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From: TSS ()
Subject: Statement by Acting FDA Commissioner Dr. Andrew von Eschenbach on the Opening of the Japanese Market to U.S. Beef
Date: December 13, 2005 at 12:50 pm PST

FDA Statement
FOR IMMEDIATE RELEASE
Statement
December 12, 2005
Media Inquiries:
Rae Jones, 301-827-6242
Consumer Inquiries:
888-INFO-FDA


Statement by Acting FDA Commissioner Dr. Andrew von Eschenbach on the Opening of the Japanese Market to U.S. Beef
FDA is encouraged by the decision of the Japanese government to lift the temporary ban on imports of United States beef products. We believe that this decision by Japan acknowledges the effectiveness of U.S. measures adopted over the years -- one of the most critical measures being FDA's ruminant feed ban -- to protect our country from BSE or bovine spongiform encephalophathy, also known as mad cow disease.

The Food and Drug Administration erected one of the most crucial defenses against this disease in 1997, when it issued a rule prohibiting the use in feed for cattle and other ruminants of some mammalian tissues that might contain the BSE infective agent. Since then, FDA and state health authorities have carried out more than 41,000 inspections of feed manufacturers, renderers, and other producers of feeds for cattle and other ruminant animals to ensure that the rule is rigorously implemented to protect the public health. Over the years, the compliance rate with the FDA regulation has exceeded 99 percent for renderers, protein blenders, and feed mills.

Together with the preventive steps adopted by the U.S. Department of Agriculture, FDA's animal feed rule has erected a firewall that has protected our country against the spread of BSE within our cattle herd. FDA continues to work with its partners, such as the U.S. Department of Agriculture, to ensure that effective measures are in place to protect the United States from BSE.

####

http://www.fda.gov/bbs/topics/NEWS/2005/NEW01273.html


GAO ON USA BSE 2002

http://www.gao.gov/new.items/d02183.pdf

GAO 2003


http://www.gao.gov/new.items/d04259t.pdf


http://www.gao.gov/cgi-bin/getrpt?GAO-04-588T

* GAO-05-51 October 2004 FOOD SAFETY (over 500 customers receiving
potentially BSE contaminated beef) - TSS 10/20/04


October 2004 FOOD SAFETY
USDA and FDA Need
to Better Ensure
Prompt and Complete
Recalls of Potentially
Unsafe Food

snip...

