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From: TSS ()
Subject: Background on Importation of Processed Canadian Beef Products Between August 2003 and April 2004
Date: March 16, 2005 at 12:49 pm PST

-------- Original Message --------
Subject: Background on Importation of Processed Canadian Beef Products Between August 2003 and April 2004
Date: Wed, 16 Mar 2005 13:51:31 -0600
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy

Background on Importation of Processed Canadian Beef Products
Between August 2003 and April 2004

In May 2003, USDA closed the border to entry of Canadian cattle and beef
products after
the discovery of a BSE-positive animal in Canada. On August 8, 2003,
Secretary Ann M.
Veneman announced a list of low-risk products, including boneless beef
from cattle
under 30 months of age and veal meat from calves under 36 weeks of age,
that would be
allowed into the United States from Canada, under certain predetermined
Shortly thereafter, USDA published a proposed rule in the Federal
Register to create a
low-risk category for countries with BSE, place Canada on that list, and
allow imports of,
among other things, low-risk beef products and live cattle under 30
months of age to
resume. This rulemaking for live animals and processed meat products
continues at this

Secretary Venemans August 8 announcement regarding low-risk products
USDAs review of the results of Canadas epidemiological investigation
into the
detection of BSE in that country. Based on the results of the
investigation, as well as
international guidelines that indicate that products derived from young
animals do not
pose a risk to human health, USDA utilized existing regulatory authority
to allow these
products into the Untied States under import permits.

Officials with USDAs Animal and Plant Health Inspection Service (APHIS)
examined requests for these import permits, taking into account the
steps Canada had
takensuch as, among others, mandating the removal of specified risk
materials from
certain cattle at slaughterto further reduce any risks associated with
the meat products.
The import permits issued by APHIS required that these types of
risk-reducing steps be
taken in order for the permit to be valid.

On August 15, 2003, APHIS posted a list of allowable products on its
website as a
clarification of the Secretarys August 8, announcement. The list
included trim, which
is boneless beef trimmed from carcasses originating from cattle under 30
months of age
and veal (including carcasses) from calves 36 weeks of age or under.
Following this
clarification, APHIS received requests to allow imports of processed
products from
Canada that were made from approved trim and other low-risk cuts of
meat. APHIS
determined that the processing of the approved trim and other low-risk
cuts of meat under
strict conditions would not increase the risk associated with these
products. The Agency
allowed the entry of these products, under permit, on a case-by-case
basis. APHIS issued
the first import permit for approved ground/further processed product on
August 27.
USDAs Food Safety and Inspection Service maintains records of the
volume of product
that is imported into the United States, reinspected, and cleared for
entry at the Agencys
import establishments, or I-houses. These records provide the volume,
type, and source
of product imported into the United States. Other sources of data,
including that used by
the Department of Commerce and collected by the Department of Homeland
Bureau of Immigration and Customs Enforcement, generically identifies
meat products
for tariff purposes and does not distinguish between, for instance, veal
(which has been
and remains allowable for entry into the United States from Canada) and
other cuts of
meat. Often, import brokers do not use the correct tariff code or may
consolidate a
shipment under one code, such as boneless beef and bone-in beef, instead
of using a
separate code to specifically identify each commodity in the shipment.
FSIS is currently
working to modify its data entry system to achieve harmonization with
other import data.
FSIS records indicate that a total of 5,611,580 million pounds of
further processed
product and ground beef were imported into the United States between
August 27, 2003,
and April 26, 2004. It is important to recognize that more than half of
this product was
not Canadian origin, but rather it was product produced in Canada from
beef that
originated in the United States (or another recognized BSE-free country
such as Australia
or New Zealand). This product was imported under conditions designed to
ensure that
there was no commingling with Canadian product.

The remaining portion2,232,459 pounds of productwas imported on
permits that
allowed for importation of product that either originated in the United
States (or another
BSE free country) or that originated in Canada, provided that the
product was processed
strictly from animals under 30 months of age, and in accordance with a
number of
processing requirements designed to further mitigate any risk.

