Decree Filed Against H & I Dairy

On November 28, 2000, a Consent Decree of Permanent
Injunction was
filed
in the Eastern District of California against Heduino
Brasil (dba H & I
Dairy) of Tipton, California. Despite repeated
warnings during FDA and
the State of California inspections, including six
USDA warning letters
for illegal drug residue findings in cull cows sold or
consigned for
slaughter, Mr. Brasil failed to take adequate
corrective action. The
consent decree permanently restrains and enjoins Mr.
Brasil from
selling
cattle for human food until all the specifications of
the decree are
met
including animal identification, medication record
keeping, drug
inventory, quarantine, and sales certification
systems.


Arie C. Van Leeuwen Sentenced


Violation of Probation Leads to Prison
Sentence

United States v. Arie C. Van Leeuwen, (E.D. Cal.) On
July 9, 2001,
United States District Judge Robert E. Coyle sentenced
Arie Van Leeuwen
to six months imprisonment and one year of supervised
release for
probation violations. In 2000, Van Leeuwen pled guilty
to two charges
of
criminal contempt and one felony charge of introducing
adulterated food
into interstate commerce, resulting from his repeated
violations of the
statutory and regulatory requirements for
administering new animal
drugs
to food-producing animals.

Van Leeuwen admitted to the following probation
violations: failure to
obey all laws; failure to submit certain monthly
report forms; failure
to comply with home confinement conditions; and
transporting animals to
cattle auctions in violation of the probation terms.
In light of Van
Leeuwen's history of repeat violations, the Court
sentenced him to six
months in prison followed by a year of supervised
release that includes
mandatory attendance in dairy management classes.


http://www.fda.gov/ora/about/enf_story/archive/2001/ch5/default.htm


Veterinary Drugs


Warning Letter to Veterinary Drug Firm

The FDAs New Orleans District Office Nashville Branch
issued a Warning
Letter on April 10, 2001, to Classic Care Products,
Inc., d.b.a. The
River City Co., Chattanooga, Tennessee, as the result
of an inspection
of the firm on March 20 and 22, 2001. The inspection
found topical
veterinary drug products being manufactured under
inadequate
conditions.
Deviations from the CGMPs included no component
testing; no master
production records; failure to conduct stability
studies on finished
products and to assign expiration dates based on these
studies; and no
label control. The firm also was not registered and
the veterinary drug
products were not listed.


Unapproved Veterinary Drugs Promoted on the
Internet

On June 28, 2001, the FDAs Minneapolis District
Office issued a
Warning
Letter to Vets Plus, Inc., Knapp, Wisconsin. FDA
conducted an
inspection
of the firms veterinary drug and nutritional
supplement manufacturing
facility on March 7 and 13, 2001.

The inspection disclosed that the firm was
manufacturing veterinary
products that, based on the labels and well as product
catalogs,
contained therapeutic and structure-function claims
causing the
products
to be unapproved new animal drugs. The firms web
sites contained
numerous promotional statements and claims for four
lines of products
marketed by the firm that established that the firm
clearly intended
the
product to be used as animal drugs. In addition, the
firm failed to
list
any of the products with the Center for Veterinary
Medicine, and the
products were not manufactured in compliance with CGMP
regulations.


Distributor of Prescription Veterinary Drugs
Receives Warning

On August 27, 2001, the FDAs Philadelphia District
Office issued a
Warning Letter to the president of Equirace Health and
Speed Products,
Washington, Pennsylvania. The firm is an exclusive
distributor of
prescription veterinary and human drugs to horse
owners. The FDA
conducted an inspection of Equirace on December 5,
2000. The inspection
and a review of information from the New Mexico
Livestock Board
disclosed that the firm was distributing prescription
veterinary and
human drugs to lay persons without a lawful order from
a licensed
veterinarian who has a valid
veterinarian-client-patient relationship
with customers.

The Warning Letter advised the owner that Equiraces
distribution
business violates several sections of the FD&C Act.
For example, the
firms prescription veterinary drugs are misbranded
because they are
not
dispensed by or upon the lawful written or oral order
of a licensed
veterinarian in the course of the veterinarians
professional practice.
Although there was a licensed veterinarian at the
firm, he did not have
a valid veterinarian-client-patient relationship with
any of Equiraces
customers. The Warning Letter also noted that certain
prescription
veterinary and human drugs offered for sale by
Equirace were
adulterated
because they were new animal drugs that were not
approved by the FDA
for
use in horses.


Illegal Veterinary Drugs Exported

On March 5, 2001, the FDAs San Juan District Office
found that a
shipment of veterinary drugs from Santo Domingo to the
U.S. Virgin
Islands, consisting of drugs such as antibiotics,
hormones and dietary
supplements, contained numerous unapproved drugs for
veterinary use.
The
drugs were placed on hold by the U.S. Customs at the
Aguadilla airport.
The shipment was exported under Custom's supervision.


FDA Assists Customs in Seizure of Illegal
Vet Drugs

On July 10, 2001, the FDAs San Juan District Office,
in conjunction
with U.S. Customs, detained and seized a shipment of
veterinary drugs
not approved for sale in the U.S. that was imported
from Santo Domingo.
U.S. Customs agents notified San Juan District Office
that the shipment
was imported as "Hair Products," but actually
contained veterinary
drugs. FDAs inspection of the shipment revealed that
the veterinary
drugs were smuggled among a variety of soaps. The
shipment, which was
originally thought to consist of a few bottles,
contained a total of
793
bottles/pouches of a variety of illegal veterinary
drugs. The shipment
was detained by FDA and seized by U.S. Customs agents.
The value of the
shipment was approximately $7,000.


Importer Attempts to Re-Enter Vet Drugs
Previously Refused
Entry

On May 2, 2001, the FDAs San Juan District Office, in
conjunction with
U.S. Customs Service seized a shipment of IVOMEC-F, a
veterinary drug
not approved for sale in the U.S. The shipment was
from importer
Hacienda Las Carolinas, Santo Domingo. The San Juan
District Office was
notified by U.S. Customs agents that a shipment that
had been refused
entry on February 10, 2001, and had been exported
under Customs
supervision was re- introduced through the same port
on March 16, 2001,
by the same importer. The value of the shipment was
$3,500.00.


Seizure at Veterinary Pharmacy

On December 20, 2000, an FDA investigator accompanied
the U.S. Marshals
Service in a seizure of unapproved new animal drugs at
Veterinary
Pharmacy Corporation (d.b.a. Vet Rx Pharmacy), St.
Peter, Minnesota.
The
firm is a compounding pharmacy for veterinary drugs.
The firm has a
history of serious violations of the FD&C Act,
particularly the 1994
Animal Medicinal Drug Use Clarification Act (AMDUCA).
The seized drugs,
valued at approximately $50,000, were intended for
administration to
food-producing animals, and were unapproved new drugs
in that they were
compounded from the bulk active ingredients. Such
compounding violates
AMDUCA and the implementing regulations, 21 C.F.R.
Part 530. The FDA
conducted inspections at the firm on June 27 - 29, and
July 6 - 7,
2000.
These inspections disclosed the above violations.


Consent Decree of Condemnation and Permanent
Injunction

U.S. v. Sulfadiozie Sodium and Veterinary Pharmacy
Corp. d.b.a. Vet Rx
Pharmacy (D. Minn.) On February 28, 2002, a U.S.
District Judge signed
a
Consent Decree of Condemnation and Permanent
Injunction against this
veterinary pharmacy and two corporate officers, as
well as the drugs
seized in this action. The Decree orders the
defendants to destroy the
seized drugs and enjoins them from engaging in
compounding activities
that fail to conform to the AMDUCA regulations.

http://www.fda.gov/ora/about/enf_story/archive/2001/ch5/cvm2.htm

http://www.fda.gov/ora/about/enf_story/archive/2001/ch5/cvm3.htm

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

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

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

Animal Food or Feed; Animal Proteins Prohibited in
Ruminant Feed

Comment Number: EC -10

Accepted - Volume 2


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

PART 2


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


APHIS Statement: June 29 Inconclusive BSE Test is
Negative

http://www.usda.gov/Newsroom/0275.04.html
07/02/2004

APHIS Statement: First Inconclusive BSE Test is
Negative


http://www.usda.gov/Newsroom/0272.04.html
06/30/2004

APHIS Statement Regarding Second Inconclusive BSE Test

http://www.usda.gov/Newsroom/0266.04.html
06/29/2004

APHIS Statement Regarding First Inconclusive BSE Test


http://www.usda.gov/Newsroom/0198.04.html 06/25/2004


January 14, 2005

Dr. John R. Clifford, Deputy Administrator, Chief
Veterinary Officer

Animal Plant Health Inspection Service

1400 Independence Ave. SW, Room 317-E

Jamie L. Whitten Federal Building

Washington, DC 20250

Dear Deputy Administrator Clifford,

We have a number of questions about your November 23,
2004 announcement
that a cow, which had tested â¬Snot negative⬝ in two
runs of the
Bio-Rad
ELISA quick test for mad cow disease, was â¬Sindeed
negative for
BSE.⬝ We
are concerned because New Scientist reported last June
that the false
positive rate after such repeated testing is â¬Saround
one in 100,000
for
Bio-Rad.⬝ We would appreciate a chance to meet with
you this month to
discuss the questions below.

1. You have indicated that the Biorad screening test
was run twice and
got a positive result both times. Were the two runs
conducted by the
same or different technicians? Did they use the same
or different brain
samples?

2. When the immunohistochemistry (IHC) test was
conducted, what was the
condition of the brain when it arrived at the National
Veterinary
Services Laboratory in Ames, Iowa? Did scientists note
any
deterioration?

3. How many slides were made and examined for the IHC
test? Were they
from only the obex, or other areas of the brain?
Atypical strains of
BSE
have been found in Italy and Japan where the level of
PrPres in the
obex
was low or non-detectable, unlike in traditional BSE.
What portion(s)
of
the brain were examined?

4. Experienced technicians can sometimes disagree on
the interpretation
of IHC slides. Does one technician review the slides
or more than one
technician? If the latter, how many? Did they all
agree on the
conclusion?

5. The World Organization of Animal Health, known as
O.I.E., recognizes
use of immunoblotting (also know as Western Blot) as a
further
confirmation of the IHC test, and it is used in Japan
and most European
countries. USDA used the Western Blot test in December
2003 along with
IHC to confirm the first case of mad cow disease in
the United States .
In Japan and Belgium cows that tested positive on two
quick tests (in
both cases using a Bio-Rad test), negative on IHC, yet
positive on
Western Blot and are considered to be confirmed BSE
cases. Was Western
blot or any other technique besides IHC used to
confirm or rule out a
positive result on this November 2004 cow? If so, what
was the result?
If not used, why not?

6. Were all the procedures referred to in your March
15, 2004
announcement of protocols to confirm any suspect
positives utilized,
particularly the reference to use of â¬Sfull battery
of tests⬝ that
includes, but is not limited to IHC? If not, what
protocol was used and
what is your rationale for the differences?

7. Does USDA still have brain material from the cow in
question? If so,
could it be sent to the World BSE reference laboratory
in Weybridge,
United Kingdom for IHC and Western Blot analysis to
confirm the USDA
finding? If not, why not?

8. Canadian press has reported that â¬SCanadian
authorities have been
told
that the cow, from Texas, didnâ¬"t have the metal ID
tags that cows
born
here are given.⬝ Is this correct? What was the age
of the cow and
where
had it lived?

We would like to request a meeting with you between
now and the end of
January about these questions, which are very
important to consumer
confidence in the safety of the food supply.

Sincerely,

Jean Halloran, Director Michael Hansen, Ph.D.

Senior Research Associate

From
http://www.ars.usda.gov/is/AR/archive/dec04/tse1204.htm

Yamakawa, Y. et al. 2003. op cit.

De Bosschere, H., Roels, S. and E. Vanopdenbosch.
2004. Atypical case
of
bovine spongiform encephalopathy in an East-Flemish
Cow in Belgium. The
International Journal of Applied Research, 2(4).
Accessed at
http://www.jarvm.com/articles/Vol2Iss1/DEBOSSCHERE.htm

In a technical briefing on the new BSE sureveillance
plan, Dr. Ron
DeHaven clearly stated that USDA would use multiple
tests that included
IHC: â¬SThe Department at NVSL will continue to use
the
immunohistochemistry, or IHC, for quality control
testing, and in
addition if any of the rapid screen test comes back
with a suspect
positive then NVSL will use the IHC as well as other
tests necessary to
confirm the results. . . Let me say up front that we
expect that there
will be positive results on these screening tests, and
that's just the
nature of the beast. That's because screening tests by
design are
intended to be very sensitive and not to miss any
positive animals. But
with that high degree of sensitivity also comes the
possibility for
false positive test results. And again that's to be
expected. any
suspect test results will be sent to NVSL for
confirmatory testing with
the full battery of tests. That would include the IHC.
From:
http://www.usda.gov/Newsroom/0106.04.html

>From
http://edmonton.cbc.ca/regional/servlet/View?filename=ed-mad-cow20041122

Greetings again,

I was told that they were to meet on Feb. 9, 2005
about these
inconclusives.

I have heard nothing of the outcome. Maybe we will
hear soon.

BUT of course we will never know the results of that
first TEXAS mad

cow they covered up, the stumbling and staggering one
they refused to

test, and decided to render, head and all...

Experts doubt USDA's mad cow results

By Steve Mitchell
Medical Correspondent

Published 11/24/2004 4:34 PM


WASHINGTON, Nov. 24 (UPI) -- U.S. Department of
Agriculture officials
said a cow that initially tested positive for mad cow
disease was found
to be negative on follow-up tests, but both domestic
and international
experts told United Press International the way the
agency handled the
situation leaves them skeptical about the validity of
the results.

"The testing process does indeed make experts scratch
their heads,"
said
Markus Moser, a molecular biologist and chief
executive officer of the
Swiss firm Prionics, which manufactures tests for
detecting mad cow
disease, also known as bovine spongiform
encephalopathy.

"I think some, but not all, BSE people internationally
have some degree
of cynical de facto doubt about everything the United
States does or
doesn't do, mostly as a result of seeing so many
similar situations
where countries at risk deny and deny and deny and
then end up having
big problems," said Elizabeth Mumford, a veterinarian
and BSE expert at
Safe Food Solutions in Bern, Switzerland, a company
that provides
advice
on reducing mad cow risk to industry and governments.
Several countries, including Germany and Austria, that
had been thought
to be free of the disease, found out it was
circulating in their herds
after they initiated large-scale testing.
The U.S. cow in question tested positive last week on
two so-called
rapid tests manufactured by Bio-Rad Laboratories in
Hercules, Calif.
The
USDA said Tuesday the animal had tested negative on
more sophisticated
confirmatory tests called immunohistochemistry or IHC
tests.

John Clifford of the USDA said in a statement that the
negative IHC
results "makes us confident that the animal in
question is indeed
negative."

A U.S. veterinarian knowledgeable about mad cow tests
told UPI that
experts she has spoken with are "very, very skeptical
about" the USDA's
negative test result.

The veterinarian, who requested anonymity because she
feared
repercussions for speaking out against the USDA, said
the skepticism
arose because the agency did not run another kind of
mad cow test
called
a Western blot. The test sometimes can pick up
positive cases that IHC
misses and the agency has used it in the past to rule
out suspect
cases.
Moser said a Western blot test would make sense for
the United States,
where the prevalence of mad cow is thought to be low.
Other countries
--
including Australia, New Zealand, Canada and Mexico --
that are either
free of the disease or have low rates, have elected to
use the Western
blot as part of their surveillance programs, he said.

The veterinarian said concerns also have emerged
because the USDA has
not made a sample from the cow in question available
for examination by
outside experts. She added that the USDA did not
notify state
officials,
as officials previously said they would about positive
results on rapid
tests.
Knowledgeable people are saying "wait a minute, this
doesn't add up
here," the veterinarian said.
At stake is the $70 billion U.S. beef industry,
including a $3.3
billion
export market. More than 60 countries, including
Japan, closed their
borders to U.S. beef last December after the first --
and so far only
--
U.S. case of mad cow was detected.

Asked whether state officials were notified, USDA
spokesman Ed Loyd
told
UPI the agency had not released any information about
the cow in
question. Loyd also said the false positives on the
rapid test were not
unexpected. Since June, the USDA has reported three
false positives out
of more than 121,000 cows tested.

Bio-Rad spokeswoman Sam Kennedy told UPI the company
was unfamiliar
with
the details of this incident and thus could not
comment.

Mumford said experts were surprised the USDA did not
send samples from
the cow in question for independent analysis by one of
the three
worldwide labs recognized as the foremost authorities
on mad cow
testing
by the World Animal Health Organization. One of these
facilities is
located in Weybridge, England, where the USDA had sent
the first U.S.
case of mad cow disease for confirmation in December
2003.

Loyd said USDA officials who would know whether USDA
planned to release
a sample for verification by an outside party could
not be reached
Wednesday.

"Full transparency and cooperation would certainly
promote the idea
internationally that the U.S. is doing everything it
can do," Mumford
said. "But somehow the U.S. consumer doesn't seem to
think that way, or
has been appeasable at least up until now, so there
seems to be no
impetus to do anything more."

The concern is humans can contract a fatal brain
illness known as
variant Creutzfeldt Jakob disease from eating beef
products
contaminated
with the mad cow pathogen.

Moser said despite USDA's reliance on the IHC test
results, repeated
negatives on that test does not necessarily rule out
the cow being
infected.