Page 38 GAO-05-51 Food Recall Programs
To examine the voluntary recall of beef products associated with the
December 2003 discovery of an animal infected with BSE, we analyzed the
distribution lists USDA collected from companies and the verification
checks it conducted to develop a diagram illustrating the location and
volume of recalled beef that reached different levels of the distribution
chain. We compared the distribution lists and verification checks to
identify how many customers listed on the distribution lists did not
receive
the recalled beef and the number of customers not listed on distribution
lists that received the recalled beef. We interviewed USDA and FDA staff
involved with the recall to understand the timing of recall actions and the
challenges encountered during the recall.
To develop information on the 2002 recall of ground beef by a ConAgra
plant in Greeley, Colorado, we reviewed USDAs recall file and other
documents on the recall. We also met with the departments Office of
Inspector General and reviewed the Inspector Generals September 2003
report.1
We conducted our review from May 2003 through August 2004 in
accordance with generally accepted government auditing standards.
1U.S. Department of Agriculture, Office of Inspector General, Great
Plains Region Audit
Report: Food Safety and Inspection Service: Oversight of Production
Process and Recall at
ConAgra Plant (Establishment 969), Report No. 24601-2-KC (September 2003).
Page 39 GAO-05-51 Food Recall Programs
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE Appendix II
On December 23, 2003, USDA announced that a cow in the state of
Washington had tested positive for BSEcommonly referred to as mad
cow disease. This appendix describes the actions USDA took to recall the
meat and the actions FDA took with respect to FDA-regulated products,
such as animal feed and cosmetics, made from rendered parts of the
animal.
Beef Recall Was
Triggered by a BSEPositive
Sample from
One Cow
On December 9, 2003, the recalling company slaughtered 23 cows. USDA,
in accordance with its BSE surveillance policy at the time, took a
sample of
1 cow that was unable to walk, although the condition of the tested cow is
now disputed. USDA did not process the sample in its Ames, Iowa National
Veterinary Services Laboratory in an expedited manner because the cow
did not show symptoms of neurological disorder. USDA test results
indicated a presumptive positive for BSE on December 23, 2003.
Recall Begun in
December 2003 Was
Completed in March
2004
On December 23, 2003, after learning about the positive BSE test, USDA
headquarters notified the Boulder District Office, which is the field
office
with jurisdiction over the recalling firm. The Boulder District began
gathering information about the recalling companys product distribution.
Field staff telephoned the recalling company and were on-site at 7:00 p.m.
The Boulder District initially thought 3 days of the recalling companys
production would have to be recalled, but further examination of facility
cleanup and shipping records revealed that it was only necessary to
recall 1
day of production. USDA recall staff convened at 9:15 p.m. and discussed
the science related to BSE and whether the recalling companys cleanup
practices were sufficient to limit the recall to 1 day of production.
Following USDAs determination to conduct a Class II recallthat is, the
beef posed a remote possibility of adverse health consequencesUSDA
contacted the recalling company to discuss recall details and the press
release. The press release and Recall Notification Report were released
that evening.
On December 24, 2003, USDAs Food Safety and Inspection Service (FSIS)
sent inspectors to the recalling companys primary customers to obtain
secondary customer distribution lists and product shipping records. USDA
conducted 100 percent verification checks for this recallit contacted
every customer that received the recalled meat. This level of verification
checks is well above the percentage of checks conducted by USDA district
offices for the Class I recalls we reviewed.
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 40 GAO-05-51 Food Recall Programs
On December 26, 2003, USDA began checking the primary and secondary
customers of the recalling company that it was aware of, although the
entire product distribution chain was unknown. During the checks, USDA
tried to determine if the product was further distributed, and it used
verification checks to acquire distribution lists for secondary and
tertiary
customers of the recalling company.
Verification checks continued until February 25, 2004. Three USDA
districts conducted these verification checks. The Boulder District
coordinated the checks and assigned checks to the Minneapolis District
Office for customers in Montana and to the Alameda District Office for
customers in California. USDA required that 100 percent of the primary
checks, 50 percent of the secondary checks, and 20 percent of the tertiary
checks be conducted on-site. According to USDA, more than 50 percent of
the secondary checks were actually conducted on-site. FDA officials
helped conduct verification checks. According to USDA, the recall took a
long time to complete because USDA contacted each customer at least
twice. USDA first contacted each customer to conduct the check and again
to verify product disposition.
On February 25, 2004, the Boulder District concluded that the recall was
conducted in an effective manner. On March 1, 2004, USDAs Recall
Management Division recommended that the agency terminate the recall,
and USDA sent a letter to the recalling company to document that USDA
considered the recall to be complete.
Recall Was
Complicated by
Inaccurate Distribution
Lists and Mixing of