In addition, 1,504,656 pounds of beef organs and offal from Canada were
imported into
the United States. In October 2003, APHIS added these products to the
list of approved
low-risk products from Canada and began issuing import permits to allow
shipments to
enter the United States. APHIS expectation was that these products would be
transshipped to Mexico because of the lack of a sizeable U.S. market for
this product.
On April 19, 2004, APHIS posted information on the Agencys website
outlining these
import revisions, including those pertaining to approved processed
products, as well as
the Agencys intention to begin allowing the importation of Canadian
bone-in beef from
animals under 30 months of age, under permit. However, this revised list
of products, as
well as the Agencys intention to allow imports of bone-in beef from
Canada under
permit, was voided by an April 26, 2004, temporary restraining order
issued by a U.S.
District Court Judge in Montana and subsequent agreement with the
plaintiff in the legal
action against USDA. USDA is closely adhering to this agreement. (Some
pounds of bone-in product were imported during the April 19, 2004, to
April 26 time

Although properly employing risk mitigation measures for animal and
public health,
APHIS should have alerted the public of the further processing permitted
for products
deemed enterable under APHIS permit. USDA has clarified the protocols by
which these
determinations are made and publicized. Nevertheless, USDA is confident
in the system
used for determining the safety of imported products. Again, the
Canadian products that
have entered the United States over recent months were produced under
strict guidelines
and pose no threat to public health. In the meantime, USDA continues its
work to finish
the rulemaking process on allowable imports, which is an open, public
June 10, 2004

> On August 8, 2003, Secretary Ann M.
> Veneman announced a list of low-risk products, including boneless beef
> from cattle
> under 30 months of age and veal meat from calves under 36 weeks of
> age, that would be
> allowed into the United States from Canada,

> ___under certain predetermined conditions.___


> Although properly employing risk mitigation measures for animal and
> public health,
> APHIS should have alerted the public of the further processing
> permitted for products
> deemed enterable under APHIS permit. USDA has clarified the protocols
> by which these
> determinations are made and publicized. Nevertheless, USDA is
> confident in the system
> used for

> ___determining the safety of imported products___.

I have FAILED to see the first bit of SCIENTIFIC evidence that
has been put forth to date, that support these lies...TSS

May 21, 2003
Subject: Clarification of the Prohibition of the Importation of all Live
Ruminants, Ruminant Meat, Ruminant Meat Products and Other Ruminant
Protein Products from Canada Due to Bovine Spongiform Encephalopathy (BSE)
To: Regional Directors, VS
Veterinary Regulatory Support, PPQ

On May 20, 2003, Mr. Bobby R. Acord, Administrator, Animal and Plant
Health Inspection Service (APHIS) received information from D. Sarah
Kahn, Deputy Chief Veterinary Officer and Director, Animal Health and
Production Division, Canadian Food Inspection Agency, reporting a
confirmed case of bovine spongiform encephalopathy. Due to this
reporting, the U.S. Department of Agriculture (USDA), APHIS, Veterinary
Services (VS) is placing a prohibition on the importation of all live
ruminants (such as cattle, sheep, goats, cervids, camelids), ruminant
meat, ruminant meat products, and other ruminant products from Canada.
This prohibition is effective as of 1:30 p.m. e.s.t., May 20, 2003.
APHIS believes that emergency measures are necessary to minimize risk to
livestock, livestock producers and other industries in the United States.

We are suspending the following animals and animal products from Canada:

1. Live ruminants (imports and transits (except for transits of U.S.
origin ruminants));
2. Processed animal protein (such as meat and bone meal, meat meal, bone
meal, blood meal, protein meal, etc.), regardless of species of origin
(not intended to exclude human food in prepackaged, final form);
3. Animal feed (unless demonstrated to be of exclusively milk or
non-animal origin);
4. Pet food (unless animal protein is non-mammalian origin, under permit
5. Milk replacers containing animal fat or non-milk animal protein;
6. Ruminant blood and blood products;
7. Animal vaccines containing ruminant-derived products;
8. Ruminant offal (internal organs, intestines and tissues not otherwise
9. Ruminant casings (except for collagen casings derived from ruminant
10. Ruminant glands (including but not limited to adrenal, pancreas,
thymus, thyroid, pituitary, etc.);
11. Ruminant gland extracts/derivatives;
12. Unprocessed ruminant fat;
13. Processed fats and oils;
14. Nutritional supplements containing specified risk materials (SRMs) 
both in bulk and in final finished package for human or animal consumption;
15. Ruminant bones;
16. Tankage;
17. Tallow, except for tallow derivatives;
18. Ruminant bone-derived gelatin for animal use (permit and additional
conditions will allow imports for non-animal/industrial use);
19. Ruminant-derived cartilage and/or chondroitin sulfate;
20. Non-hide derived collagen (exemptions similar to those for gelatin
for non-animal use); and
21. Ruminant urine/urine derivatives.
22. Ruminant meat and meat products

The following animal and animal products are still eligible for entry:
milk, milk products, ruminant hides and ruminant hide derived products,
ruminant semen and embryos. Semen and embryo import protocols that
include the BSE certification statements will be completed shortly. As
we learn more information about the case of BSE in Canada, the
restrictions placed on Canadian imports will be re-evaluated.

Thank you for your cooperation and support.

Karen A. James-Preston, DVM
Technical Trade Services
National Center for Import and Export

United States Department of Agriculture
Marketing and Regulatory Programs
Animal and Plant Health Inspection Service
Veterinary Services
National Center for Import and Export
4700 River Road, Unit 40
Riverdale, MD 20737

Phone: 301-734-3277
Fax: 301-734-8226

APHIS - Protecting American Agriculture
An Equal Opportunity Employer

Click here for printable version

U.S. Importers, Brokers and Other Interested Parties

Release No. 0166.03

Statement by Agriculture Secretary Ann M. Veneman
Regarding Canada's Announcement of BSE Investigation
May 20, 2003

"I have spoken with Canada's Agriculture and Agri-Food Minister Lyle Vanclief a short time ago about Canada's investigation and feel that all appropriate measures are being taken in what appears to be an isolated case of bovine spongiform encephalophathy. Information suggests that risk to human health and the possibility of transmission to animals in the United States is very low.

"USDA is placing Canada under its BSE restriction guidelines and will not accept any ruminants or ruminant products from Canada pending further investigation. We are dispatching a technical team to Canada to assist in the investigation and will provide more detailed information as it becomes available."

"The United States remains diligent in its BSE surveillance and prevention efforts. In 1997, the Food and Drug Administration prohibited the use of most mammalian protein in the manufacture of animal feed intended for cows and other ruminants to stop the way the disease is thought to spread.

"Since 1989, the U.S. government has taken a series of preventive actions to protect against this animal disease. This includes USDA prohibitions on the import of live ruminants, such as cattle, sheep, goats and most ruminant products from countries that have or are considered to be at risk for having BSE.
"In fiscal year 2002, USDA tested 19,990 cattle for BSE using a targeted surveillance approach designed to test the highest risk animals, including downer animals (animals that are non-ambulatory at slaughter), animals that die on the farm, older animals and animals exhibiting signs of neurological distress."


202 720-9035


USDA Reopens Comment Period on Proposed Rule to Allow Live

Animal Imports from Canada
Press Release)
-- Explanatory Note: Risk Analysis

-- Federal Register Notice

-- previously submitted comments
-- Government of Canada
Comments on Proposed Rule




Bovine Spongiform Encephalopathy; Minimal Risk Regions and Importation
of Commodities

- proposes to add Canada to Minimal Risk Category
-- Risk Analysis

(APHIS/Veterinary Services report)
-- Economic Analysis
and U.S. Commerce Dept.) 11/04/2004


USDA Issues Proposed Rule to Allow Live Animal Imports from Canada

-- Q&ACurrent USDA Actions and the Canadian Situation
-- Webcast
Announcing Proposed rule: audio
| transcript

Import Permit Applications for Certain Ruminant Products From
Canada Will Be Accepted
-- Media briefing:
-- Q&A's
-- Beef Export
Verification Program
-- Information on
Hunter-harvested wild ruminant meat


Statement by USDA Secretary Regarding Canadas Decision to Remove
Specified Risk Material from Food Products

USDA Tele-news Conference: USDA Officials' Background

Briefing on Canada's New BSE Measures

"Terry S. Singeltary Sr."