"The reason for this is that the IHC test ... is done
on a different
piece of tissue" than that used for the rapid test, he
said. Prions,
the
pathogen thought to cause mad cow disease, tend to
concentrate in a
region of the brain called the obex, so the different
outcomes of the
different tests could be due to sampling a brain
region that contains
little or no prions.
This could be made worse if the animal had lay dead
for several days
before its brain was collected. The brain might be so
degraded that it
would be difficult to locate the obex region for
confirmatory testing
and a sample might mistakenly be taken from a region
that contains no
prions.
"So with these samples, the confirmatory testing would
be even less
reliable, not because of the confirmatory test itself,
but because of
the sampling," he said.
--

E-mail sciencemail@upi.com

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-------- Original Message --------
Subject: Update/R-Calf Suit against USDA March 7, Canadian Border
Re-opening
Date: Sat, 26 Feb 2005 05:26:52 -0800 (PST)
From: Gary Burkholder
To: "Terry S. Singletary, Sr."

Dear Terry, Just wanted to take a minute or two to
thank you for what all you've sent my way. R-Calf has
now garnered additional support from several state
attorney generals, several Congressmen, the National
Farmer's Union and Consumer Reports organization.
I've only two of your e-mails on to R-Calf so
far....but the impact was absolutely perfectly timed
for them to receive it.

R-Calf is primarily an organization of cow/calf
producers, and these are the people that will have to
bear the burden of implementing the National Livestock
Animal I.D. program, as the plan is to have them tag
or chip all calves born in the USA, from now on. Of
course, USDA is going to administrate this program.
Most all farmers and ranchers are about
equally-divided on this program. There will be alot
of book-keeping, and time spent to make it happen, and
alot of them don't see how they will be compensated to
comply.

One of the biggest problems associated with all these
changes for cow/calf people is that, in the past, the
cattle nutritionists, feed manufacturers, used the
Bible of Beef Nutrition, Ensminger's Feeds and
Feeding, to design and create beef cattle rations.
When that was written, BSE was unheard of. Studying
that book, Ensminger used Meat and Bone Meal, Blood
Meal, and other by-products as standard methodology in
creating beef rations. This was standard practice.
So, all those people who studied Beef Cattle
Nutrition, now have to modify their thinking. This is
a very real challenge. Old habits are very hard to
break....

snip...END


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

Subject: Re: Update/R-Calf Suit against USDA March 7, Canadian Border
Re-opening
Date: Sat, 26 Feb 2005 13:18:59 -0800 (PST)
From: Gary Burkholder
To: "Terry S. Singeltary Sr."

Dear Terry: We've got a chance to make some progress.

Your research will be essential. Are you willing to
testify?

I need to know what you want me to do.


Gary
------------------------------------------------------
--- "Terry S. Singeltary Sr." wrote:

> >
> >
> >I am still puzzled as to why our USDA is such a
> puppet
> >to the OIE. That's bothered me ever since I got
> >involved in all the FAD news world-wide in
> 2000-2001.
> >
>
> hey there burkie, my comments on OIE below.
> if you do not hear from me sometimes, i am here,
> just sometimes
> i don't look up for days and reply to my email.
> every now and then
> i come up for air and read and reply to emails. just
> not enough time in
> the day.............later..........terry.
>
snip...
>
> -------- Original Message --------
> Subject: USDA RELEASES TECHNICAL ASSESSMENT ON THE
> IMPLEMENTATION OF THE
> CANADIAN FEED BAN
> Date: Fri, 25 Feb 2005 14:30:30 -0600
> From: "Terry S. Singeltary Sr."
> Reply-To: Bovine Spongiform Encephalopathy
>
> To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE
>
>
>
> ##################### Bovine Spongiform
> Encephalopathy #####################
>
> Release No. 0066.05
>
> Ed Loyd (202) 720-4623
> Jim Rogers (202) 690-4755
>
> USDA RELEASES TECHNICAL ASSESSMENT ON THE
> IMPLEMENTATION OF THE CANADIAN FEED BAN
>
> WASHINGTON, Feb. 25, 2005-The U.S.
> Department of Agriculture today released its
> assessment of the Canadian ruminant-to-ruminant feed
> ban. Agriculture Secretary Mike Johanns in a
> hearing Feb. 3 before the Senate Agriculture
> Committee stated that USDA would be "absolutely
> transparent" with the results of the assessment and
> would immediately release it when it was available.
>
> "After the two recent BSE finds in Canada, it was
> important to get a team up there to conduct a
> firsthand assessment of Canada's compliance with the
> feed ban," said Dr. Ron DeHaven, Administrator of
> USDA's Animal and Plant Health Inspection Service
> (APHIS). "This assessment affirms our science-based
> decision to begin lifting the ban on live ruminants
> and ruminant products from Canada that have
> virtually no risk to human or animal health."
>
> USDA assembled a team of technical experts that
> arrived in Canada on Jan. 24 to gather all relevant
> information to do an in-depth assessment on Canada's
> ruminant-to-ruminant feed ban and their feed ban
> inspection program. USDA took this additional step
> to ensure compliance with Canada's feed ban control
> measures. The feed ban has been determined to be an
> important BSE risk mitigation measure to protect
> animal health.
>
> The inspection team's report states that "Canada has
> a robust inspection program, that overall compliance
> with the feed ban is good and that the feed ban is
> reducing the risk of transmission of bovine
> spongiform encephalopathy in the Canadian cattle
> population."
>
> In both the risk assessment conducted by APHIS as
> part of the BSE minimal-risk rule and the feed ban
> assessment announced today, the agency found that
> compliance by feed mills and rendering facilities in
> Canada to their feed ban regulations is good and,
> just like the United States, Canada is continually
> looking for ways to make it even better.
>
> USDA is confident that the animal and public health
> measures that Canada has in place to prevent BSE,
> combined with existing U.S. domestic safeguards and
> additional safeguards provided in the final rule,
> provide the utmost protections to U.S. consumers and
> livestock. When Canadian ruminants and ruminant
> products are presented for importation into the
> United States, they become subject to domestic
> safeguards as well.
>
> On Jan. 4, USDA published a final rule that amends
> the regulations to provide for the importation of
> certain ruminants, ruminant products and byproducts
> from regions that pose a minimal risk of introducing
> BSE. Canada will be the first country recognized as
> a minimal-risk region and, as such, will be eligible
> to export to the United States live cattle, as well
> as certain other animals and products, from animals
> under 30 months of age. Live cattle imported from
> Canada under this rule will be subject to
> restrictions designed to ensure that they are
> slaughtered by the time they reach 30 months of age.
> These include permanent marking of the animals as to
> their origin, requiring them to move in sealed
> containers to a feedlot or to slaughter, and not
> allowing them to move to more than one feedlot while
> in the United States. The rule is to go into effect
> on March 7, 2005.
>
> For a copy of the feed ban assessment, the final
> rule, and other documents pertaining to BSE, visit
> the APHIS BSE website at
> http://www.aphis.usda.gov/lpa/issues/bse/bse.html
>
> #TSS
>
> USDA News
> oc.news@usda.gov
> 202 720-4623
>
>
>
> >"This assessment affirms our science-based decision
> to begin lifting the ban on live ruminants and
> ruminant products from Canada that have virtually no
> risk to human or animal health."
>
>
> THEY don't know what science base means...
>
>
> >The inspection team's report states that "Canada
> has a robust inspection program, that overall
> compliance with the feed ban is good and that the
> feed ban is reducing the risk of transmission of
> bovine spongiform encephalopathy in the Canadian
> cattle population."
>
>
> sure it does??? this is what happens when you stack
> the
> deck with corporate industry for decision making
> while
> ignoring all the science $$$
>
> the only thing that matters to these people is
> opening
> up the borders for the global trading again. IF this
>
> happens, they will also be opening the door for the
> legal
> trading of all strains of TSEs. THAT is all in the
> world
> GWs MRR will do, and exactly what it was suppose to
> do.
>
> Working Group Report on
> the Assessment of the Geographical BSE-Risk (GBR) of
> CANADA
>
> snip...
>
=== message truncated ===

snip...END-------- Original Message --------
Subject: Re: Update/R-Calf Suit against USDA March 7, Canadian Border
Re-opening
Date: Sat, 26 Feb 2005 13:33:29 -0800 (PST)
From: Gary Burkholder
To: "Terry S. Singeltary Sr."

Stand by for a phone call. Gary
------------------------------------------------------
--- "Terry S. Singeltary Sr." wrote:


---------------------------------
if i testify to anything, it will be everything. all
or none.

testify to whom? where? when? cost$

snip...END


-------- Original Message --------
Subject: Re: Update/R-Calf Suit against USDA March 7, Canadian Border
Re-opening
Date: Sun, 27 Feb 2005 15:54:21 -0600
From: "Terry S. Singeltary Sr."
To: Gary Burkholder
References: <20050226213329.92856.qmail@web14606.mail.yahoo.com>

hey there burkie,

hello. good speaking with you last night. left me thinking about
the wyoming governor. did he really change his mind due to the
info i sent you? i was trying to explain this to the wife and she
did not understand why r-calf would want me to testify, then
i tried to explain to her about the this and that and then got
confused myself. thought in case some one was to knock on the
door, i would put something together, some good stuff, ill be damn
if i did not run of of ink again. i had already had a briefcase ready...

snip...end...TSS

To The Honorable Hon. Richard F. Cebull, District Judge 316 N. 26th,
Room 5405 Billings, Montana 59101 Telephone: (406) 247-4490 Fax: (406)
247-7023 -------- Original Message --------
Subject: R-CALF VS USDA i would love to testify...TSS
Date: Wed, 02 Mar 2005 11:19:38 -0600
From: "Terry S. Singeltary Sr."
To: sdodson@r-calfusa.com
CC: rccattle@ria.net, sraabe@Denverpost.com, jenniries@r-calfusa.com,
r-calfusa@r-calfusa.com


WE MUST KEEP CANADIAN BORDER CLOSED OR 25+
YEARS OF TRYING TO ERADICATE THIS HIDEOUS DISEASE
BY THE REST OF THE GLOBE WILL GO FOR NAUGHT.
THE BSE MRR GW ET AL ARE TRYING TO SHOVE DOWN
THE THROATS OF EVERY OTHER COUNTRY WILL DO NOTHING
MORE THAN LEGAL TRADING OF ALL STRAINS OF TSEs.

THIS IS ABOUT NOTHING MORE THAN COMMODITIES AND
FUTURES, SCIENCE HAS NOTHING TO DO WITH IT.

WHY DON'T WE TALK TSE SCIENCE?

BASE ???

IMPORTS FROM UK AND OTHER BSE COUNTRIES TO
CANADA INCLUDING MBM ?

I HAVE ALL IMPORTS LISTED IN PDF FILES...

LETS TALK PLEASE...TSS

snip...