Potentially
Contaminated and
Noncontaminated Beef
USDA used distribution lists and shipping records to piece together where
the recalled product was distributed. According to USDA, one of the
recalling companys three primary customers was slow in providing its
customer list. USDA could not begin verification activities for that
primary
customer without this list. Furthermore, some customers of the recalling
company provided USDA with imprecise lists that did not specify which
customers received the recalled product. As a consequence, USDA could
not quickly determine the scope of product distribution and had to take
time conducting extra research using shipping invoices to determine which
specific customers received the product.
Even when USDA determined the amount and location of beef, the agency
still had trouble tracking the beef in certain types of establishments,
such
as grocery store distributors. USDA could not easily track the individual
stores where those distributors sent the beef because of product mixing
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 41 GAO-05-51 Food Recall Programs
and the distributors record-keeping practices. Generally, distributors
purchase beef from multiple sources, mix it in their inventory, and lose
track of the source of the beef they send to the stores that they
supply. To
deal with this problem, USDA first identified the dates when recalled beef
was shipped to the distributors and then asked for a list of the stores
that
were shipped any beef after those dates. Consequently, some stores were
included in the recall that may never have received recalled beef.
The recall was also complicated by repeated mixing of recalled beef with
nonrecalled beef, thereby increasing the amount of meat involved in the
recall. The recalling company slaughtered 23 cows on December 9, 2003,
and shipped those and 20 other carcasses to a primary customer on
December 10, 2003. The recalling companys carcasses were tagged to
identify the slaughter date and the individual cow. The primary customer
removed the identification tags and mixed the 23 recalled carcasses with
the 20 nonrecalled carcasses. Because the carcasses could not be
distinguished, the recall included all 43 carcasses at the primary
customer.
After one round of processing at the primary customer, the meat from the
carcasses was shipped to two other processing facilities. Both
establishments further mixed the recalled meat from the 43 carcasses with
meat from other sources. In all, the mixing of beef from 1 BSE-positive cow
resulted in over 500 customers receiving potentially contaminated beef.
Imprecise distribution lists and the mixing of recalled beef combined to
complicate USDAs identification of where the product went. Specifically,
on December 23, 2003, USDAs initial press release stated that the
recalling
company was located in Washington State. Three days later, on December
26, 2003, USDA announced that the recalled beef was distributed within
Washington and Oregon. On December 27, 2003, USDA determined that one
of the primary customers of the recalling firm distributed beef to
facilities
in California and Nevada, in addition to Washington and Oregon, for a total
of four states. On December 28, 2003, USDA announced that some of the
secondary customers of the recalling company may also have distributed
the product to Alaska, Montana, Hawaii, Idaho, and Guam, for a total of
eight states and one territory.
On January 6, 2004, over 2 weeks from recall initiation, USDA determined
that the beef went to only six statesWashington, Oregon, California,
Nevada, Idaho, and Montanaand that no beef went to Alaska, Hawaii, or
Guam. To reach that conclusion, USDA used the distribution lists, shipping
records, and sales invoices that it received from companies to piece
together exactly where the recalled beef may have been sent. The lists
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 42 GAO-05-51 Food Recall Programs
showed that 713 customers may have received the recalled beef; 6 of those
may have received beef from more than one source. USDA determined that
176 customers on the lists did not actually receive recalled beef,
including
the customers in Guam and Hawaii. USDAs review also indicated that
recalled beef was probably not shipped to Alaska or Utah, and USDA
checked 2 retailers in Alaska and 3 retailers in Utah to confirm that
was the
case. In total, USDA conducted verification checks on 537 of the 713
customers on the lists. USDAs initial checks identified an additional 45
customers that may have received the recalled beef that were not included
on the distribution lists, for a total of 582 verification checks. Figure 4
summarizes USDAs verification efforts during the recall.
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 43 GAO-05-51 Food Recall Programs
Figure 4: USDAs Recall Verification Checks by Location and Customer
Type for Meat Associated with the Animal Infected with
BSE
Note: USDA checked 15 primary, 40 secondary, and 526 tertiary customers
plus the recalling
company, for a total of 582 verification checks.
USDAs press release stated that the recall involved 10,410 pounds of beef
products, and the USDA recall coordinator for this recall told us that
downstream processors mixed the recalled beef with nonrecalled beef, for
a total of more than 38,000 pounds of beef that was distributed at the
secondary customer level. According to USDA officials involved with the
D = Distributor
R = Retailer
SF = Storage facility
P = Processor
Primary customers
(15 total)
Recalling
slaughterhouse
(WA) 1 R
(OR)
1 P
(WA) 1 P
(OR)
1 P
(OR)
11 R
(WA)
Secondary customers
(40 total)
Tertiary customers
(526 total)
1 R
(OR)
1 SF
(OR)
3 D
(OR)
3 D
(WA)
2 dual D
(OR)
59 R
(OR)
79 R
(WA)