11/03/2003 01:19 PM






I would like to kindly comment on Docket No. 03-080-1


>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;

>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

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

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.

> 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

>5) cervids for immediate slaughter;

are you going to test all cervids coming into the USA from Canada for
(this should be mandatory).

Commentary by European Microbiologist Roland Heynkes

August 26, 2003 Posted to BSE-L@UNI-KARLSRUHE.DE

> SECRETARY VENEMAN: "Well, thank you, Tony, for your question. As
> you know, we've spent a considerable amount of time on this issue
> of Canada and the single case of BSE. The announcement we made on
> the 8th had several aspects. One was we were going to use a permit
> process to open the border with respect to boxed beef from animals
> under 30 months. As you know, animals under 30 months are generally
> thought to be of virtually no risk of having BSE. Now, we will also
> begin a regulatory process to look at the lowest risk animals,
> those under 30 months. That regulation is in process at this point,
> but it will take some time to actually do the regulation. That will
> include a risk assessment and so forth.

in my opinion this is a statement with intent to deceive and it is not
correct. There have been several cases of clinical BSE in British cattle
under 30 months and it is therefore hardly possible to think that cattle
under 30 months have virtually no risk of having BSE. In 1988 the
youngest British BSE case was 24, the second youngest 27 months old. In
1989 the youngest British BSE case was 21 and there were 4 cases only 24
months old. In 1990 there were two cases only 24 and one 26 months old.
In 1991 the youngest British BSE case was 24 and there were 3 cases only
26 months old. In 1992 the youngest British BSE case was 20!, the second
youngest 26 months old. In 1993 there was was a 29 months old case, in
1995 the UK had a 24 months old case and in 1996 one British BSE case
was 29 months old.

But mainly this wrong statement is misleading, because not the
clinically sick cows are the problem for consumers. The real problem are
those animals that became infected as calves and are still incubating
the infectivity during the incubation time of 5-6 years. For consumers
it is therefore totally irrelevant that cattle are at low risk to reach
the clinical stage before being 30 months old. Important for consumers
is the fact that most British BSE cases became infected as calves
( and that infected calves are already
amplifying the infectivity. The advantage of young calves for consumers
is that the infectivity in infected animals is low and still
concentrated around the gastro- intestinal tract. But this is not
necessarily true for bulls, which are usually slaughtered when they are
19-22 months old. They are too young to give positive results in the
actual BSE tests, but they might be infective for consumers.

For US consumers it is of no importance whether a BSE-infected Canadian
cow will show the first symptoms before or after it becomes 30 months
old. Interesting for the consumers is only

1) if cattle are infected or not,

2) where in the animal is how much of the infectivity and

3) what happens to the infectivity during slaughtering?

If the US government is really interested to reduce consumers risk, it
has to

1) stop cannibalism among farm animals (no farm animal protein and fat
in feeding stuff for farm animals, no possibility of cross contamination
of concentrate feed in mills and no lambing on pastures where scrapie
might be a problem)

2) test slaughter cattle above 24 months for BSE,

3) avoid contamination of the beef with prions from CNS by changing
slaughter methods (electrical stunning instead of captive bolt, no
immobilisation with a pithing rod, no spreading of infectivity by sawing
through the spinal cord),

4) destroy the high risk materials (brain, eyes, spinal cord, dorsal
root ganglia and other peripheral ganglia, nervous and lymphatic tissue
associated with intestine)

5) commit the whole chain from abattoir to counter in shop and
restaurant to label products from cattle and sheep, because it is only a
myth that scrapie is less infective than BSE.