Working Group Report on the Assessment of the Geographical BSE-Risk
(GBR) of CANADA snip... Annex to the EFSA Scientific Report (2004) 2,
1-15 on the Assessment of the Geographical BSE Risk of Canada - 11 -
snip... - 2 - 2. EXTERNAL CHALLENGES 2.1 Import of cattle from BSE-Risk2
countries An overview of the data on live cattle imports is presented in
table 1 and is based on data as provided in the country dossier (CD) and
corresponding data on relevant exports as available from BSE risk
countries that exported to Canada. Only data from risk periods are
indicated, i.e. those periods when exports from a BSE risk country
already represented an external challenge, according to the SSC opinion
on the GBR (SSC July 2000 and updated January 2002). • According to the
CD, 231 cattle were imported from UK during the years 1980 to 1990 and
no cattle imports from UK were recorded after 1990. • According to
Eurostat, altogether 198 cattle have been imported from the UK during
the years 1980 to 1990, Additionally 500 were recorded in 1993; this
import is 1 For the purpose of the GBR assessment the abbreviation “MBM”
refers to rendering products, in particular the commodities Meat and
Bone Meal as such; Meat Meal; Bone Meal; and Greaves. With regard to
imports it refers to the customs code 230110 “flours, meals and pellets,
made from meat or offal, not fit for human 2 BSE-Risk countries are all
countries already assessed as GBR III or IV or with at least one
confirmed Annex to the EFSA Scientific Report (2004) 2, 1-14 on the
Assessment of the Geographical BSE Risk of Canada - 3 - mentioned in
Eurostat and the updated UK export statistic as male calves, but not
mentioned in the original UK export statistics. According to the CD,
detailed investigations were carried out and it is very unlikely that
the 500 calves have been imported. Therefore, they were not taken into
account. • According to the CD, in 1990 all cattle imported from UK and
Ireland since 1982 were placed in a monitoring program. • Following the
occurrence of the BSE index case in 1993 (imported from UK in 1987 at
the age of 6 months), an attempt was made to trace all other cattle
imported from UK between 1982 and 1990. • Of the 231 cattle imported
from the UK between 1980 and 1990, 108 animals had been slaughtered and
9 had died. From the remaining, 37 were exported, 76 were sent to
incineration and one was buried; these were not entering the rendering
system and therefore not taken into account. • According to the CD, 16
cattle were imported from Ireland (according to Eurostat 20), of which 9
were slaughtered, 3 died. The remaining 4 were incinerated and did
therefore not enter the rendering system. According to the CD, the 6
animals which were imported in 1990 according to Eurostat, were never
imported. • Moreover 22 cattle have been imported from Japan (through
USA), of which 4 were exported (excluded from the table) and 14 were
destroyed and therefore not entering the rendering system, 4 were
slaughtered. • Of 28 imported bovines from Denmark, 1 was destroyed and
1 was exported. Of the 19 buffalos imported in 2000, 1 was incinerated
and the others were ordered to be destroyed. • Additionally in total 264
cattle according to the CD (276 according to other sources) were
imported from Austria, France, Germany, Hungary, Italy, The Netherlands
and Switzerland. • The numbers imported according to the CD and Eurostat
are very similar. Some discrepancies in the year of import can be
explained by an extended quarantine; therefore it is likely that imports
according to Eurostat in 1980 and imports according to the CD in 1981
are referring to the same animals. • Additionally, between 16.000 and
340.000 bovines have annually been imported from US, almost all are
steers and heifers. In total, between 1981 and 2003, according to the CD
more than 2.3 million, according to other sources 1.5 million cattle
have been imported. • According to the CD, feeder/slaughter cattle
represent typically more than 90% of the imported cattle from the USA;
therefore, only 10% of the imported cattle have been taken into account.
snip... Annex to the EFSA Scientific Report (2004) 2, 1-15 on the
Assessment of the Geographical BSE Risk of Canada - 5 - 2.2 Import of
MBM or MBM-containing feedstuffs from BSE-Risk countries An overview of
the data on MBM imports is presented in table 2 and is based on data
provided in the country dossier (CD) and corresponding data on relevant
exports as available from BSE risk countries that exported to Canada.
Only data from risk periods are indicated, i.e. those periods when
exports from a BSE risk country already represented an external
challenge, according to the SSC opinion on the GBR (SSC, July 2000 and
updated January 2002). According to the CD, no imports of MBM took place
from UK since 1978 (initially because of FMD regulations). • According
to Eurostat data, Canada imported 149 tons MBM from the UK in the period
of 1993 to 2001. According to up-dated MBM statistics from UK (August
2001) no mammalian MBM was exported to Canada from 1993 – 1996. As it
was illegal to export mammalian meat meal, bone meal and MBM from UK
since 27/03/1996, exports indicated after that date should only have
included nonmammalian MBM. Therefore, these imports were not taken into
account. • According to the CD, imports of MBM have taken place from
Denmark, Germany, France, Japan and US. • According to Eurostat Canada
imported MBM from Denmark, Belgium, France and Ireland. • According to
the CD further investigations concluded that all imported MBM from
Denmark consisted of pork and poultry origin and was directly imported
for aquaculture, the imported MBM from France was feather meal, the
imported MBM from Germany was poultry meal for aquaculture and the
imported MBM from Belgium was haemoglobin; therefore these imports were
not taken into account. • The main imports of MBM were of US origin,
according to the CD around 250.000 tons, according to other sources
around 310.000 tons between 1988 and 2003. snip... Annex to the EFSA
Scientific Report (2004) 2, 1-15 on the Assessment of the Geographical
BSE Risk of Canada - 7 - 2.3 Overall assessment of the external
challenge The level of the external challenge that has to be met by the
BSE/cattle system is estimated according to the guidance given by the
SSC in its final opinion on the GBR of July 2000 (as updated in January
2002). Live cattle imports: In total the country imported according to
the CD more than 2.3 million, according to other data 1.5 million live
cattle from BSE risk countries, of which 231 (CD) respectively 698
(other sources) came from the UK. The numbers shown in table 1 are the
raw import figures and are not reflecting the adjusted imports for the
assessment of the external challenge. Broken down to 5 year periods the
resulting external challenge is as given in table 3. This assessment
takes into account the different aspects discussed above that allow to
assume that certain imported cattle did not enter the domestic
BSE/cattle system, i.e. were not rendered into feed. In the case of
Canada, the 500 cattle imported from UK according to Eurostat were not
taken into account and it is assumed that all incinerated, buried,
exported animals and the animals still alive did not enter the rendering
system and were therefore excluded from the external challenge. MBM
imports: In total the country imported according to the CD around
300.000 tons, according to other sources nearly 360.000 tons of MBM from
BSE risk countries, of which 149 tons came from the UK. The majority
consisted of MBM imported from the US. The numbers shown in table 2 are
the raw import figures and are not reflecting the adjusted imports for
the assessment of the external challenge. Broken down to 5 year periods
the resulting external challenge is as given in table 3. This assessment
takes into account the different aspects discussed above that allow to
assume that certain imported MBM did not enter the domestic BSE/cattle
system or did not represent an external challenge for other reasons. As
it was illegal to export mammalian meat meal, bone meal and MBM from UK
since 27/03/1996, exports indicated after that date should only have
included non-mammalian MBM. In the case of Canada all imported MBM from
UK, Germany, Belgium, Denmark and France was not taken into account. On
the basis of the available information, the overall assessment of the
external challenge is as given in table 3 below. Annex to the EFSA
Scientific Report (2004) 2, 1-15 on the Assessment of the Geographical
BSE Risk of Canada - 8 - External Challenge experienced by CANADA
External challenge Reason for this external challenge Period Overall
Level Cattle imports MBM imports Comment 1980 to 1990 Low Low Negligible
1991 to 1995 High Moderate High 1996 to 2000 Extremely high High
Extremely high 2001 to 2003 Very high High Very high Table 3: External
challenge resulting from live cattle and/or MBM imports from the UK and
other BSE risk countries. The challenge level is determined according to
the SSC-opinion on the GBR of July 2000 (as updated in January 2002). 3.
STABILITY 3.1 Overall appreciation of the ability to avoid recycling of
BSE infectivity, should it enter processing Feeding The annual Canadian
production of MBM is approximately 575,000 tons of which approx. 40,000
tons are exported each year, mainly to USA. Use of MBM in cattle feed •
Before the feed ban, dairy cattle received supplementary feed containing
MBM during their productive life (maximum 200-400 g MBM per day). Beef
cattle in the western part of the country do not usually receive
complementary feed. Beef cattle in the eastern part receive normally no
supplement protein but the calves could have access to creep feeds
containing MBM, after weaning the ratios may have contained supplemental
protein containing MBM (100-400 g per day). • According to the CD, MBM
is mainly fed to pigs and poultry and included in pet food. • According
to the CD, only a proportion of dairy cattle may have received MBM. Feed
bans • Before 1997, there was no legal restriction to include MBM into
cattle feed. • An MBM-ban was introduced in August 1997; it is forbidden
since to feed mammalian MBM to ruminants except if of pure porcine,
equine and non mammalian origin, i.e. in practice a ruminant-to-ruminant
ban (RMBM-ban). Annex to the EFSA Scientific Report (2004) 2, 1-15 on
the Assessment of the Geographical BSE Risk of Canada - 9 - Potential
for cross-contamination and measures taken against • Cross-contamination
in the about 600 feed mills is assumed to be possible as long as cattle
and pig feed is produced in the same production lines, and premises. •
Cross-contamination during transport is possible, particularly if the
same trucks are used for transporting ruminant MBM (RMBM) and
non-ruminant MBM (porcine or poultry MBM which still might be included
into cattle feed) or for transporting pig/poultry feed and cattle feed.
• On-farm cross-contamination is regarded to be possible. •
Cross-contamination of cattle feed with RMBM can not be excluded. Hence,
as reasonable worst case scenario, it has to be assumed that cattle, in
particular dairy cattle, can still be exposed to RMBM and hence to
BSE-infectivity, should it enter the feed chain. Control of Feed bans
and cross-contamination • With the introduction of the RMBM ban (1997)
the feed mills (approximately 600) were checked for compliance with the
ban, including good manufacturing practices (GMP) and record keeping,
i.e. the separation in production of MBM containing ruminant material
(RMBM) from non-ruminant MBM. • The feed mills had previously – since
1983 – been regularly checked in relation to production of medicated
feed. • No examinations are performed to assess cross-contamination with
RMBM of the protein (e.g. non ruminant MBM) that enters cattle feed.
Differentiation would anyway be difficult. Rendering Raw material used
for rendering • Ruminant material is rendered together with material
from other species, but according to the CD only in the production of
MBM prohibited for use in ruminant feeds. • Slaughter by-products,
including specified risk material (SRM) and fallen stock are rendered. •
The country expert estimated that 20% of the rendering plants,
processing 20% of the total amount of raw material, are connected to
slaughterhouses. Their raw material is more than 98 % animal waste from
these slaughterhouses while less than 2 % is fallen stock. No estimation
was given for the remaining 80% of the rendering capacity. • There are
32 rendering plants of which 3 are processing blood exclusively.
Rendering processes • The rendering systems (parameters) were specified
for 6 plants producing mixed MBM, none of these fulfilled the 133/20/3
standard. Of these, 5 have dedicated facilities to produce products for
use in ruminant feed and products not permitted for use in ruminant
feed. • The remaining plants process porcine or poultry material
exclusively. SRM and fallen stock • There is an SRM ban for human food
in place since 2003. Annex to the EFSA Scientific Report (2004) 2, 1-15
on the Assessment of the Geographical BSE Risk of Canada • However, SRM
are rendered together with other slaughter waste and fallen stock.
However, according to the CD, MBM with SRM is not permitted to be fed to
ruminants. Conclusion on the ability to avoid recycling • Between 1980
and 1997 the Canadian system would not have been able to avoid recycling
of the BSE-agent to any measurable extent. If the BSE-agent was
introduced into the feed chain, it could have reached cattle. • Since
1997 this ability gradually improved with the introduction of the
ruminant MBM ban and its implementation. • Since cross-contamination
cannot be excluded, and as SRM is still rendered by processes unable to
significantly reduce BSE-infectivity, the system is still unable to
avoid recycling of BSE-infectivity already present in the system or
incoming. 3.2 BSE surveillance laboratory tests). i.e. formalin
fixation. snip... In 1990, when BSE was made notifiable, this awareness
was extended to suspicions of BSE. " Since 1993 the number of brains
examined per year did exceed the number recommended by OIE (300 - 336
for countries with a cattle population over 24 months of age of 5.0 to
7.0 Million) PLEASE NOTE BEFORE GOING ANY FURTHER THAT MOST EVERY
COUNTRY THAT WENT BY THOSE SAME OIE BSE GUIDELINES HAVE BSE NOW. THE
ONLY REASON IT WAS NOT DETECTED SOONER IN THESE COUNTRIES WERE BECAUSE
OF THESE SAME OIE GUIDELINES. SIMPLY PUT, THEY ARE WRONG IN RELATIONS TO
TSEs. IT'S NOTHING MORE THAN AN EXCUSE, ONE THAT FLIES ABOUT LIKE A COW
WOULD...TSS in all years, except in 1995 (table 4). year 1992 1993 1994
1995 1996 1997 1998 1999 2000 2001 2002 2003 samples 225 645 426 269 454
759 940 895 1´020 1´581 3´377 3´361 Table 4: Number of bovine brains
annually examined for CNS diseases, including BSE. " According to the CD
approx. 98% of the examined cattle were older than 24 months and approx.
90% exhibited neurological symptoms. Although the identification system
of Canada does not document the birth date or age of the animals,
according to the CD, examination of the dentition is used to ascertain
the maturity of the animals. " The list of neurological differential
diagnoses for the 754 brains examined in 1997 included encephalitis (70
cases), encephalomalacia (19), hemophilus (7), hemorrhage (2),
listeriosis (38), meningoencephalitis (36), rabies (22), tumors (2),
other conditions (135) and no significant findings (423). " Compensation
is paid for suspect BSE cases as well as for animals ordered to be
destroyed (90-95% of market value with a maximum of 2,500 Can$ per cow).
" Diagnostic criteria developed in the United Kingdom are followed at
ADRI, Nepean. According to the very detailed protocol for the
collection, fixation and submission of Bovine Spongiform Encephalopathy
(BSE) specimens at abattoirs under inspection by the Canadian Food
Inspection Agency, the specimen shall be shipped to National Center for
Foreign Animal Disease, Winnipeg, Manitoba. " In 2003, around 3000
animals from risk populations have been tested. " According to the CD,
it is aimed to test a minimum of 8000 risk animals (animals with
clinical signs consistent with BSE, downer cows, animals died on farm
animals diseased or euthanized because of serious illness) in 2004 and
then continue to progressively increase the level of testing to 30,000.
" In May 2003, Canada reported its first case of domestic BSE. A second
case was detected in the US on 23 December 2003 and traced back to
Canadian origin. Both were born before the feed ban and originated from
Western Canada. 3.3 Overall assessment of the stability For the overall
assessment of the stability, the impact of the three main stability
factors (i.e. feeding, rendering and SRM-removal) and of the additional
stability factor, surveillance, has to be estimated. Again, the guidance
provided by the SSC in its opinion on the GBR of July 2000 (as updated
January 2002) is applied. Until 1997, it was legally possible to feed
ruminant MBM to cattle and a certain fraction of cattle feed (for calves
and dairy cattle) is assumed to have contained MBM. Therefore feeding
was Not OK. In August 1997 a ruminant MBM ban was introduced but
feeding of non-ruminant MBM to cattle remained legal as well as feeding
of ruminant MBM to non-ruminant animals. This makes control of the feed
ban very difficult because laboratory differentiation between ruminant
and non ruminant MBM is difficult if not impossible. Annex to the EFSA
Scientific Report (2004) 2, 1-15 on the Assessment of the Geographical
BSE Risk of Canada - 12 - Due to the highly specialised production
system in Canada, various mammalian MBM streams can be separated. Such a
feed ban would therefore be assessed as "reasonably OK", for all regions
where this highly specialised system exists. However, several areas in
Canada do have mixed farming and mixed feed mills, and in such regions,
an RMBM ban would not suffice. Additionally, official controls for
cattle feeds to control for the compliance with the ban were not started
until the end of 2003. Thus, for the whole country, the assessment of
the feeding after 1997 remains "Not OK". Rendering The rendering
industry is operating with processes that are not known to reduce
infectivity. It is therefore concluded that the rendering was and is
Not OK. SRM-removal SRM and fallen stock were and are rendered for
feed. Therefore SRM-removal is assessed as Not OK BSE surveillance
Before 1989, the ability of the system to identify (and eliminate)
BSE-cases was limited. Since 1990 this ability is improved, thanks to a
specific (passive) BSE surveillance. Today the surveillance should be
able to detect clinical BSE-cases within the limits set by an
essentially passive surveillance system. " Passive surveillance has been
carried out since 1990. In 1993 surveillance was intensified and has
considerably improved with mandatory reporting and basic compensation
ensured, awareness raising measures and education of veterinarians, and
a specific BSE-surveillance programme targeting cattle showing clinical
signs that could be compatible with BSE. " The initiated introduction of
active surveillance should improve the system significantly. Stability
of the BSE/cattle system in CANADA over time Stability Reasons Period
Level Feeding Rendering SRM removal BSE surveillance 1980 to 2000 Mainly
passive 2001 to 2003 Extremely unstable Not OK Not OK Not OK Improving
with some testing of risk groups Table 5: Stability resulting from the
interaction of the three main stability factors and the BSE
surveillance. The stability level is determined according to the
SSC-opinion on the GBR of July 2000 (as updated in 2002). Annex to the
EFSA Scientific Report (2004) 2, 1-15 on the Assessment of the
Geographical BSE Risk of Canada - 13 - On the basis of the available
information, it has to be concluded that the country's BSE/cattle system
was extremely unstable until today, i.e., it would have recycled and
amplified BSE-infectivity very fast, should it have entered the system.
The stability of the BSE/cattle system in Canada overtime is as given in
table 5 above. 4. CONCLUSION ON THE RESULTING RISKS 4.1 Interaction of
stability and challenges In conclusion, the stability of the Canada
BSE/cattle system in the past and the external challenges the system has
coped with are summarised in the table 6. INTERACTION OF STABILITY AND
EXTERNAL CHALLENGE IN CANADA Period Stability External Challenge
Internal challenge 1980 to 1990 Low Unlikely but not excluded 1991 to
1995 High 1996 to 2000 Extremely high Likely and rapidly growing 2001 to
2003 Extremely unstable Very high Confirmed at a lower level Table 6:
Internal challenge resulting from the interaction of the external
challenge and stability. The internal challenge level is determined
according to guidance given in the SSC-opinion on the GBR of July 2000
(as updated in 2002). From the interaction of the two parameters
stability and external challenge a conclusion is drawn on the
level of internal challenge that emerged and had to be met by the
system, in addition to external challenges that occurred. An external
challenge resulting from cattle import could only lead to an internal
challenge once imported infected cattle were rendered for feed and this
contaminated feed reached domestic cattle. Cattle imported for slaughter
would normally be slaughtered at an age too young to harbour plenty of
BSE infectivity or to show signs, even if infected prior to import.
Breeding cattle, however, would normally live much longer and only
animals having problems would be slaughtered younger. If being 4-6 years