In addition the US government should test all cattle and sheep which
died or had to be killed because of illness. This measure should be hold
out for at least one year in order to see the real BSE- and
scrapie-incidence in the USA....

Microbiologist Roland Heynkes

Furthermore, for the USA to continue to flagrantly ignore the findings
from Collinge/Asante 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. These
findings could have
major implications for the medical and surgical arena and human health.
this type sporadic CJD
is very prevalent in the USA ;

> USDA also released the findings of a second assessment conducted by the
> Harvard Center for Risk Analysis (HCRA) that confirms the findings of the
> initial study released in 2001...

GAO proved this;

Reanalysis of Mad Cow Disease Confirms Risk is Low in the U.S.

Policies put in place in 1997 would reverse any possible disease spread

For immediate release: Friday, October 31, 2003

Boston, MA A study by the Harvard Center for Risk Analysis (HCRA) at
the Harvard School of Public Health, assessing the likelihood of mad cow
disease spreading in the United States cattle population, confirms the
findings of the initial HCRA analysis done in 2001; that even if
infected animals or contaminated ruminant feed material entered the
American animal agriculture system from Canada, the risk of mad cow
spreading extensively within the American herd would be low, and that
any possible spread would by now have been reversed by controls put in
place in the late 1990s.

The new study was initiated at the request of the United States
Department of Agriculture following discovery in the summer of 2003 of a
Canadian cow infected with bovine spongiform encephalopathy (BSE). The
reanalysis also finds that any disease that might have been introduced
would eventually be eliminated from the United States.

The reanalysis, done by George Gray, executive director and Joshua
Cohen, senior researcher, both at HCRA, specifically examined scenarios
for the likely introductions of BSE from Canada into the U.S. These
hypothetical introductions included both infected animals (the study
assumed 5 infected animals imported even though Canada has only
identified one case to date) and contaminated animal feed. These
scenarios were evaluated using the HCRA computer model that simulates
conditions in the American agricultural system. The analysis found that
if BSE infected animals had been introduced as early as 1990, up to
500-600 cattle in the U.S. might have become infected, and approximately
20-25 percent would have demonstrated signs of BSE. Such an outbreak was
never detected, though it would have been below the prevalence level
that surveillance systems in place at that time would likely have found.
If the introduction took place later, the total number of animals
infected in the U.S. would have been smaller.

The HCRA study found that the 1997 U.S. imposition of a ban on feeding
rendered ruminant protein back to other ruminants essentially chokes off
and then reverses any possible spread of the disease. Even accounting
for incomplete compliance with that feed ban, the HCRA analysis found
that had infected animals or contaminated feed come in from Canada or
elsewhere, the spread of BSE in the American cattle population would
have been reversed by now and that human exposure to contaminated animal
tissue would have been very low.

HCRA has also delivered to the USDA the revised version of the November,
2001 BSE report following extensive peer review by both American and
European experts.

The revised document is available on the HCRA website at and the HCRA
BSE computer model is available by contacting Joshua Cohen at HCRA
( ).
For further information, please contact:

George Gray
Executive Director
Harvard Center for Risk Analysis

Kevin C. Myron
Office of Communications
Harvard School of Public Health

Harvard School of Public Health is dedicated to advancing the public's
health through learning, discovery, and communication. More than 300
faculty members are engaged in teaching and training the 800-plus
student body in a broad spectrum of disciplines crucial to the health
and well being of individuals and populations around the world. Programs
and projects range from the molecular biology of AIDS vaccines to the
epidemiology of cancer; from risk analysis to violence prevention; from
maternal and children's health to quality of care measurement; from
health care management to international health and human rights.