old when slaughtered, they could suffer from early signs of BSE, being
approaching the end of the BSE-incubation period. In that case, they
would harbour, while being pre-clinical, as much infectivity as a
clinical BSE case. Hence cattle imports could have led to an internal
challenge about 3 years after the import of breeding cattle (that are
normally imported at 20-24 months of age) that could have been infected
prior to import. In case of Canada this implies that cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early 90s. On the other
hand imports of contaminated MBM would lead to an internal challenge in
the year of import, if fed to cattle. The feeding system is of utmost
importance in this context. If it could be excluded that imported,
potentially contaminated feed stuffs reached cattle, such imports might
not lead to an internal challenge at all. In case of Annex to the EFSA
Scientific Report (2004) 2, 1-15 on the Assessment of the Geographical
BSE Risk of Canada - 14 - Canada this implies that it was possible that
imported MBM reached domestic cattle and lead to an internal challenge
in the early 90s. 4.2 Risk that BSE infectivity entered processing A
certain risk that BSE-infected cattle entered processing in Canada, and
were at least partly rendered for feed, occurred in the early 1990s when
cattle imported from UK in the mid 80s could have been slaughtered. 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. 4.3 Risk
that BSE infectivity was recycled and propagated A risk that
BSE-infectivity was recycled and propagated exists since a processing
risk first appeared; i.e. in the early 90s. Until today this risk
persists and increases fast because of the extremely unstable BSE/cattle
system in Canada. 5. CONCLUSION ON THE GEOGRAPHICAL BSE-RISK 5.1 The
current GBR as function of the past stability and challenge The current
geographical BSE-risk (GBR) level is III, i.e. it is confirmed at a
lower level that domestic cattle are (clinically or pre-clinically)
infected with the BSE-agent. This assessment deviates from the previous
assessment (SSC opinion, 2000) because at that time several exporting
countries were not considered a potential risk. 5.2 The expected
development of the GBR as a function of the past and present stability
and challenge " As long as the system remains unstable, it is expected
that the GBR continues to grow, even if no additional external
challenges occur. " Since recent improvements in the safety of MBM
production in many countries or significant recent reductions in the
incidence of BSE are not taken into account for the assessment of the
external challenge, the external challenge assessed after 2001 could be
overestimated and is the worst case assumption. However all current GBR
conclusions are not dependent on these assumptions in any of the
countries assessed. For future assessments and when the impact of the
production, surveillance and true incidence changes has been fully
quantified, these developments should be taken into account. 5.3
Recommendations for influencing the future GBR " Enhancing the stability
of the system, in particular by ensuring that cattle have no access to
mammalian MBM in combination with appropriate rendering and exclusion of
SRM and fallen stock from any feed chain could lead, over time, to a
reduction of the GBR. " Improved passive and active surveillance, i.e.
sampling of animals not showing signs compatible with BSE from at-risk
cattle populations, such as adult cattle in Annex to the EFSA Scientific
Report (2004) 2, 1-15 on the Assessment of the Geographical BSE Risk of
Canada - 15 - fallen stock and emergency slaughter, by means of rapid
screening, would allow monitoring the efficiency of stability enhancing
measures. Documentation provided to EFSA " Letter with the ref
D(2003)KVD/ip/420722 from the European Commission requesting a
geographical risk assessment for the appearance of BSE in a country. "
Country Dossier as prepared by the country in response to the EC and
EFSA data collection request. " Other sources of data information i.e.
exports from third countries and Eurostat data. " SSC, July 2000. Final
opinion on the Geographical Risk of Bovine Spongiform Encephalopathy
(GBR). " SSC, January 2002. Updated opinion on the Geographical Risk of
Bovine Spongiform Encephalopathy (GBR). Acknowledgment Members of the
EFSA Scientific Expert Working Group on GBR are acknowledged for their
valuable contribution to this mandate. The members are: Didier Calavas,
Aline De Koeijer, Michael Gravenor, John Griffin, Dagmar Heim, Matthias
Kramer, Riitta Maijala, Mo Salman, Vittorio Silano, Emmanuel
Vanopdenbosch, and Stig Widell. CANADA
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/563/sr02_biohaz02_canada_report_annex_en1.pdf
Geographical BSE Risk of USA European Food Safety Authority Scientific
Expert Working Group on GBR Working Group Report on the Assessment of
the Geographical BSE-Risk (GBR) of UNITED STATES OF AMERICA 2004 snip...
- 12 - 3.3 Overall assessment of the stability For the overall
assessment of the stability, the impact of the three main stability
factors, (i.e. feeding, rendering and SRM-removal) and of the additional
stability factor surveillance has to be estimated. Again, the guidance
provided by the SSC in its opinion on the GBR of July 2000 (as updated
in 2002) is applied. Annex to the EFSA Scientific Report (2004) 3, 1-17
on the Assessment of the Geographical BSE Risk of USA - 13 - Feeding
Until August 1997, RMBM was legally fed to cattle. Feeding was therefore
"not OK". In August 1997 an RMBM-ban was introduced but feeding of
non-ruminant MBM to cattle remained legal as well as feeding of RMBM to
non-ruminant animals (farm animals and pets). An RMBM ban is difficult
to maintain, as only labels can distinguish the various MMBMs. This
makes control of the feed ban very difficult because analytical
differentiation between ruminant and non-ruminant MBM is difficult if
not impossible. Due to the highly specialised production system in the
USA, various mammalian MBM streams can be separated. Such a feed ban
would therefore be assessed as "reasonably OK", for all regions where
this highly specialised system exists. However, several areas in the USA
do have mixed farming and mixed feed mills, and in such regions an RMBM
ban would not suffice. Additionally, official controls for cattle feeds
to control for compliance with the ban started in 2002. Thus, for the
whole country, the assessment of the feeding after 1997 remains "not
OK", but improving. Rendering The rendering industry is operating with
processes that are not known to reduce infectivity. It is therefore
concluded that rendering was and is "not OK". SRM-removal SRM were and
are still rendered for feed, as are (parts of) the fallen stock.
SRMremoval is therefore regarded as "not OK". BSE-surveillance Before
1989, the ability of the system to identify (and eliminate) BSE-cases
was limited. Since 1990 this ability is improved, thanks to a specific
(passive) BSE surveillance. The initiated introduction of active
surveillance in risk populations should improve the system
significantly. Stability of the BSE/cattle system in the USA over time
Stability Reasons Period Level Feeding Rendering SRM removal BSE
surveillance 1980 to 2003 Extremely unstable Not OK Not OK Not OK
Passive but improving with some testing of risk groups Table 4:
Stability resulting from the interaction of the three main stability
factors and the BSE surveillance. The stability level is determined
according to the SSC-opinion on the GBR of July 2000 (as updated in
2002). Annex to the EFSA Scientific Report (2004) 3, 1-17 on the
Assessment of the Geographical BSE Risk of USA - 14 - On the basis of
the available information, it has to be concluded that the country's
BSE/cattle system was extremely unstable until today, i.e., it would
have recycled and amplified BSE-infectivity very fast, should it have
entered the system. The stability of the BSE/cattle system in the USA
overtime is as given in table 4. The present assessment modifies the
stability assessment of the previous GBR report in 2000 mainly due to a
different perception of the impact of BSE surveillance on stability and
of the efficiency of the RMBM feed ban. 4. CONCLUSION ON THE RESULTING
RISKS 4.1 Interaction of stability and challenges In conclusion, the
stability of the USA BSE/cattle system in the past and the external
challenge the system has coped with, are summarised in table 5 below.
From the interaction of the two parameters “stability” and “external
challenge” a conclusion is drawn on the level of “internal challenge”
that emerged and had to be met by the system, in addition to external
challenges that occurred. Interaction of stability and external
challenge in the USA Period Stability External Challenge Internal
challenge 1980 to 1985 1986 to 1990 Moderate Possibly present 1991 to
1995 Very high 1996 to 2000 2001 to 2003 Extremely unstable Extremely
high Likely to be present and growing Table 5: Internal challenge
resulting from the interaction of the external challenge and stability.
The internal challenge level is determined according to guidance given
in the SSC-opinion on the GBR of July 2000 (as updated in 2002). An
external challenge resulting from cattle import could only lead to an
internal challenge once imported infected cattle were rendered for feed
and this contaminated feed reached domestic cattle. Cattle imported for
slaughter would normally be slaughtered at an age too young to harbour
plenty of BSE infectivity or to show signs, even if infected prior to
import. Breeding cattle, however, would normally live much longer and
only animals having problems would be slaughtered younger. If being 4-6
years old when slaughtered, they could suffer from early signs of BSE,
being approaching the end of the BSE-incubation period. In that case,
they would harbour, while being pre-clinical, as much infectivity as a
clinical BSE case. Hence cattle imports could have led to an internal
challenge about 3 years after the import of Annex to the EFSA Scientific
Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of
USA - 15 - breeding cattle (that are normally imported at 20-24 months
of age) that could have been infected prior to import. In the case of
the USA a few potentially infected cattle were imported from the UK and
more from other BSE-risk countries. Furthermore, large numbers of
imported animals came from Canada. This implies that cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early 90s. On the other
hand imports of contaminated MBM would lead to an internal challenge in
the year of import, if fed to cattle. The feeding system is of utmost
importance in this context. If it could be excluded that imported,
potentially contaminated feed stuffs reached cattle, such imports might
not lead to an internal challenge at all. In case of the USA this
implies that it was possible that imported MBM reached domestic cattle
and lead to an internal challenge in the early 90s. If Canadian imports
would be excluded from this assessment, we find that the USA receives a
moderate challenge for all 5-year intervals since 1980, a high challenge
between 1985 and 2000 and a low challenge thereafter. If combining these
moderate to high challenges due to imports with the extremely unstable
system, the conclusion would still be that the occurrence of an internal
challenge is possible during the early 80s and likely in the late 80s.
4.2 Risk that BSE infectivity entered processing 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. 4.3 Risk that BSE infectivity was recycled
and propagated A risk that BSE-infectivity was recycled and propagated
exists since a processing risk first appeared, i.e. in the early 90s.
Until today this risk persists and increases fast because of the
extremely/very unstable BSE/cattle system in the USA. 5. CONCLUSION ON
THE GEOGRAPHICAL BSE-RISK 5.1 The current GBR as function of the past
stability and challenge • The current geographical BSE risk (GBR) level
is III, i.e. it is likely but not confirmed that domestic cattle are
(clinically or pre-clinically) infected with the BSE-agent. Note1: It is
also worth noting that the current GBR conclusions are not dependent on
the large exchange of imports between USA and Canada. External challenge
due to exports to the USA from European countries varied from moderate
to high. These Annex to the EFSA Scientific Report (2004) 3, 1-17 on the
Assessment of the Geographical BSE Risk of USA challenges indicate that
it was likely that BSE infectivity was introduced into the North
American continent. Note2: This assessment deviates from the previous
assessment (SSC opinion, 2000) because at that time several exporting
countries were not considered a potential risk. 5.2 The expected
development of the GBR as a function of the past and present stability
and challenge • 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 (preclinically or clinically) infected with
the BSE-agent persistently increases. • Since recent improvements in the
safety of MBM production in many countries or significant recent
reductions in the incidence of BSE are not taken into account for the
assessment of the external challenge, the external challenge assessed
after 2001 could be overestimated and is the worst case assumption.
However all current GBR conclusions are not dependent on these
assumptions in any of the countries assessed. For future assessments and
when the impact of the production, surveillance and true incidence
changes have been fully quantified, these developments should be taken
into account. 5.3 Recommendations for influencing the future GBR •
Measures that improve the stability of the system, will, over time,
reduce the probability that cattle could get infected with the
BSE-agent. Possible actions include - removal of SRM and/or fallen stock
from rendering of animal by-products into feed, - high pressure
standards in rendering processes, - significant improvement of ban on
use of ruminant MBM in cattle feed, supported by regular sampling of
feed for the occurrence of such MBM. • Improved passive and active
surveillance, i.e. sampling of animals not showing signs compatible with
BSE from “at-risk” cattle populations, such as adult cattle in fallen
stock and emergency slaughter, by means of rapid screening, would allow
monitoring the efficiency of stability enhancing measures.
Documentation... snip...
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/574/sr03_biohaz02_usa_report_annex_en1.pdf
Annex to the EFSA Scientific Report (2004) 4, 1-13 on the Assessment of
the Geographical BSE Risk of Mexico European Food Safety Authority
Scientific Expert Working Group on GBR Working Group Report on the
Assessment of the Geographical BSE-Risk (GBR) of MEXICO 2004 snip...
Annex to the EFSA Scientific Report (2004) 4, 1-13 on the Assessment of
the Geographical BSE Risk of Mexico - 7 - 2.3 Overall assessment of the
external challenge The level of the external challenge that has to be
met by the BSE/cattle system is estimated according to the guidance
given by the SSC in its final opinion on the GBR of July 2000 (as
updated in January 2002). Live cattle imports: According to the CD the
country imported in total over the period 1980 to 2003, approximately
3.2 million live cattle from BSE - risk countries, of which conclusively
none came from the UK. The numbers shown in table 1 are the raw import
figures and are not reflecting the adjusted imports for the assessment
of the external challenge. Broken down to 5 - years periods the
resulting external challenge is as given in table 3. This assessment
takes into account the evidence that certain imported cattle did not
enter the domestic BSE/cattle system, i.e. were not rendered into feed.
In the case of Mexico, it is assumed that “cattle still alive” (imports
from Spain) did not enter the rendering system. MBM imports: According
to the CD the country imported in total over the period 1980 - 2003
approximately 826,000 tons MBM from BSE - risk countries (according to
“other data”: ~ 919,000 tons), of which none came from the UK. The
numbers shown in table 2 are the raw import figures and are not
reflecting the adjusted imports for the assessment of the external
challenge. Broken down to 5 - years periods the resulting external
challenge is as given in table 3. This assessment takes into account the
evidence that certain imported MBM did not enter the domestic BSE/cattle
system or did not represent an external challenge for other reasons.
However, in the case of Mexico, there was not sufficient evidence to
remove any quantities of MBM from the external challenge. External
Challenge experienced by MEXICO External challenge Reason for this
external challenge Period Overall Level Cattle imports MBM imports
Comment 1980 to 1985 1986 to 1990 Negligible Negligible Negligible 1991
to 1995 Very high High Very high Due to MBM imports from USA since 1993
and cattle imports from USA/Canada since 1994 1996 to 2000 Extremely
high Due to imports from USA / Canada 2001 to 2003 Extremely high Very
high Extremely high Due to imports from USA / Canada Table 3: External
challenge resulting from live cattle and/or MBM imports from the UK and
other BSE - risk countries. The challenge level is determined according
to the SSC - opinion on the GBR of July 2000 (as updated in January
2002). Annex to the EFSA Scientific Report (2004) 4, 1-13 on the
Assessment of the Geographical BSE Risk of Mexico - 8 - On the basis of
the available information, the overall assessment of the external
challenge is as given in the table above. 3. STABILITY 3.1 Overall
appreciation of the ability to avoid recycling of BSE infectivity,
should it enter processing Feeding Use of MBM in cattle feed Until 11th
October 2000, MBM could and was legally included in cattle feed. Feed
bans The law prohibiting the use of ruminant MBM in ruminant feed was
published on 11th October 2000. According to the FAO mission,
implementation of the ban began in 2002. Potential for cross -
contamination and measures taken against In feed mills, lines are not
always separated. According to the CD flushing is used to clean in -
between lines, and feed mills carry out in - house controls. According
to the CD, controls during transport and on farms are not regularly
carried out, but inspections may occur on the farm. No details are
provided on the kind or frequency of these control measures, the dates
checking of cross contamination began, or on the results of these
inspections. Control of feed bans and cross - contamination According to
the CD, checks occur to ensure that plants do not use ruminant MBM in
feed stuff production for ruminants. This may have been helped by
regulations defined in 1999 that allowed ruminant feed production to use
MBM only from rendering plants that do not process ruminant material.
However, detailed outcomes of control procedures, tests carried out or
quality control are not provided. It is concluded that cross
contamination is possible. Rendering • A rendering industry exists in
Mexico and raw bovine materials are normally rendered. This includes fat
tissue, bones, horns and hooves but not usually viscera, eyes, brains or
spinal cords. About 90 % of the rendered material is of bovine origin
and the rest consists mainly of pork material. 58 plants produce MBM,
with an annual production of between 150,000 and 250,000 tons per year.
It is estimated that about 6 % was destined for bovines in 2000. • The
rendering process standard (133° C/20min/3bar) is not applied. According
to the CD, there are guidelines in place so that the standard process
will be used in the event that a BSE case is discovered. • According to
the CD, regulations were introduced in 1999 to ensure that the
processing of animal offal and its employment in animal food took place
in two Annex to the EFSA Scientific Report (2004) 4, 1-13 on the
Assessment of the Geographical BSE Risk of Mexico - 9 - plant types: 1).
plants processing material of ruminant origin plus other species (such
as pig) and 2). plants processing only non-ruminant material. Plants
corresponding to the first category are prohibited from the preparation
of foodstuffs intended for ruminants. The fulfillment of this procedure
is checked annually through veterinarians. Specific results of checking
procedures are not supplied in the CD. Specified Risk Material (SRM) and
fallen stock There is no SRM-ban. SRM is normally destined for human
consumption. According to the CD, fallen stock from pasture and diseased
animals are incinerated and not rendered. Conclusion on the ability to
avoid recycling In light of the above information, it has to be assumed
that the BSE agent, should it have entered Mexico, could have been
recycled and potentially amplified. 3.2 Overall appreciation of the
ability to identify BSE - cases and to eliminate animals at risk of
being infected before they are processed Cattle population structure
Detailed information is provided in the CD on the cattle population and
their husbandry system. Approximately 30 million cattle is the national
population of which the majority is for beef production, and
approximately 6 % dairy. Approximately 34 % of animals are over 24
months old. In dairy cattle, 59 % of the milk production is derived from
intensive production. The average age and weight at slaughter varies
according to rearing system. Slaughter tends to occur at approximately 3
years on extensive pasture, 2 years on semiintensive, 1.3 years on
intensive fattening, 6 - 7 years for dairy cows and 10 years for
breeding cows. BSE surveillance Notification of BSE is compulsory since
21 September 1994. Awareness/training measures were initially put in
place in 1994 and increased in intensity since 1997 (leaflets, training
scheme on BSE - related issues, sampling manual). Laboratory personnel
have been trained since 1997 in surveillance, diagnostic techniques and
risk management in Mexico but also in Canada and USA. Since November
1998 a trilateral agreement (Mexico - USA - Canada) on an exchange
program in relation to BSE has been set up, that focuses on diagnostics
and surveillance. The methods used for BSE suspects are described. Since
the end of 1996, histopathology has been used. Together with Canada and
USA, a project on immunohistochemistry as a diagnostic technique has
been jointly set up, and the same monoclonal commercial antibodies will
be used in the three countries. In the years 1996 to 2003, a total of
2047 animals have been tested for BSE (1726 > 29 months of age), with
active surveillance in place since 1997. Since 2000, some fallen stock
has also been targeted. No positive test results have occurred. Annex to
the EFSA Scientific Report (2004) 4, 1-13 on the Assessment of the
Geographical BSE Risk of Mexico - 10 - The CD describes a program for
increased BSE surveillance beginning in 2004 (“Program of
Epidemiological Vigilance and Prevention of BSE for 2004”). This is a
programme developed in conjunction with the “Commission of Mexico to the
United States for the Prevention of Foot and Mouth Disease and other
Exotic Illnesses of Animals”. 3.3 Overall assessment of the stability
For the overall assessment of the stability, the impact of the three
main stability factors (i.e. feeding, rendering and SRM - removal) and
of the additional stability factor, BSE-surveillance, has to be
estimated. The guidance provided by the SSC in its opinion on the GBR of
July 2000 (as updated in 2002) is applied. Feeding: Feeding MBM to
cattle was legally possible until October 2000 and the information
provided indicates that it was common practice for both dairy and beef
cattle. Therefore feeding was assumed to be “not OK” for the period
1980-2000. The feed ban is of ruminant MBM only and good evidence of its
effectiveness is not provided. Therefore feeding remains “not OK” also
for the period 2000-2003. Rendering: Rendering is and was common
practice in Mexico. Ruminant material is included, excluding most SRM
and most fallen stock. The process used was and is not adequate for
reducing BSE - infectivity. Therefore rendering is assessed as having
been "not OK" throughout the reference period (i.e. 1980-2003).
SRM-removal: There is no SRM ban. However, SRM is consumed by humans and
it does not tend to enter the feed chain and fallen stock and diseased
animals are incinerated. Hence SRM-removal it is assessed as "reasonably
OK" throughout the reference period (i.e. 1980-2003). BSE surveillance
There is some passive and active BSE surveillance. However, given the
large cattle population size, the BSE surveillance system in Mexico is
insufficient. Recent plans have been introduced to increase surveillance
efforts since 2004. On the basis of the available information it has to
be concluded that the country’s BSE/cattle system was and is very
unstable. Incoming BSE - infectivity would have been recycled and
quickly amplified. The stability of the BSE/cattle system in Mexico
overtime is as given in table 4. Annex to the EFSA Scientific Report
(2004) 4, 1-13 on the Assessment of the Geographical BSE Risk of Mexico
- 11 - Stability of the BSE/cattle system in MEXICO over time Stability
Reasons Period Level Feeding Rendering SRM removal BSE surveillance 1980
to 2003 Very unstable Not OK Not OK Reasonably OK 1996 – 2003: passive
and some active surveillance Table 4: Stability resulting from the
interaction of the three main stability factors and the BSE
surveillance. The stability level is determined according to the SSC -
opinion on the GBR of July 2000 (as updated in 2002). 4. CONCLUSION ON
THE RESULTING RISKS 4.1 Interaction of stability and challenges In
conclusion, the stability of the Mexico BSE/cattle system in the past
and the external challenges the system has coped with are summarized in
the table 5 below. From the interaction of the two parameters
“stability” and “external challenge” a conclusion is drawn on the level
of “internal challenge” that emerged and had to be met by the system, in
addition to external challenges that occurred. INTERACTION OF STABILITY
AND EXTERNAL CHALLENGE IN MEXICO Period Stability External Challenge
Internal challenge 1980 to 1985 1986 to 1990 Negligible Highly unlikely
1991 to 1995 Very high 1996 to 2000 2001 to 2003 Very unstable Extremely
high Likely to be present and growing since 1993 Table 5: Internal
challenge resulting from the interaction of the external challenge and
stability. The internal challenge level is determined according to
guidance given in the SSC - opinion on the GBR of July 2000 (as updated
in 2002). An external challenge resulting from cattle import could only
lead to an internal challenge once imported infected cattle were
rendered for feed and this contaminated feed reached domestic cattle.
Cattle imported for slaughter would normally be slaughtered at an age
too young to harbour large amounts of BSE infectivity or to show signs,
even if infected prior to import. Breeding cattle, however, would
normally live much longer and only animals having problems would be
slaughtered younger. If being 4 - 6 years old when slaughtered, they
could suffer from early signs of BSE, being approaching the end of the
BSE - incubation period. In that case, they Annex to the EFSA Scientific
Report (2004) 4, 1-13 on the Assessment of the Geographical BSE Risk of
Mexico - 12 - would harbour, while being pre - clinical, as much
infectivity as a clinical BSE case. Hence cattle imports could have led
to an internal challenge about 3 years after the import of breeding
cattle (that are normally imported at 20 - 24 months of age) that could
have been infected prior to import. In case of Mexico this implies that
an internal challenge caused by live cattle imports (predominantly from
USA or Canada) first occurred in the mid to late 1990’s and continued to
the present. On the other hand imports of contaminated MBM would lead to
an internal challenge in the year of import, if fed to cattle. The
feeding system is of utmost importance in this context. If it could be
excluded that imported, potentially contaminated feed stuffs reached
cattle, such imports might not lead to an internal challenge at all. In
case of Mexico this implies that an internal challenge caused by MBM
imports (predominantly from USA or Canada) first occurred around 1993
and continued to the present. In view of the above - described
consideration the combination of the very / extremely high external
challenges with a very unstable system makes the occurrence of an
internal challenge likely in Mexico from approximately 1993 onwards. 4.2
Risk that BSE infectivity entered processing It is likely that BSE
infectivity entered processing at the time of imported ‘at - risk’ MBM
(1993) and at the time of slaughter of imported live ‘at - risk’ cattle
(mid to late 1990’s). The high level of external challenge is maintained
throughout the reference period, and the system has not been made
stable, leading to increased internal challenge. 4.3 Risk that BSE
infectivity was recycled and propagated It is likely that BSE
infectivity was recycled and propagated from approximately 1993. The
risk has since grown consistently due to a maintained internal and
external challenge and lack of a stable system. 5. CONCLUSION ON THE
GEOGRAPHICAL BSE - RISK 5.1 The current GBR as function of the past
stability and challenge The current geographical BSE risk (GBR) level is
III, i.e. it is likely but not confirmed that domestic cattle are
(clinically or pre-clinically) infected with the BSE-agent. 5.2 The
expected development of the GBR as a function of the past and present
stability and challenge • The GBR is likely to increase due to continued
internal and external challenge, coupled with a very unstable system. •
Since recent improvements in the safety of MBM production in many
countries or significant recent reductions in the incidence of BSE are
not taken into account for the assessment of the external challenge, the
external Annex to the EFSA Scientific Report (2004) 4, 1-13 on the
Assessment of the Geographical BSE Risk of Mexico challenge assessed
after 2001 could be overestimated and is the worst case assumption.
However all current GBR conclusions are not dependent on these
assumptions in any of the countries assessed. For future assessments and
when the impact of the production, surveillance and true incidence
changes has been fully quantified, these developments should be taken
into account. 5.3 Recommendations for influencing the future GBR •
Measures that improve the stability of the system, will, over time,
reduce the probability that cattle get infected with the BSE-agent.
Possible actions include - strict removal of SRM and/or fallen stock
from rendering, - pressurized rendering processes, - significant
improvement of ban on use of ruminant MBM in cattle feed, supported by
regular sampling of such feed for the non-occurrence of MBM. • Improved
passive and active surveillance, i.e. sampling of animals not showing
signs compatible with BSE from “at - risk” cattle populations, such as
adult cattle in fallen stock and emergency slaughter, by means of rapid
screening, would allow monitoring the efficiency of the stability
enhancing measures. Documentation... snip...
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/566/sr04_biohaz02_mexico_report_annex_en1.pdf
From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Tuesday, July 29,
2003 1:03 PM To: fdadockets@oc.fda.gov Cc: ggraber@cvm.fda.gov;
Linda.Grassie@fda.gov; 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
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
"Terry S. Singeltary Sr." 07/11/2004 09:34 PM To: fdadockets@oc.fda.gov
cc: regulations@aphis.usda.gov, burt.pritchett@fda.gov bcc: Subject:
Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW
BSE SAFEGUARDS (comment submission) Docket No. 04-047-l No. 04-021ANPR
No. 2004N-0264 NEW BSE SAFEGUARDS Federal Measures to Mitigate BSE
Risks: Considerations for Further Action
http://www.fda.gov/cvm/index/updates/bseanprm.htm Greetings FDA, USDA
and APHIS et al, I would kindly like to comment on the continued delay
of the regulations that have been proposed for years to reduce the risk
of BSE/TSE in the USA. Each day that is wasted debating this issue
allows this agent to spread, and many many more humans and animals
become needlessly exposed to this agent via a multitude of potential
routes and sources right here in the USA. TO continue to ignore the new
findings from several scientists about the fact that BSE is not the only
strain of TSE in cattle, the fact that new atypical strains of TSE are
showing up in not only cattle, but sheep and the fact that the new
strain of TSE in cattle seems to be more similar to sporadic CJD as
opposed to the nv/v CJD, to continue to ignore these findings will only
further spread this agent. CWD and Scrapie have been running rampant in
the USA for decades. BOTH of which have been rendered and fed back to
animals for human/animal consumption for decades. All of which transmits
to primates by the natural and non-forced oral consumption of TSE
scrapie, CJD, Kuru agent (and CWD by inoculation). Strong Scientific
evidence discovered back in the 80s support the fact that a TSE has been
prevalent in the USA bovine for decades, either undetected or ignored.
IF you consider the recent stumbling and staggering TEXAS cow that was
showing all signs of a CNS/TSE disorder that was ordered to be rendered
without BSE/TSE test, brains, spinal cord, head and all (as to no
possible evidence left of TSE), I would think the 'ignored' or 'covered
up' to be the better terminology. Then you have the Downer in Washington
state that was actually a good walker and then all the banned Canadian
products that some how found it's way across the border into the USA,
considering all this, it is very difficult for me to believe that the
FDA/USDA/APHIS et al are doing everything possible to protect the
'consumer'. Hardly the case; snip... Congressman Henry Waxmans Letter to
the Honorable Ann Veneman
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
snip... USA BSE RED BOOK > October 1998 > > BSE Red Book 2.1-36 > >
7.2.1.7 Laboratory Coordination--The Laboratory Coordination Officer >
will advise the READE(3 Director concerning laboratory capabilities and
> appropriate laboratory examinations to be conducted to provide needed
> results as rapidly as possible. This individual will assist with >
interpretation of results. seems that if the 'enhanced BSE/TSE testing
program' is to test some 400,000+ animals in 1 1/2 years, they better
hurry up, times a wasting. > BSE Red Book 2.1-39 > > 7.6 Depopulation
Procedures > > Under no > circumstances may BSE suspects be sent fo
slaughhter or rendering. snip... > BSE Red Book 2.1-40 > > 7.7 Disposal
> Under no circumstances may BSE suspects be sent to slaughter or >
rendering. Notify FDA, CVM if you suspect that the carcass of a >
BSE-confirmed animal has moved to rendering or animal feed >
manufacturing. Field personel should arrange for the carcass to be >
transported to and examined by a qualified veterinary pathologist or >
field veterinary medical officer. After the pathologic examination has >
been completed and the necessary diagnostic specimens have been >
obtained, field personnel should arrange for disposal of the carcass. >
Before a method of disposal is selected, there are many factors that >
must be considered, and often other State and Federal agencies must be >
consulted. The environmental and legal impacts of the operation must be
> considered. Upon recommendation of the State or Federal agencies, VS
may > consider other disposal methods. > snip... > 7.7.3 Rendering >
Because BSE is spread by rendered animal protein, BSE-suspect and >
confirmed carcasses must not be rendered, unless the rendered material >
is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or
> carcasses have moved to rendering or animal feed manufacturing. >
snip... > 7.10.11 Prevention--Suspects and animals confirmed to have BSE
must not > be rendered. Producers, feed mills, and rendering
establishments should > adhere to U.S. State and local rendering
policies and FDA regulations > concerning the feeding of rendered animal
protein to ruminants. TSS Terry S. Singeltary Sr. wrote: > ########
Bovine Spongiform Encephalopathy > ######### > > ONE HUNDRED EIGHTH
CONGRESS > CONGRESS OF THE UNITED STATES > HOUSE OF REPRESENTATIVES >
COMMITTEE ON GOVERNMENT REFORM > 2157 RAYBURN HOUSE OFFICE BUILDING >
WASHINGTON, DC 20515-6143 > > > www.house.gov/reform > > May 13, 2004 >
> > The Honorable Ann M. Veneman > Secretary of Agriculture >
Department of Agriculture > 1400 Independence Avenue, SW > Washington,
DC 20250 > > Dear Madam Secretary: > > 1 am writing to express concern
that the recent failure of the U.S. > Department of > Agriculture (USDA)
to test a Texas cow with neurological symptoms for > bovine spongiform >
encephalopathy (BSE) may reflect wider problems in the surveillance >
program. USDA > apparently does not keep track of how many cows
condemned for central > nervous system > symptoms are tested for BSE nor
does it require that suspect carcasses > be held pending testing.
snip... USDA/APHIS ET AL MUST GET BSE/TSE TESTING DONE CORRECTLY THE
recent findings of positive 'inconclusives' that turned up negative was
not only a nightmare to the consumer, but also to the farmers and
industry as well. Using Prionics or Bio-Rad or whatever rapid TSE test
will never eliminate the potential for human error. IF we look at the
recent discovery of the BSE in Switzerland in the Zoo Zebu, the testing
they perform would have eliminated this mix-up; Diagnosis: A. Laboratory
where diagnosis was made: Institute of Animal Neurology, University of
Bern (OIE Reference Laboratory for bovine spongiform encephalopathy). B.
Diagnostic tests used: - histology; - immunohistochemistry; - ELISA (two
different kits); - western blot. All tests gave positive results.
http://www.oie.int/eng/info/hebdo/AIS_38.HTM#Sec9 ALSO, if we look at
the USA BSE EMERGENCY RESPONSE PLAN, where it states; Subject: U.S.
Emergency Bovine Spongiform Encephalopathy Response Plan Summary Date:
Tue, 4 May 1999 18:25:12 -0500 From: "Terry S. Singeltary Sr." Reply-To:
BSEL To: BSEL snip... If additional tests do suggest a presumptive
diagnosis of BSE, an NVSL pathologist will hand carry the sample to the
United Kingdom for confirmation. It is at this critical point, when NVSL
suggests a diagnosis of BSE and is preparing to send the sample to the
United Kingdom, that this BSE Response Plan is initiated. The Plan
begins the preliminary notification from NVSL to APHIS. Preliminary
Notification The director of NVSL is responsible for immediately
notifying the APHIS, Veterinary Services (VS) deputy administrator when
tests suggest a presumptive diagnosis of BSE. Once NVSL has made a
presumptive diagnosis of BSE, APHIS and FSIS field activities will also
be initiated. APHIS will receive notification (either confirming or not
confirming NVSL's diagnosis) from the United Kingdom anywhere between 24
and 96 hours. (The international animal health community has recognized
the United Kingdom's Central Veterinary Laboratory {CVL} as the world's
reference laboratory for diagnosing BSE. Other countries, including
Belgium, France, Ireland, Luxembourg, the Netherlands, Portugal, and
Switzerland, have all sent samples to this lab to confirm their first
case of BSE). snip...end...TSS WHY is the UK not going to verify the
findings of BSE/TSE in tissue samples as the original BSE emergency
response plan told them too? I think that having several different rapid
TSE test kits (Prionics, Bio-Rad etc.) along with the IHC and finally
the OIE reference laboratory for confirmation is the best possible
answer. Prusiner et al have a test that is some 1,000 times more
sensitive and I only ponder why we are not using it? My fear is that
once testing becomes more sensitive, more tissue/organ will become known
to hold infectivity of some titre of the TSE agent. THEN we must ponder
if _accumulation_ may play a role? With the threat from new atypical
TSEs in many species and the real threat from iatrogenic CJD, the fact
that we do not yet know how these new 'atypical' phenotpyes will
transmit and how infectious there tissues may be, we must act now, we
cannot flounder any longer. Docket No. 03-080-1 -- USDA ISSUES PROPOSED
RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to
load]
https://web01.aphis.usda.gov/BSEcom.nsf/BSEFrameset?OpenFrameSet&Frame=BottomFrame&Src=_25t156hb3dtmisrjjconjcc9n6ph6ccr66oqjgdpo74qm6e1l68qjcp9hc4o30dhgckq34phfc8rjgoj16orjep9ic8o66c9i64s3achl6pi68cpg60r38eb675i3ujrgcln48rr3elmmarjk4p0nat3f8pp62rb5cg0_
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment
Number: EC -10 Accepted - Volume 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be07.html
PART 2
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be09.html
PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page
1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr.
[flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Asante/Collinge et al, that BSE transmission to the 129-methionine
genotype can lead to an alternate phenotype that is indistinguishable
from type 2 PrPSc, the commonest _sporadic_ CJD;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm Docket
Management Docket: 96N-0417 - Current Good Manufacturing Practice in
Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number:
EC -2 Accepted - Volume 7
http://www.fda.gov/ohrms/dockets/dailys/03/Mar03/031403/96N-0417-EC-2.htm
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1
File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass
Destruction Operations Unit Federal Bureau of those who provided
comments in response to Docket No. ... Meager 8/18/01 Terry S.
Singeltary Sr ... www.aphis.usda.gov/lpa/pubs/pubs/PL107-9_Appen.pdf
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO
DOCKET 2003N-0312]
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of
2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] -
TSS 1/27/03 (0) Docket Management Docket: 02N-0276 - Bioterrorism
Preparedness; Registration of Food Facilities, Section 305 Comment
Number: EC-254 [TSS SUBMISSION]
http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title,
1978N-0301, OTC External Analgesic Drug Products, ... EMC 7, Terry S.
Singeltary Sr. Vol #: 1, ...
www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm Daily
Dockets Entered on 02/05/03 DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry
S. Singeltary Sr. Vol#: 2. ... Vol#: 1. 03N-0009 Federal Preemption of
State & Local Medical Device Requireme. ...
www.fda.gov/ohrms/dockets/dailys/03/Feb03/020503/020503.htm Docket
Management Docket: 02N-0370 - Neurological Devices; Classification of
Human Dura Mater Comment Number: EC -1 Accepted - Volume 1
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html
http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html
Daily Dockets - 04/10/03 ... 00D-1662 Use of Xenotransplantation
Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...
www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003
- Cached > 2003D-0186 Guidance for Industry: Use of Material From Deer
and Elk In Animal Feed EMC 1 Terry S. Singeltary Sr. Vol #: 1 --------
Original Message -------- Subject: DOCKET-- 03D-0186 -- FDA Issues Draft
Guidance on Use of Material >From Deer and Elk in Animal Feed;
Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S.
Singeltary Sr." To: fdadockets@oc.fda.gov Greetings FDA, i would kindly
like to comment on; Docket 03D-0186 FDA Issues Draft Guidance on Use of
Material From Deer and Elk in Animal Feed; Availability Several factors
on this apparent voluntary proposal disturbs me greatly, please allow me
to point them out; 1. MY first point is the failure of the partial
ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed
ban of some ruminant materials being fed back to cattle is terribly
flawed. without the _total_ and _mandatory_ ban of all ruminant
materials being fed back to ruminants including cattle, sheep, goat,
deer, elk and mink, chickens, fish (all farmed animals for human/animal
consumption), this half ass measure will fail terribly, as in the past
decades... 2. WHAT about sub-clinical TSE in deer and elk? with the
recent findings of deer fawns being infected with CWD, how many could
possibly be sub-clinically infected. until we have a rapid TSE test to
assure us that all deer/elk are free of disease (clinical and
sub-clinical), we must ban not only documented CWD infected deer/elk,
but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL
tissues. recent new and old findings support infectivity in the rump or
ass muscle. wether it be low or high, accumulation will play a crucial
role in TSEs. 4. THERE are and have been for some time many TSEs in the
USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in
USA cattle. all this has been proven, but the TSE in USA cattle has been
totally ignored for decades. i will document this data below in my
references. 5. UNTIL we ban all ruminant by-products from being fed back
to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle
in sufficient numbers to find (1 million rapid TSE test in USA cattle
annually for 5 years), any partial measures such as the ones proposed
while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not
closing down feed mills that continue to violate the FDA's BSE feed
regulation (21 CFR 589.2000) and not making freely available those
violations, will only continue to spread these TSE mad cow agents in the
USA. I am curious what we will call a phenotype in a species that is
mixed with who knows how many strains of scrapie, who knows what strain
or how many strains of TSE in USA cattle, and the CWD in deer and elk
(no telling how many strains there), but all of this has been rendered
for animal feeds in the USA for decades. it will get interesting once
someone starts looking in all species, including humans here in the USA,
but this has yet to happen... 6. IT is paramount that CJD be made
reportable in every state (especially ''sporadic'' cjd), and that a CJD
Questionnaire must be issued to every family of a victim of TSE. only
checking death certificates will not be sufficient. this has been proven
as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE) 7. WE must learn
from our past mistakes, not continue to make the same mistakes...
REFERENCES Six white-tailed deer fawns test positive for CWD MADISON --
Six fawns in the area of south central Wisconsin where chronic wasting
disease has been found in white-tailed deer have tested positive for the
disease, according to Department of Natural Resources wildlife health
officials. These are the youngest wild white-tailed deer detected with
chronic wasting disease (CWD) to date. Approximately 4,200 fawns,
defined as deer under 1 year of age, were sampled from the eradication
zone over the last year. The majority of fawns sampled were between the
ages of 5 to 9 months, though some were as young as 1 month. Two of the
six fawns with CWD detected were 5 to 6 months old. All six of the
positive fawns were taken from the core area of the CWD eradication zone
where the highest numbers of positive deer have been identified. snip...
http://www.dnr.state.wi.us/org/caer/ce/news/on/2003/on20030513.htm#art4
=================================================== Issued: Monday, 28
August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT
RESEARCH FINDINGS RELEVANT TO CJD AND BSE A team of researchers led by
Professor John Collinge at the Medical Research Council Prion Unit1
report today in the Proceedings of the National Academy of Sciences, on
new evidence for the existence of a 'sub-clinical' form of BSE in mice
which was unknown until now. The scientists took a closer look at what
is known as the 'species barrier' - the main protective factor which
limits the ability of prions2 to jump from one species to infect
another. They found the mice had a 'sub-clinical' form of disease where
they carried high levels of infectivity but did not develop the clinical
disease during their normal lifespan. The idea that individuals can
carry a disease and show no clinical symptoms is not new. It is commonly
seen in conventional infectious diseases. Researchers tried to infect
laboratory mice with hamster prions3 called Sc237 and found that the
mice showed no apparent signs of disease. However, on closer inspection
they found that the mice had high levels of mouse prions in their
brains. This was surprising because it has always been assumed that
hamster prions could not cause the disease in mice, even when injected
directly into the brain. In addition the researchers showed that this
new sub-clinical infection could be easily passed on when injected into
healthy mice and hamsters. The height of the species barrier varies
widely between different combinations of animals and also varies with
the type or strain of prions. While some barriers are quite small (for
instance BSE easily infects mice), other combinations of strain and
species show a seemingly impenetrable barrier. Traditionally, the
particular barrier studied here was assumed to be robust. Professor John
Collinge said: "These results have a number of important implications.
They suggest that we should re-think how we measure species barriers in
the laboratory, and that we should not assume that just because one
species appears resistant to a strain of prions they have been exposed
to, that they do not silently carry the infection. This research raises
the possibility, which has been mentioned before, that apparently
healthy cattle could harbour, but never show signs of, BSE. "This is a
timely and unexpected result, increasing what we know about prion
disease. These new findings have important implications for those
researching prion disease, those responsible for preventing infected
material getting into the food chain and for those considering how best
to safeguard health and reduce the risk that theoretically, prion
disease could be contracted through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS
SET BY THE JOURNAL. FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE
ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357
(OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760.
PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL
ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN
ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A
CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE
UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING
OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE
THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME. NOTES FOR EDITORS
Professor Collinge is a consultant neurologist and Director of the newly
formed MRC Prion Unit based at The Imperial College School of Medicine
at St Mary's Hospital. He is also a member of the UK Government's
Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit
is was set up in 1999, and its work includes molecular genetic studies
of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such
as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad
cow disease) in animals. In some circumstances prions from one species
of animals can infect another and it is clear that BSE has done this to
cause the disease variant CJD in the UK and France. It remains unclear
how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain
(also known as 263K) which infects hamsters, and until now was assumed
not to infect mice. This research was funded by the Medical Research
Council and Wellcome Trust. The Medical Research Council (MRC) is a
national organisation funded by the UK tax-payer. Its business is
medical research aimed at improving human health; everyone stands to
benefit from the outputs. The research it supports and the scientists it
trains meet the needs of the health services, the pharmaceutical and
other health-related industries and the academic world. MRC has funded
work which has led to some of the most significant discoveries and
achievements in medicine in the UK. About half of the MRC's expenditure
of ÂŁ345 million is invested in over 50 of its Institutes and Units,
where it employs its own research staff. The remaining half goes in the
form of grant support and training awards to individuals and teams in
universities and medical schools. The Wellcome Trust is the world's
largest medical research charity with a spend of some ÂŁ600 million in
the current financial year 1999/2000. The Wellcome Trust supports more
than 5,000 researchers, at 400 locations, in 42 different countries to
promote and foster research with the aim of improving human and animal
health. As well as funding major initiatives in the public understanding
of science, the Wellcome Trust is the country's leading supporter of
research into the history of medicine. ©2002 Medical Research Council
Data Protection policy | Contact the MRC
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
====================================== Oral transmission and early
lymphoid tropism of chronic wasting disease PrPres in mule deer fawns
(Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2,
Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and
Edward A. Hoover1 Department of Pathology, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University, Fort
Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences,
University of Wyoming, 1174 Snowy Range Road, University of Wyoming,
Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife
Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097,
USA3 Colorado State University Veterinary Diagnostic Laboratory, 300
West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease
Research Unit, Agricultural Research Service, US Department of
Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA
99164-7030, USA5 Author for correspondence: Edward Hoover.Fax +1 970 491
0523. e-mail ehoover@lamar.colostate.edu Mule deer fawns (Odocoileus
hemionus) were inoculated orally with a brain homogenate prepared from
mule deer with naturally occurring chronic wasting disease (CWD), a
prion-induced transmissible spongiform encephalopathy. Fawns were
necropsied and examined for PrP res, the abnormal prion protein isoform,
at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an
immunohistochemistry assay modified to enhance sensitivity. PrPres was
detected in alimentary-tract-associated lymphoid tissues (one or more of
the following: retropharyngeal lymph node, tonsil, Peyer's patch and
ileocaecal lymph node) as early as 42 days p.i. and in all fawns
examined thereafter (53 to 80 days p.i.). No PrPres staining was
detected in lymphoid tissue of three control fawns receiving a control
brain inoculum, nor was PrPres detectable in neural tissue of any fawn.
PrPres-specific staining was markedly enhanced by sequential tissue
treatment with formic acid, proteinase K and hydrated autoclaving prior
to immunohistochemical staining with monoclonal antibody F89/160.1.5.
These results indicate that CWD PrP res can be detected in lymphoid
tissues draining the alimentary tract within a few weeks after oral
exposure to infectious prions and may reflect the initial pathway of CWD
infection in deer. The rapid infection of deer fawns following exposure
by the most plausible natural route is consistent with the efficient
horizontal transmission of CWD in nature and enables accelerated studies
of transmission and pathogenesis in the native species. snip... These
results indicate that mule deer fawns develop detectable PrP res after
oral exposure to an inoculum containing CWD prions. In the earliest
post-exposure period, CWD PrPres was traced to the lymphoid tissues
draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph
nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which
probably received the highest initial exposure to the inoculum. Hadlow
et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal
and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally
infected lamb by mouse bioassay. Eight of nine sheep had infectivity in
the retropharyngeal lymph node. He concluded that the tissue
distribution suggested primary infection via the gastrointestinal tract.
The tissue distribution of PrPres in the early stages of infection in
the fawns is strikingly similar to that seen in naturally infected sheep
with scrapie. These findings support oral exposure as a natural route of
CWD infection in deer and support oral inoculation as a reasonable
exposure route for experimental studies of CWD. snip...
http://vir.sgmjournals.org/cgi/content/full/80/10/2757
=================================== now, just what is in that deer feed?
_ANIMAL PROTEIN_ Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr."
Reply-To: BSE-L To: BSE-L 8420-20.5% Antler Developer For Deer and Game
in the wild Guaranteed Analysis Ingredients / Products Feeding
Directions snip... _animal protein_ http://www.surefed.com/deer.htm
BODE'S GAME FEED SUPPLEMENT #400 A RATION FOR DEER NET WEIGHT 50 POUNDS
22.6 KG. snip... _animal protein_ http://www.bodefeed.com/prod7.htm
Ingredients Grain Products, Plant Protein Products, Processed Grain
By-Products, Forage Products, Roughage Products 15%, Molasses Products,
__Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate,
Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal
Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12
Supplement, Riboflavin Supplement, Niacin Supplement, Calcium
Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite
Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin,
Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt
Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles,
Cellulose gum, Artificial Flavors added.
http://www.bodefeed.com/prod6.htm ===================================
MORE ANIMAL PROTEIN PRODUCTS FOR DEER Bode's #1 Game Pellets A RATION
FOR DEER F3153 GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat
(Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca)
(Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Ingredients Grain Products, Plant Protein Products, Processed Grain
By-Products, Forage Products, Roughage Products, 15% Molasses Products,
__Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate,
Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal
Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12
Supplement, Roboflavin Supplement, Niacin Supplement, Calcium
Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite
Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin,
Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt
Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles,
Cellulose gum, Artificial Flavors added. FEEDING DIRECTIONS Feed as
Creep Feed with Normal Diet http://www.bodefeed.com/prod8.htm
INGREDIENTS Grain Products, Roughage Products (not more than 35%),
Processed Grain By-Products, Plant Protein Products, Forage Products,
__Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt,
Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt
Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide,
Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium
Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A
Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium
Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite
Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,
Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate DIRECTIONS
FOR USE Deer Builder Pellets is designed to be fed to deer under range
conditions or deer that require higher levels of protein. Feed to deer
during gestation, fawning, lactation, antler growth and pre-rut, all
phases which require a higher level of nutrition. Provide adequate
amounts of good quality roughage and fresh water at all times.
http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html
=================================================== DEPARTMENT OF HEALTH
& HUMAN SERVICES PUBLIC HEALTH SERVICE FOOD AND DRUG ADMINISTRATION
April 9, 2001 WARNING LETTER 01-PHI-12 CERTIFIED MAIL RETURN RECEIPT
REQUESTED Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O.
Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT Tel: 215-597-4390
Dear Mr. Raymond: Food and Drug Administration Investigator Gregory E.
Beichner conducted an inspection of your animal feed manufacturing
operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and
determined that your firm manufactures animal feeds including feeds
containing prohibited materials. The inspection found significant
deviations from the requirements set forth in Title 21, code of Federal
Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant
Feed. The regulation is intended to prevent the establishment and
amplification of Bovine Spongiform Encephalopathy (BSE) . Such
deviations cause products being manufactured at this facility to be
misbranded within the meaning of Section 403(f), of the Federal Food,
Drug, and Cosmetic Act (the Act). Our investigation found failure to
label your swine feed with the required cautionary statement "Do Not
Feed to cattle or other Ruminants" The FDA suggests that the statement
be distinguished by different type-size or color or other means of
highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of
cracked corn to flush your mixer used in the manufacture of animal feeds
containing prohibited material. This flushed material is fed to wild
game including deer, a ruminant animal. Feed material which may
potentially contain prohibited material should not be fed to ruminant
animals which may become part of the food chain. The above is not
intended to be an all-inclusive list of deviations from the regulations.
As a manufacturer of materials intended for animal feed use, you are
responsible for assuring that your overall operation and the products
you manufacture and distribute are in compliance with the law. We have
enclosed a copy of FDA's Small Entity Compliance Guide to assist you
with complying with the regulation... blah, blah, blah...
http://www.fda.gov/foi/warning_letters/g1115d.pdf
================================== snip... posted here;
http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed EMC 7 Terry S. Singeltary Sr. Vol #: 1 2003D-0186 Guidance
for Industry: Use of Material From Deer and Elk In Animal Feed EMC 7
Terry S. Singeltary Sr. Vol #: 1
http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm
Chronic Wasting Disease and Potential Transmission to Humans Ermias D.
Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W.
Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for
Disease Control and Prevention, Atlanta, Georgia, USA; University of
Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort
Collins, Colorado, USA; and §Case Western Reserve University, Cleveland,
Ohio, USA Suggested citation for this article: Belay ED, Maddox RA,
Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting
disease and potential transmission to humans. Emerg Infect Dis [serial
on the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
------------------------------------------------------------------------
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner
area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been
detected in other parts of the United States. Although detection in some
areas may be related to increased surveillance, introduction of CWD due
to translocation or natural migration of animals may account for some
new foci of infection. Increasing spread of CWD has raised concerns
about the potential for increasing human exposure to the CWD agent. The
foodborne transmission of bovine spongiform encephalopathy to humans
indicates that the species barrier may not completely protect humans
from animal prion diseases. Conversion of human prion protein by
CWD-associated prions has been demonstrated in an in vitro cell-free
experiment, but limited investigations have not identified strong
evidence for CWD transmission to humans. More epidemiologic and
laboratory studies are needed to monitor the possibility of such
transmissions. snip... Transmission to Other Animals Concerns have been
raised about the possible transmission of the CWD agent to domestic
animals, such as cattle and sheep, which may come in contact with
infected deer and elk or CWD-contaminated environments. If such
transmissions were to occur, they would potentially increase the extent
and frequency of human exposure to the CWD agent. In addition, passage
of the agent through a secondary host could alter its infectious
properties, increasing its potential for becoming more pathogenic to
humans. This phenomenon may have occurred with BSE when a strain of
scrapie, a possible original source of the BSE outbreak, changed its
pathogenic properties for humans after infecting cattle. However, the
exact origin of BSE remains unknown. Although CWD does not appear to
occur naturally outside the cervid family, it has been transmitted
experimentally by intracerebral injection to a number of animals,
including laboratory mice, ferrets, mink, squirrel monkeys, and goats (1
,26 ). In an experimental study, the CWD agent was transmitted to 3 of