Return to News, Events, and Publications

Return to the HSPH Home Page

Contact HSPH

BOUGHT AND PAID FOR (in partial or whole) by your local cattle dealler ;

In addition, USDA cannot rely on the Food and Drug Administrations
(FDAs) 1997 BSE feed rule being rigorously enforced. Because of serious
lapses, increased surveillance is needed. The USDA-sponsored Harvard
risk assessment of the risk of BSE in the U.S. noted that compliance
with FDAs 1997 BSE feed rule is the most important factor in preventing
a BSE outbreak. Yet a pair of reports by GAOone published in September
2000 and the other published in January 2002have shown how lax FDA has
been in ensuring compliance with the feed rule. The first report,
published some three years after the BSE feed rule went into effect
found fairly widespread non-compliance: inspection results of the 2,481
firms that were identified as handling prohibited materials . . . 699,
or 28 percent, did not label their products with the required cautionary
statements that the feed should not be fed to cattle or other ruminants.
. . . In addition, of the 1,771 firms that manufacture both prohibited
and non-prohibited material, 361, or 20 percent, did not have a system
in place to prevent commingling and cross contamination, as required by
the regulation (pp. 11-12 in

The 2002 GAO report found that, (C)oncerning the feed ban, FDA has not
acted promptly to compel firms to keep prohibited proteins out of cattle
feed and to label animal feed that cannot be fed to cattle. . . .
Moreover, FDAs data on inspections are severely flawed and, as a
result, FDA does not know the full extent of industry compliance. FDA
acknowledges that it has not yet identified and inspected all firms
subject to the ban (pg. 3 in
The report concludes that federal actions do not sufficiently ensure
that all BSE-infected animals or products are kept out or that if BSE
were found it would be detected promptly and not spread to other cattle
through animal feed or enter the human food chain italics added (pg. 3
in The failure of FDA to fully
implement the 1997 BSE feed ban should spur USDA to exercise greater
vigilance to ensure that if BSE occurred in the US that it would be
found quickly. USDA should therefore dramatically expand the testing of
cattle to ensure, at a minimum, that all downer cows (e.g. all emergency
slaughter and all fallen stock) are tested for BSE using one of the
rapid tests, preferably the one found to be the most accurate (e.g. with
the lowest rate of false positives and false negatives).

We also believe that USDA should act to ensure that no CNS tissue is
found in meat destined for human consumption. We note that the results
of the Food Safety Inspection Services 2002 AMR survey found that
about 74 percent (25 of 34) of the establishments tested in the AMR
Survey of 2002 had positive laboratory results for CNS tissue in their
final beef AMR products; the other 26 percent had negative laboratory
results (see pg. 2 of
The USDA should take appropriate action to ensure that there is zero CNS
contamination of meat destined for human consumption...

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


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


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


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



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

Evidence That Transmissible Mink Encephalopathy
Results from Feeding Infected Cattle

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

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

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


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


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

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

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

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

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


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


SCRAPIE 'USA' ANNUAL REPORT (105 newly infected flocks
2002) & CWD IN USA

As of September 30, 2002, there were 45 scrapie infected and source
flocks (figure 3). There were 105 newly infected flocks, reported in
FY2002 (figure 4). In addition, 379 scrapie cases were confirmed and
reported by the National Veterinary Services Laboratories (NVSL) in FY
2002 (figure 5) and (figure 6). Five cases of scrapie in goats were
reported in FY 2002 (figure 7), the last of which was confirmed in
August 2002. New infected and source flocks numbers and the number of
these flocks released in FY 2002 are depicted in chart 4. One hundred
(100) flocks which is 67 percent of the scrapie infected and source
flocks present in FY 2002 were released or put on clean-up plans in FY2002.

Slaughter Surveillance

Slaughter Surveillance is currently in Phase II which is intended to
determine the prevalence of scrapie in the US culled sheep population.
Through September 2002 samples from 3,269 sheep were submitted to NVSL
for testing. Samples from a total of 6,795 sheep have been submitted
since the beginning of Phase II on April 1, 2002. Surveillance regions
are depicted in (figure 8).

Scrapie Testing

During FY 2002 11,751 animals have been tested for scrapie which
includes: 2,711 regular necropsy cases, 1,343 third eyelid biopsies for
the test validation project, 546 third eyelid biopsies for the
regulatory program, and approximately 7,151 animals for Phase I & II of
SOSS (chart 5). Laboratory testing has been taking 10 - 11 days on
average with a range of 3 - 34 days.