13 intracerebrally injected cattle after an incubation period of 22 to
27 months (27 ). The susceptibility of cattle intracerebrally challenged
with the agent of this disease was substantially less than that observed
after intracerebral scrapie challenge: nine of nine cattle succumbed to
scrapie challenge after intracerebral injection (28 ). In ongoing
experimental studies, after >6 years of observation, no prion disease
has developed in 11 cattle orally challenged with the CWD agent or 24
cattle living with infected deer herds (E.S. Williams and M.W. Miller,
unpub. data) (1 ). In addition, domestic cattle, sheep, and goat
residing in research facilities in close contact with infected cervids
did not develop a prion disease. [PLEASE NOTE, THIS HAS BEEN UPDATED TO
AN ADDITIONAL 2 COWS AND ONE SHEEP, making the total transmission of CWD
to cattle at 5 and one transmission of CWD to one sheep, MILLER ET AL
BSE-L...TSS] Conclusions The lack of evidence of a link between CWD
transmission and unusual cases of CJD, despite several epidemiologic
investigations, and the absence of an increase in CJD incidence in
Colorado and Wyoming suggest that the risk, if any, of transmission of
CWD to humans is low. Although the in vitro studies indicating
inefficient conversion of human prion protein by CWD-associated prions
raise the possibility of low-level transmission of CWD to humans, no
human cases of prion disease with strong evidence of a link with CWD
have been identified. However, the transmission of BSE to humans and the
resulting vCJD indicate that, provided sufficient exposure, the species
barrier may not completely protect humans from animal prion diseases.
Because CWD has occurred in a limited geographic area for decades, an
adequate number of people may not have been exposed to the CWD agent to
result in a clinically recognizable human disease. The level and
frequency of human exposure to the CWD agent may increase with the
spread of CWD in the United States. Because the number of studies
seeking evidence for CWD transmission to humans is limited, more
epidemiologic and laboratory studies should be conducted to monitor the
possibility of such transmissions. Studies involving transgenic mice
expressing human and cervid prion protein are in progress to further
assess the potential for the CWD agent to cause human disease.
Epidemiologic studies have also been initiated to identify human cases
of prion disease among persons with an increased risk for exposure to
potentially CWD-infected deer or elk meat (47 ). If such cases are
identified, laboratory data showing similarities of the etiologic agent
to that of the CWD agent would strengthen the conclusion for a causal
link. Surveillance for human prion diseases, particularly in areas where
CWD has been detected, remains important to effectively monitor the
possible transmission of CWD to humans. Because of the long incubation
period associated with prion diseases, convincing negative results from
epidemiologic and experimental laboratory studies would likely require
years of follow-up. In the meantime, to minimize the risk for exposure
to the CWD agent, hunters should consult with their state wildlife
agencies to identify areas where CWD occurs and continue to follow
advice provided by public health and wildlife agencies. Hunters should
avoid eating meat from deer and elk that look sick or test positive for
CWD. They should wear gloves when field-dressing carcasses, bone-out the
meat from the animal, and minimize handling of brain and spinal cord
tissues. As a precaution, hunters should avoid eating deer and elk
tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes,
spleen, tonsils, lymph nodes) from areas where CWD has been identified.
snip... see full text ;
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm Diagnosis and
Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001;
285: 733-734.
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States Email Terry S. Singeltary: flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
comment on the CDC's attempts to monitor the occurrence of emerging
forms of CJD. Asante, Collinge et al [1] have reported that BSE
transmission to the 129-methionine genotype can lead to an alternate
phenotype that is indistinguishable from type 2 PrPSc, the commonest
sporadic CJD. However, CJD and all human TSEs are not reportable
nationally. CJD and all human TSEs must be made reportable in every
state and internationally. I hope that the CDC does not continue to
expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in
the USA in both animal and man. CWD in deer/elk is spreading rapidly and
CWD does transmit to mink, ferret, cattle, and squirrel monkey by
intracerebral inoculation. With the known incubation periods in other
TSEs, oral transmission studies of CWD may take much longer. Every
victim/family of CJD/TSEs should be asked about route and source of this
agent. To prolong this will only spread the agent and needlessly expose
others. In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535 BRITISH MEDICAL
JOURNAL http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2
http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 IN SHORT, we have
floundered to long in the regulation of human/animal TSEs. EACH day
longer, more and more people will become exposed. YOU can step up to the
plate and act now, forget about corporate/political interest, act in the
best of public health, with the available science to date (it's all
there), or you can pay later. AT what cost you ask, depends which loved
one you loose to this agent. THIS goes far beyond the bad hamburger.
85%+ of all CJD (sporadic), did not just happen. sporadic CJD simply
means CJD from unknown route and source of agent, and we have many of
both right here in the USA. What phenotype is anyone's guess? ALL SRM
must be removed. ALL animals for human/animal consumption must be tested
for TSE. ALL human TSEs must be made reportable Nationally and
Internationally. with CJD/TSE questionnaire asking real questions as to
route and source of agent. THIS must pertain to all ages! CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm CJD Watch
message board http://disc.server.com/Indices/167318.html full text;
https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
-------- Original Message -------- Subject: Atypical Case of Bovine
Spongiform Encephalopathy in an East-Flemish Cow in Belgium Date: Fri,
04 Feb 2005 10:59:33 -0600 From: "Terry S. Singeltary Sr." To: Bovine
Spongiform Encephalopathy CC: cjdvoice@yahoogroups.com 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. INTRODUCTION Transmissible spongiform
encephalopathies (TSEs), or prion diseases, are a group of fatal
neurodegenerative diseases including sheep and goat scrapie, bovine
spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease (CJD) in
humans. They are characterized by the accumulation of an abnormal
protein, called PrPsc, which is formed post-translationally from the
normal isoform (PrPc).1,2 At present, the agent causing TSEs is still
incompletely characterized, although PrPsc is believed to be its major
if not unique constituent.3 Research in mice showed the existence of
different scrapie strains.4,5 Scrapie strain discrimination is currently
based on biologic typing in a panel of inbred mice, using incubation
time and brain pathology scoring as criteria.6 However, no large-scale
studies of the molecular features of PrPsc have been reported for bovine
BSE to date. Till now, the BSE strain seemed to maintain constant
biologic and molecular properties even after experimental or accidental
passages into different species, such as mice, humans, primates, and
sheep.710 However, very recently, variant forms of BSE have been
reported in Japan, Italy, and France.11-13 These forms were
characterized by atypical histopathologic, immunohistochemical, or
biochemical phenotypes. The present case is the description of the first
atypical BSE case in Belgium. MATERIALS AND METHODS Since January 2001,
all cattle older than 30 months are tested for TSE via a rapid test
(TeSeE-kit, Bio-Rad, Nazareth, Belgium) after EC regulation
999/2001.14,15 Samples positive according to the enzyme-linked
immunosorbent assay (ELISA) screening are further subjected to
scrapie-associated fibrils (SAF), histopathology, immunohistochemistry,
and Western blot (WB) testing16,17 at the National Reference Laboratory
(NRL). RESULTS A positive ELISA sample from a 64-month-old East-Flemish
cow or Belgian white and red (Figure 1) was presented at the NRL for
confirmation. The animal was reported healthy before slaughter. The
optical density (OD) titers at the local laboratory were 2.324 and
2.116.16 The OD titers at the NRL were 0.953 and 0.708 (sample taken at
the contralateral side of the first sampling side of the obex region).
The histopathology of the obex, pons, and midbrain showed no spongiform
changes; immunohistochemistry of the brainstem revealed no signal of
PrPsc accumulation typical for BSE; and SAF was negative. However, WB
analysis (Bovine WB, Bio-Rad, France; antibodies 12F10 and SAF60) of the
same homogenate that was prepared from the obex region for ELISA
revealed a small amount of PrPsc with an electrophoretic profile
different from that of typical BSE-associated PrPsc.18,19 The band on
the gel of the non-glycosylated form of PrPsc of the present case
clearly showed a lower migration pattern compared with that of a typical
BSE case (Figure 2). 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. ACKNOWLEDGMENTS The
authors wish to thank Rita Geeroms, Patrick Van Muylem, Stephanie
Durand, Raphaël Foubert and Amina Chama for their technical assistance.
Mario Vanpoucke is acknowledged for providing references. REFERENCES 1.
Oesch B, Westaway D, Walchii M, et al: A cellular gene encodes PrP 2730
protein. Cell 40:735746, 1985. 2. Prusiner SB, De Armond SJ: Prion
diseases and neurodegeneration. Annu Rev Neurosci 17:311339, 1994. 3.
Prusiner SB: Scrapie prions. Annu Rev Microbiol 43:345374, 1989. 4.
Bruce M, Dickinson AG: Biological evidence that scrapie agent has an
independent genome. J Gen Virol 68:7989, 1987. 5. Fraser H, Dickinson
AG: Scrapie in mice: Agent strain differences in the distribution and
intensity of grey matter vacuolation. J Comp Pathol 83:2940, 1973. 6.
Bruce M, McConnell I, Fraser H, Dickinson AG: The disease
characteristics of different strains of scrapie in Sinc Congenic mice
lines: Impications for the nature of the agent and host control of
pathogenesis. J Virol 72:595603, 1991. 7. Bruce M, Chree A, McDonnell
I, et al: Transmission of bovine spongiform encephalopathy and scrapie
to mice: Strain variation and the species barrier. Philos Trans R Soc
Lon Ser B 343:405411, 1994. 8. Bruce M, Will RG, Ironside JW, et al:
Transmissions to mice indicate that new variant CJD is caused by the
BSE agent. Nature 389:498501, 1997. 9. Foster JD, Bruce M, McDonnell I,
et al: Detection of BSE infectivity in brain and spleen of
experimentally infected sheep. Vet Rec 138:546548, 1996. 10. Lasmezas
CI, Fournier J-G, Nouvel V, et al: Adaptation of the bovine spongiform
encephalopathy agent to primates and comparison with Creutzfeldt-Jakob
disease: Implications for human health. Proc Natl Acd Sci U S A
98:41424147, 2001. 11. Yamakawa Y, Hagiwara K, Nohtomi K, et al, for
the Expert Commitee for BSE Diagnosis, Ministry of Health, Labour and
Welfare of Japan: Atypical proteinase K-resistant prion protein (PrPres)
observed in an apparently healthy 23-month-old Holstein steer. Jpn J
Infect Dis 56:221222, 2003. 12. Casalone C, Zanusso G, Acutis PL, et
al: Identification of a novel molecular and neuropathological BSE
phenotype in Italy: International Conference on Prion Disease: from
basic research to intervention concepts. Gasreig, München, 810 October,
2003. 13. Biacabe AG, Laplanche JL, Ryder S, Baron T: A molecular
variant of bovine spongiform encephalopathy. International Conference on
Prion Disease: From basic research to intervention concepts. Gasreig,
München, 810 October, 2003. 14. De Becker D, Roels S, Vanopdenbosch E:
BSE onderzoek: opsporen van PrPres door middel van de BIO-RAD Platelia
BSE-kit. Vlaams Diergeneeskundig Tijdschrift 69:382384, 2000. 15. Roels
S, Demeyer G, Tedik K, et al: Variance of mass (volume) taken with the
calibrated syringe and of the results provided by the Bio-Rad Platelia
BSE test upon storage of brainstem samples at 20°C. Anim Res
51:493499, 2002. 16. Roels S, De Bosschere H, Saegerman C, et al: BSE
and scrapie testing in Belgium: general overview. New Food: accepted,
2004. 17. Vanopdenbosch E, Dechamps P, Dufey J, et al: Le premier cas
dencephalopathie spongioforme bovine diagnostique en Belgique. Annales
de Médicine Vétérinaire 142:111118, 1998. 18. Collinge J, Sidle KCL,
Meads J, et al: Molecular analysis of prion strain variation and the
aetiology of new variant CJD. Nature 383:685690, 1996. 19. Hill AF,
Desbruslais M, Joiner S, et al: The same prion strain causes vCJD and
BSE. Nature 389:448450, 1997. Figure 1. Photograph of the East-Flemish
cattle breed or the Belgian white and red. Figure 2. Bovine Western blot
(Bio-Rad, France) using antibodies 12F10 and SAF60. MM, Magic mark;
Atyp. BSE, Atypical BSE case (present case); Ref1, Reference 1 of a
classical BSE case; Ref2, Reference 2 of a classical BSE case. The third
band of the non-glycosylated PrPsc of the Atyp. BSE case (left
rectangle) shows a markedly faster migration compared to the Ref1 and
Ref2 cases (right rectangle).
http://www.jarvm.com/articles/Vol2Iss1/DEBOSSCHERE.htm SURE MAKES THEM
VERMONT ATYPICAL TSE SHEEP MORE AND MORE INTERESTING, ESPECIALLY SINCE
THE PUT OFF MOUSE BIO ASSAYS FOR 2 YEARS, AFTER THEY SAID THEY WOULD
START IMMEDIATELY??? I HAVE DOCUMENTATION OF THAT FOR ANYONE INTERESTED,
WITH COMMENTS FROM DEFRA, DETWILER ET AL... "Terry S. Singeltary Sr."
11/03/2003 01:19 PM To: regulations@aphis.usda.gov cc: bcc: Subject:
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA I would like to kindly comment on Docket No.
03-080-1 USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM
CANADA ; >Under this proposal, ruminant and ruminant products eligible
for entry into >the United States from a BSE minimal risk region would
include: > >1) bovine >animals less than 30 months of age for immediate
slaughter; > >2) bovine >animals for feeding to be moved to a designated
feedlot and then to >slaughter at less than 30 months of age; > snip...
>6) fresh (chilled or frozen) >meat from bovines less than 30 months of
age; 7) fresh (chilled or frozen) >whole or half carcasses of bovines
less than 30 months of age; 8) fresh >(chilled or frozen) bovine liver;
9) fresh (chilled or frozen) bovine >tongues; the myth that cattle under
30 months of age are free from BSE/TSE is just that, a myth, and it's a
false myth ! 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
http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html
http://www.defra.gov.uk/animalh/bse/index.html 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.
http://www.sare.org/htdocs/hypermail/html-home/28-html/0359.html > 3)
sheep and goats less than 12 >months of age for immediate slaughter; 4)
sheep and goats for feeding to be >moved to a designated feedlot and
then to slaughter at less than 12 months >of age; > even if one believes
that scrapie does not transmit to humans (without scientific proof and
realizing scrapie transmits to primates) what about the potential for
BSE in sheep/goats and what about the many different tissues that are
infectious ? Research into sheep TSEs - audit reports & IAH's response
http://www.defra.gov.uk/animalh/bse/bse-publications/bse-publications-index.html#audit
snip... full text;
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
ORAL 1 Variant Creutzfeldt-Jakob Disease Ironside JW, Head MW, Knight R,
Ward H National CJD Surveillance Unit, University of Edinburgh,
Edinburgh, UK Variant Creutzfeldt-Jakob disease (vCJD) is a novel human
prion disorder which on the basis of experimental strain typing appears
to result from human exposure to the bovine spongiform encephalopathy
(BSE) agent, probably by the consumption of BSE-contaminated meat
products. This disorder tends to present in young adults (median age 28
y) as a psychiatric disorder often accompanied by sensory abnormalities
and later followed by ataxia, myoclonus and other movement disorders.
Death occurs after a median duration of illness of 13 months. MRI brain
scans have shown that abnormal areas of high signal occur in T2 and
proton density images in the posterior thalamus. All patients with vCJD
have been homozygous for methionine at codon 129 in the PrP gene.
Pathologically, vCJD is characterised by florid plaques in the cerebrum
and cerebellum, and by the presence of a PrP isotype (2B), which is
distinct from other human prion diseases. vCJD also differs from other
human prion disorders in that abnormal PrP is widely distributed outside
the nervous system in lymphoid tissues. This has given rise to concerns
that vCJD may be transmitted by surgical instruments used on these
tissues, even if infectivity appears to be at lower levels than in the
brain. 2 cases of iatrogenic vCJD infection have recently been reported
following blood transfusion from donors who subsequently developed vCJD,
one of whom was a heterozygote at codon 129 in the prion protein gene
and died before the onset of clinical neurological disease. There are
considerable uncertainties over future numbers of vCJD cases in the UK,
since clinical cases appear to be declining in frequency, but
retrospective studies of PrP accumulation in tonsils and appendix tissue
have suggested that a few thousand individuals may be incubating the
disease in the UK. Continuing surveillance is required in the UK and in
other countries where BSE has been identified. ORAL 2 CLINICAL ASPECTS
OF VARIANT CJD Richard Knight Clinical Neurologist, National CJD
Surveillance Unit, UK 160 cases of variant CJD have been identified (149
in the UK). The clinico-pathological profile of human prion diseases is
influenced by PRNP codon-129 genotype, prion ‘agent strain’ (or prion
protein type) and mode of acquisition. All tested cases of variant CJD
have occurred in one genotype (codon 129 MM), with one presumed agent
strain/one protein type and one probable cause: BSE dietary
contamination (but for one instance of possible blood transmission).
Therefore, it is perhaps unsurprising that variant CJD has a relatively
uniform clinical picture, unlike the significant clinico-pathological
heterogeneity of sporadic CJD. Also unlike sporadic CJD, it is
predominantly affects the young with a relatively long duration (median
ages at onset: vCJD 26 years, sCJD 66 years; median durations: vCJD14
months, sCJD 4 months in sporadic CJD). Sporadic CJD typically presents
in a clearly neurological way, most often with a rapidly progressive
dementia. Variant CJD typically presents with a psychiatric or
behavioural disturbance; its essentially neurological nature may not be
apparent for some months. Social withdrawal, loss of interest,
dysphoria, anxiety, irritability and insomnia are common early symptoms;
depression being a frequent initial diagnosis. Sensory symptoms
(typically unpleasant) are reported in around two thirds of cases.
Specifically neurological signs appear at a median of around 6 months;
memory/cognitive dysfunction and cerebellar ataxia being the commonest
features. Other neurological features include: pyramidal signs, and
involuntary movements (chorea, dystonia, tremor, myoclonus). Definite
diagnosis requires neuropathology. The clinical diagnosis of variant CJD
rests on: a clinical suspicion of the condition, the exclusion of other
possible diagnoses and the appropriate use of supportive diagnostic
tests. The most useful non-invasive investigation is the cerebral MRI,
showing the so-called ‘Pulvinar sign’ in most cases. Tonsil biopsy is
useful in some. ORAL 4 CEREBROVENTRICULAR INFUSION OF PENTOSAN
POLYSULPHATE (PPS) IN HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Nikolai G Rainov 1,2 1 Department of Neurological Science, The
University of Liverpool, and 2The Walton Centre for Neurology and
Neurosurgery NHS Trust, Liverpool, UK Transmissible spongiform
encephalopathies (TSE) are diseases believed to be caused by
accumulation of an abnormal isoform of the prion protein (PrPsc) in the
central nervous system. There are sporadic, aquired and hereditary TSE.
Creutzfeld-Jacob disease (CJD) in its sporadic and variant form is the
most frequent and clinically important TSE. At present there is no
proven specific or effective treatment available for any form of CJD,
although drugs such as quinacrine are being investigated in early
clinical trials. Pentosan polysulphate (PPS), a large polyglycoside
molecule with weak heparin-like activity, has been shown to prolong the
incubation period of PrPsc infection when administered to the cerebral
ventricles in a rodent scrapie model. PPS also prevents the production
of further PrPsc in cell culture models. However, PPS penetrates poorly
the blood-brain barrier and only a minor fraction of orally administered
drug may reach the CNS. These properties of PPS prompted its
cerebroventricular administration in a total of 8 patients with vCJD and
other TSE, such as iatrogenic CJD and Gerstmann-Sträussler-Scheinker
syndrome (GSS). Long-term continuous infusion of PPS at doses from 11
µg/kg/day to 110 µg/kg/d did not cause any drug-related side effects.
Follow-up CT and MRI imaging demonstrated that brain atrophy may
progress during PPS administration. Proof of clinical efficacy has not
been the aim of these early studies, however one patient with vCJD
survived for 37 months after initial symptoms and 30 months after
diagnosis, while the median duration of illness with vCJD is 13 months
(range 6-39). Some lessons have been learned from the first cases.
Surgery in a brain affected by TSE may result in a higher rate of
surgical complications than might be expected in analogous cases without
TSE. Secondly, if clinically significant benefits are to be expected,
PPS administration should start as early as possible in the course of
the respective disease and before irreversible loss of neurological
function has occurred. Further clinical, neuroradiological and
laboratory investigations in the setting of a prospective clinical study
with standardised follow-up protocol and data collection are essential
in order to assess the efficacy of PPS administration in vCJD and in
other TSE. ORAL 5 Peripheral Pathogenesis of Human Prion Diseases Markus
Glatzel1, Eugenio Abela1, Nicolas Genoud1, James Ironside2, and Adriano
Aguzzi 1Swiss National Reference Center for Prion Diseases, University
Hospital of Zürich, CH-8091 Zürich, Switzerland 2The National
Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital,
Edinburgh EH4 2XU, UK Ante-mortem diagnosis of human prion diseases has
been attempted by brain biopsy, but is complicated by insurmountable
biosafety problems, is highly invasive, and is thus generally considered
obsolete in the diagnosis of a human prion disease. As a consequence,
there is currently no minimally invasive ante-mortem test available to
confirm the clinical suspicion of a human prion disease or to
discriminate prion strains. By studying the precise distribution of
disease-associated prion protein (PrPSc) in sporadic Creutzfeldt-Jakob
disease we have identified muscle as a putative target for the diagnosis
of Creutzfeldt-Jakob disease. These investigations are supplemented by
studies employing genetically modified mice aimed unraveling the
molecular basis of muscular prion replication. ORAL 6 Further advances
in the molecular and pathological diagnosis of sporadic
Creutzfeldt-Jakob disease subtypes. Piero Parchi, Silvio Notari, Rosaria
Strammiello, Sabina Capellari. Laboratory of Neuropathology, Department
of Neurological Sciences, University of Bologna, Italy. The
characterization of at least six clinico-pathological phenotypes of
sporadic Creutzfeldt-Jakob disease (sCJD) which largely correlate at the
molecular level with the genotype at codon 129 (MM, MV, VV) and either
one of two major types of PrPSc 27-30 with distinct physicochemical
properties (i.e. type 1 and type 2) has provided the basis for a
molecular classification of sCJD, and a potentially powerful method for
strain typing. Despite the significant advances, however, additional
work needs to be to done to fully explore the whole spectrum of sCJD
variants and the issue of the molecular basis of phenotypic variability
in sCJD. The discovery of subjects with the co-occurrence of PrPSc type
1 and type 2 constitutes a potential drawback for the widespread
application of this classification to CJD diagnostics and epidemiology.
Furthermore, there is still some disparity among laboratories regarding
the understanding and nomenclature of PrPSc types and it is still
unknown whether a specific PrPSc type is associated with each sCJD
phenotypic variant. Lastly, the recent identification of novel
C-terminal fragments of PrP (PrP-CTF) has provided a potential novel
molecular marker, but it is currently unclear to what extent PrP-CTF
properties correlate with the sCJD phenotype. We report on our recent
results on the above issues. I) Studying in detail a large series of
cases we found that the co-occurrence of types 1 and 2 is not random and
characterizes about 30% of MM cases and 20-25% of the sCJD population as
a whole. Our data show that a correct molecular classification can be
reached in the absolute majority of sCJD cases, but requires
pathological and biochemical analyses of 6-8 samples from the cerebral
cortex, thalamus and cerebellum. II) We further analyzed PrPSc 27-30
properties using a high resolution gel electrophoresis system and
varying experimental conditions and found that pH varies among CJD brain
homogenates in standard buffers thereby influencing the characteristics
of PrPSc 27-30. We also found that PrPSc 27-30 type 1 and type 2 are
heterogeneous species, which can be further distinguished into molecular
subtypes that fit the current histopathological classification of sCJD
variants. III) Finally, our latest results indicate that PrP-CTF
characterization is also useful for the molecular diagnostics of some
sCJD subtypes. Supported by the Italian Ministry of Health (Ricerca
Finalizzata 1%/2001), the EU contract QLK3-CT-2001-02345, and the G.
Galletti Foundation. ORAL 7 Chronic Wasting Disease in Cervids in North
America Elizabeth S. Williams University of Wyoming Chronic wasting
disease (CWD) is a transmissible spongiform encephalopathy of
free-ranging and farmed cervids in North America that is distinct from
scrapie of domestic sheep, bovine spongiform encephalopathy, and
Creutzfeldt-Jacob disease of humans. The purpose of this paper is to
review the current status of CWD in North America. The natural host
range of CWD includes mule deer (Odocoileus hemionus), white-tailed deer
(Odocoileus virginianus), and Rocky Mountain elk (Cervus elaphus
nelsoni). Experimentally, by intracerebral or oral exposure, the host
range is wider, but there appears to be a significant barrier to
infection of cattle and humans. The exact mechanism of CWD transmission
is not known but recent studies indicate that direct transmission,
indirect transmission via environmental contamination, and transmission
associated with carcasses are possible. Maternal transmission does not
appear to play a significant role in CWD. Although still under
investigation, polymorphisms in the prion protein influence CWD
pathogenesis in mule deer and elk. Studies of CWD pathogenesis following
oral exposure demonstrate early widespread distribution of abnormal
prion protein in the lymphoid tissue prior to invasion of the central
nervous system. These data have lead to techniques for CWD surveillance
in deer based on testing retropharyngeal lymph node. However, both brain
and lymph node must be tested in elk for highest sensitivity due to
differences in pathogenesis in this species compared to deer. The unique
nature of a transmissible spongiform encephalopathy occurring in
free-ranging cervids is a serious challenge to wildlife managers and
animal health agencies in North America. ORAL 8 Bovine spongiform
encephalopathy (BSE) in Japan Takashi Yokoyama, Kumiko M. Kimura,
Morikazu Shinagawa Prion Disease Research Center, National Institute of
Animal Health, Japan Bovine spongiform encephalopathy (BSE) has become
an important problem not only for animal industry, but also for public
health. In Japan, BSE was first recognized in September 2001 by fallen
stock surveillance. Since October 2001, BSE examination for all cattle
slaughtered at abattoirs has started. In April 2004, all dead cattle
examination (over 24 months) has been conducted at livestock hygiene
service center. Samples positive in enzyme linked immunosorbent assay
(ELISA) are further subjected to western blot (WB) and
immunohistochemistry (IHC). Thirteen BSE cases have been reported by
September 2004. Twelve cases were classified as typical BSE, and the
remained one was an atypical BSE. Variant forms of BSE with atypical
histopathological and/or biochemical phenotype were reported in Italy
and France. Further study is required for BSE prion characteristics. To
characterize BSE prion properties, brain homogenates of Japanese BSE
cases were intracerebrally inoculated into wild-type mice. The first
case (BSE/Chiba) was successfully transmitted to rodents. The mean
incubation periods (409.0 days) in this experiment was preferably longer
than that of previously reported. PrPSc distribution, prion titer, mice
susceptibility and/or storage condition of sample might be influenced
the result. Recently, we introduced transgenic mice that overexpress a
bovine PrP gene to overcome the species barrier problem. These mice are
expected to accelerate the transmission experiment of BSE prion.
Transmission of atypical BSE case is undergoing by using these
transgenic mice. ORAL 9 How does host PrP control TSE disease? Jean
Manson1, R Barron1, N Tuzi1, H Baybutt1, Enrico Cancellotti1, P Hart1, L
Aitchison1, B.Bradford1, D King1 , R Moore2, D Melton2, M Bishop3, J
Ironside3, R Will3 1Institute for Animal Health, Neuropathogenesis Unit,
Edinburgh, UK, 2University of Edinburgh, 3National CJD Surveillance
Unit, Edinburgh PrP is central to the TSE disease process and has been
hypothesised to be the infectious agent. Polymorphisms in the PrP gene
of a number of species are associated with different incubation times of
disease following exposure to an infectious agent and mutations in the
human PrP gene can apparently lead to spontaneous genetic disease.
Strains of TSE agent are proposed to be generated and maintained through
differences in glycosylation or conformation of PrP and the barrier to
infection between species is thought to be due to the differences in the
sequence of PrP between different species. In order to test these
hypotheses, we have introduced specific modifications into the
endogenous mouse Prnp gene by gene targeting. The mutated PrP gene is in
the correct location under the control of the endogenous Prnp regulatory
sequences and thus expressed in the same tissues and amounts as the wild
type Prnp gene. This strategy therefore allows the effect of specific
mutations in the PrP gene to be assessed. By altering the murine PrP
coding region to that of another species we have established that
increasing overall identity between host and donor PrP can lead to
either an increase or a decrease in incubation time of disease in a
strain dependent manner. We have introduced a point mutation (101L) into
the N-terminus of the host PrP and shown that it dramatically changes
the susceptibility of the host to infection from different species. We
have in addition demonstrated that polymorphisms in the N terminus
(L108T) and C-terminus (F189V) of host PrP both alter the incubation
time of disease but each operates by a different mechanism. We have
introduced mutations into the Prnp gene which prevent glycosylation at
each or both of the two N-linked glycosylation sites of PrP. Inoculation
of these mice with infectivity has established that glycosylation of
host PrP can influence incubation time of disease, vacuolar pathology
and strain determination. We have during these studies produced a model
of TSE disease which contains high levels of infectivity in the apparent
absence of PrPSc and we are using this model to define the nature of the
infectious agent. We have thus established that the gene targeting
approach can produce models for TSE disease which address fundamental
questions associated with these diseases. We aim to use these models to
address central issues including the origin of strains, the species
barrier and the nature of the infectious agent. ORAL 10 Prion
interactions with the immune system Neil A Mabbott Institute for Animal
Health, Edinburgh, UK Many natural prion infections are likely to be
acquired peripherally for example, following ingestion of
prion-contaminated feed. Following peripheral exposure prions accumulate
in lymphoid tissues before spreading to the brain. Using mice
experimentally infected with scrapie prions we have shown that mature
follicular dendritic cells (FDCs), expressing the host prion protein
(PrPc), are critical for replication of infection in lymphoid tissues.
Prion neuroinvasion is also dependent on FDCs as in their absence
disease susceptibility is reduced. For example, temporary depletion of
FDCs before oral inoculation with prions blocks the accumulation of
disease-specific PrP in Peyer’s patches and mesenteric lymph nodes, and
prevents neuroinvasion. Studies in mice have shown that skin
scarification is also an effective means of prion transmission.
Following inoculation via the skin scrapie prions accumulate in the
draining lymph node in association with FDCs. The accumulation of prions
in association with FDCs is also critical for the transmission of
disease from the skin to the brain, as disease susceptibility is reduced
in their absence. The mechanisms through which prions are transported
from the skin to lymphoid tissues are not known. Langerhans cells (LCs)
reside in the epidermis and migrate to the draining lymph node after
encountering antigen. Our studies show that LCs have the potential to
acquire and degrade PrPSc following in vitro exposure. To investigate
the potential role of LCs in prion transportation from the skin, we
utilized mouse models in which their migration was blocked. We show that
the early accumulation of prions in the draining lymph node and
subsequent neuroinvasion was not impaired in mice with blocked LC
migration. These data therefore demonstrate that although LCs have the
potential to acquire prions they are not involved in their
transportation to draining lymphoid tissues. Thorough analysis of the
early events in prion pathogenesis in lymphoid tissues may identify
potential targets for therapeutic intervention. ORAL 11 Scrapie
infection of SN56 cells: greater efficiency by membrane-associated
versus purified PrP-res Gerald S. Baron1, Ana C. Magalhăes2, Marco A.M.
Prado2, and Byron Caughey1 1Rocky Mountain Laboratories, Laboratory of
Persistent Viral Diseases, NIAID, NIH, 903 S. 4th St., Hamilton, MT
59840 2Program of Molecular and Biochemical Pharmacology, Department of
Pharmacology, ICB, Universidade Federal de Minas Gerais, Av. Antonio
Carlos 6627, 31270-901, Brazil The process by which transmissible
spongiform encephalopathy (TSE) agents, or prions, infect cells is
unknown. We employed a new highly susceptible cell line (SN56) and a
previously described cell line (N2a) to gain insight into the mechanism
of infection. The effect of disease-associated PrP (PrP-res) association
with membranes on infection efficiency was examined by comparing
sustained PrP-res production in cells treated with either scrapie brain
microsomes or purified, detergent-extracted PrP-res. When normalized for
quantity of input PrP-res, scrapie brain microsomes induced dramatically
enhanced persistent PrP-res formation compared to purified PrP-res.
Infected SN56 cells released low levels of PrP-res into the culture
supernatant, which also efficiently initiated infection in recipient
cells. Interestingly, microsomes labeled with a fluorescent marker were
internalized by SN56 cells in small vesicles, which were subsequently
found in neuritic processes. When bound to culture wells to reduce
internalization during the infection process, scrapie microsomes induced
less long-term PrP-res production than suspended microsomes. Our
observations suggest that efficient infection of cells may involve a
transfer and/or internalization of membranes containing PrP-res. ORAL 12
Slow dynamics of prion protein Kazuo Kuwata Division of Prion Research,
Center for Emerging Infectious Deseases (CEID), Gifu University Although
the conformational conversion mechanism from cellular (PrPC) to scrapie
(PrPSc) form of animal prion proteins has not yet been elucidated, much
evidence is accumulating that potentially provides insights into the
conversion process at atomic resolution. We characterized the critical
aspects of the slow fluctuation dynamics of the recombinant hamster
prion protein, rPrP(90-231), based on NMR relaxation analysis using
Carr-Purcell-Meiboom-Gill (CPMG) experiments, and compare them in detail
with the results from high-pressure NMR. Residues exhibiting slow
fluctuations on the time scale of microseconds to milliseconds are
mainly localized on helices B and C (172-193 and 200-227), which include
locally disordered regions in an intermediate conformer, PrP*,
identified previously by high pressure NMR (Kuwata et al., Biochemistry
12277-12283 (2002)). Moreover, chemical shift differences between two
putative exchanging conformers obtained by the CPMG relaxation analysis
and the linear component of the pressure-induced chemical shift changes
are well correlated at individual residue sites. These observations
apparently support the notion that both the CMPG relaxation and the
pressure shifts represent slow conformational fluctuations, and that
these slow motions in PrPC are fundamentally on the trajectories leading
to the transition to PrP*. Furthermore the slow conformational exchange
rates were not in proportion to the square of the static magnetic field,
indicating that the slow dynamical trajectory of the prion protein is
not simply described by the semiclassical periodic approximation, but
includes bifurcation and/or singularities. Those abnormal dynamical
characterstics of prion may be related to its pathogenicity. Department
of Prion Research Tohoku University School of Medicine 2-1 Seiryo-cho
Aoba-ku, Sendai 980-8575, JAPAN Tel: +81-22-717-8233 Fax:
+81-22-717-8148 TSS Japan Consumer Press online Nippon shouhisha shinbun
http://www.jc-press.com/eg.htm
http://www.jc-press.com/En/Latest%20News/200411/20041109BSE%20death%20cow%27s%20anomalous%20prion.htm
Last modified, 11/09/2004 13:42:49 BSE death cow's anomalous prion
detected from peripheral nerve tissue, suprarenal gland First time from
non-Specified Risk Material, or SRM By JCPRESS National Institute of
Animal Health Animal announced on November 1 that it had detected the
anomalous prion protein that was the etiologic agent of the mad cow
disease, or BSE, or bovine spongiform encephaalopathy, from the
peripheral nerve tissue and the suprarenal gland of the cow of the age
in the mad cow disease for the dying infection 94 months on March 9 this
year. Japan is obligating the removal of the Specified Risk Material, or
SRM such as the head, the spinal cord, the vertebral columns, and the
small intestines that accumulate the anomalous prion protein easily as a
BSE (bovine spongiform encephaalopathy) measures. Because the mad cow
disease etiologic agent was detected from a tissue different from the
Specified Risk Material, or SRM, the review of the Specified Risk
Material, or SRM might be urged on the Japanese Government.
International Symposium of PRION DISEASES for food and drug safety
http://www.knt.co.jp/ec/2004/prion/ national institute of animal
health(only in Japanese) http://niah.naro.affrc.go.jp/index-j.html The
statement of the Ministry of Health, Labour and Welfare (only in
Japanese) http://www.maff.go.jp/www/press/cont2/20041101press_7.htm
Yomiuri on line (only in Japanese)
http://www.yomiuri.co.jp/science/news/20041102i503.htm Asahi on
line(only in Japanese)
http://www.asahi.com/special/bse/TKY200411010291.html Mainichi on
line(only in Japanese)
http://www.mainichi-msn.co.jp/shakai/jiken/disease/news/20041102ddm041040128000c.html
1: Vet Pathol. 2005 Jan;42(1):107. Click here to read Comment on
"Failure to detect prion protein (PrPres) by immunohistochemistry in
striated muscle tissues of animals experimentally inoculated with agents
of transmissible spongiform encephalopathy". Sigurdson C, Glatzel M,
Aguzzi A. Publication Types: * Comment * Letter PMID: 15657284 [PubMed -
in process]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15657284
full text ; 107 Vet Pathol 42:107–108 (2005) Letters to the Editor
Editor: Absence of evidence is not always evidence of absence. In the
article ‘‘Failure to detect prion protein (PrPres) by
immunohistochemistry in striated muscle tissues of animals
experimentally inoculated with agents of transmissible spongiform
encephalopathy,’’ recently published in Veterinary Pathology (41:78–81,
2004), PrPres was not detected in striated muscle of experimentally
infected elk, cattle, sheep, and raccoons by immunohistochemistry (IHC).
Negative IHC, however, does not exclude the presence of PrPSc. For
example, PrPres was detected in skeletal muscle in 8 of 32 humans with
the prion disease, sporadic Creutzfeldt-Jakob disease (CJD), using
sodium phosphotungstic acid (NaPTA) precipitation and western blot.1 The
NaPTA precipitation, described by Wadsworth et al.,3 concentrates the
abnormal isoform of the prion, PrPres, from a large tissue homogenate
volume before western blotting. This technique has increased the
sensitivity of the western blot up to three orders of magnitude and
could be included in assays to detect PrPres. Extremely conspicuous
deposits of PrPres in muscle were detected by IHC in a recent case
report of an individual with inclusion body myositis and CJD.2 Here,
PrPres was detected in the muscle by immunoblotting, IHC, and paraf-
fin-embedded tissue blot. We would therefore caution that, in addition
to IHC, highly sensitive biochemical assays and bioassays of muscle are
needed to assess the presence or absence of prions from muscle in
experimental and natural TSE cases. Christina Sigurdson, Markus Glatzel,
and Adriano Aguzzi Institute of Neuropathology University Hospital of
Zurich Zurich, Switzerland References 1 Glatzel M, Abela E, et al:
Extraneural pathologic prion protein in sporadic Creutzfeldt-Jakob
disease. N Engl J Med 349(19):1812–1820, 2003 2 Kovacs GG, Lindeck-Pozza
E, et al: Creutzfeldt-Jakob disease and inclusion body myositis:
abundant diseaseassociated prion protein in muscle. Ann Neurol 55(1):
121–125, 2004 3 Wadsworth JDF, Joiner S, et al: Tissue distribution of
protease resistant prion protein in variant CJD using a highly sensitive
immuno-blotting assay. Lancet 358:171–180, 2001TSS Terry S. Singeltary
Sr. P.O. Box 42 Bacliff, Texas USA

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