Ear Tag Orders

During FY 2002 9.9 million plastic and 6.0 million metal tags were
distributed by APHIS (chart 6).


Oct. 2002)

CWD USA surveillance

DO NOT TAKE LIKELY, the early studies proving transmission of CWD to 5
cows and 1 sheep
by inoculation. The oral route will take longer, if/when transmission

-------- Original Message --------
Subject: Re: CWD TO CATTLE by inoculation (ok,is it three or four OR NOW
Date: Mon, 23 Jun 2003 12:36:59 -0500
From: "Janice M. Miller"
Reply-To: Bovine Spongiform Encephalopathy


After 5.75 years of observation we have 5 CWD transmissions to cattle
from a group of 13 inoculates. These animals, which were necropsied 23,
24, 28, 59, and 63 months after inoculation, did not show the clinical
signs or histopathologic lesions typical of a TSE, but PrPres was
detected in brain samples by both immunohistochemistry and western blot.
Five other animals necropsied during the 4th, 5th and 6th years of
observation have not shown evidence of PrPres and the remaining 3 cattle
are apparently healthy. Note that this study involved direct
intracerebral inoculation of cattle with the CWD agent, which is an
unnatural route of exposure. Likely, it would be more difficult to
infect cattle by the oral route. Cattle have been inoculated orally at
the University of Wyoming with the same inoculum used in this
experiment, and 5.75 years into the study the animals remain healthy
(personal communication, Dr. Beth Williams).

Experimental Transmission of CWD to sheep

Eight Suffolk sheep from the NADC scrapie-free flock were inoculated
intracerebrally with the CWD brain suspension used to inoculate cattle.
PRNP genotyping showed that 4 of the sheep were QQ at codon 171 and the
other four were QR. Two of the QQ sheep were euthanized during the 3rd
year of observation. At necropsy one of these animals had a urethral
obstruction and PrPres was not detected in brain or lymphoid tissues.
The other sheep, necropsied 35 months after inoculation, showed clinical
signs and histopathologic lesions that were indistinguishable from
scrapie. IHC tests showed typical PrPres accumulations in brain,
tonsil, and some lymph nodes. The 2 remaining QQ sheep and all 4 QR
sheep are apparently healthy 47 months after inoculation.

After 4 years of observation we have 1 transmission of CWD to a 171 QQ
sheep. This animal, which was necropsied 35 months after inoculation,
showed clinical signs and histopathologic lesions that were
indistinguishable from scrapie. Another QQ sheep that was necropsied
during the 3rd year showed no evidence of prion disease and all
remaining sheep (2 QQ and 4 QR) are apparently healthy.

1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under

PMID: 6997404

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by
electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral
cortex of a middle aged woman with progressive dementia were
previously implicated in the accidental transmission of
Creutzfeldt-Jakob disease (CJD) to two younger patients. The
diagnoses of CJD have been confirmed for all three cases. More than
two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the
electrodes were implanted in the cortex of a chimpanzee. Eighteen
months later the animal became ill with CJD. This finding serves to
re-emphasise the potential danger posed by reuse of instruments
contaminated with the agents of spongiform encephalopathies, even
after scrupulous attempts to clean them.

PMID: 8006664 [PubMed - indexed for MEDLINE]

> In recent correspondence, the
> Director General of the OIE acknowledged that there has been an "increase
> in unjustified restrictions in international trade, particularly as it
> relates to cattle and cattle products." The letter was in response to a
> request from Secretary Veneman, Agricultural Minister Lyle Vanclief,
> Canada, and Agriculture Secretary Javier Usabiaga, Mexico, to the OIE to
> provide more practical guidance regarding the resumption of trade with
> countries that have reported cases of BSE.

just because the USA, Canada and Mexico does not like them. then all the
work all
other countries have done to erradicate this horrible disease from the
planet over the last
3 decades will go for naught, and the agent will continue to spread...

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


Working Group Report on the Assessment of the Geographical BSE-Risk (GBR

III) of USA 2004 ''extremely/very unstable BSE/cattle system''





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