5 R
(ID)
3 R
(UT)
4 R
(MT)
161 R
(WA)
8 R
(ID)
15 R
(OR)
2 R
(AK)
31 R
(OR) 8 R
(WA)
10 R
(NV)
5 R
(ID)
10 R
(CA)
2 R
(CA)
17 R
(OR)
5 R
(WA)
1 D
(NV)
11 R
(CA)
85 R
(NV)
3 D
(OR) 11 R
(OR)
2 D
(CA) 26 R
(CA)
2 R
(WA)
( ) Acronyms in parentheses are postal abbreviations for each state.
Source: GAO analysis of USDA verification check documents.
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 44 GAO-05-51 Food Recall Programs
recall, the precise amount of meat that was sold at the retail level is
unknown because retailers at the tertiary level further mixed nonrecalled
meat with potentially contaminated meat. USDA told us that more than
64,000 pounds of beef was ultimately returned or destroyed by customers,
and that, because of the mixing, it was not able to determine how much of
the original 10,410 pounds of recalled beef was contained in the 64,000
pounds that were recovered.
FDAs Role in USDAs
Recall
Parts of the BSE-infected animal slaughtered on December 9, 2003, were
not used for food, but they were sent to renderers to be separated into raw
materials, such as proteins and blood. Rendered materials are used for
many purposes, including cosmetics and vaccines. FDA has jurisdiction
over renderers.
When USDA learned of the BSE-infected cow on December 23, 2003, the
agency immediately notified FDA. On December 24, 2003, FDA sent an
inspection team to a renderer that handled materials from the BSE cow.
Inspectors confirmed that the parts of the slaughtered BSE positive cow
were on the premises. FDA later identified a second company that
potentially rendered material from the slaughtered BSE cow. Both
renderers agreed to voluntarily hold all product processed from the
diseased cow and dispose of the product as directed by FDA and local
authorities.
On January 7, 2004, 15 containers of potentially contaminated, rendered
material (meat and bone meal) were inadvertently loaded on a ship, and on
January 8, 2004, the ship left Seattle, Washington, for Asia. The renderer
initiated steps to recover the shipped material, so it could be disposed
of as
directed by FDA and local authorities. The ship carrying the material
returned to the United States on February 24, 2004, and the material was
disposed of in a landfill on March 2, 2004.
On January 12, 2004, FDA asked both renderers to expand their voluntary
holds to rendered materials processed from December 23, 2003, through
January 9, 2004, because they may have rendered some recalled meat or
trim that was recovered from retail establishments. Both renderers agreed
to the expanded product hold. In total, FDA requested that renderers
voluntarily hold approximately 2,000 tons of rendered material. FDA
confirmed that none of the potentially contaminated, rendered material
entered commerce, because FDA accounted for all rendered material. FDA
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 45 GAO-05-51 Food Recall Programs
reported that no recall was necessary because no product was distributed
commercially by the rendering companies.
USDA and FDA
Worked Together on
the Recall
USDA and FDA worked together in two ways. First, both agencies notified
each other if their investigations yielded any information about products
within the jurisdiction of the other agency. For instance, when conducting
the second round of verification checks, USDA tracked the disposition of
the product to renderers and landfills and notified FDA when the product
went to renderers. Second, FDA officials helped conduct verification
checks. FDA conducted 32 of the 582 verification checks (approximately 5
percent) for the USDA recall. Officials from both agencies indicated they
regularly interacted and shared information. Table 3 outlines the agencies
actions.
Table 3: Detailed Timeline of USDA, FDA, and Company Actions Related to
the Discovery of an Animal Infected with BSE
Date USDA recall actions FDA actions Company actions
12/9/03 " USDA samples cow for BSE. " BSE cow is slaughtered.
12/11/03 " Sample is sent to Ames, Iowa, for BSE
testing.
" Recalling company sends
carcasses to primary customer for
processing.
12/12/03 " Primary customer sends meat
products to two other primary
customers for further processing.
12/12 -
12/23/03
" Other primary customers distribute
recalled product to secondary
customers.
" Secondary customers distribute
recalled product to tertiary
customers.
12/23/03 " BSE test results are presumptively
positive.
" Recall meeting.
" Initiation of voluntary recall.
" Press release.
" FDA notified of BSE test results.
" FDA dispatches investigation teams.
12/24/03 " FDA inspects Renderer 1.
" FDA determines some rendered
material from Renderer 1 is intended
for Indonesia.
" FDA discovers some material may
have been sent to Renderer 2.
" Renderer 1 agrees to hold remaining
rendered material.
" Recalling company contacts
primary customers.
" Primary customers contact their
customers.
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 46 GAO-05-51 Food Recall Programs
12/25/03 " USDA receives confirmation from
reference lab in England that cow in
question is BSE positive.
12/26/03 " Verification checks begin
" USDA announces recalled product in
Washington State and Oregon.
" FDA begins process of comparing
records to ensure all products from
Renderers 1 and 2 are accounted for.
" Renderer 2 agrees to hold all material
that may have been derived from
BSE cow. None of the rendered
material has been distributed.
12/27/03 " USDA announces recalled product was
distributed in Washington State,
Oregon, California, and Nevada.
" FDA issues statement confirming that
the rendering plants that processed
all of the nonedible material from the
BSE cow have placed a voluntary
hold on all of the potentially infectious
product, none of which had left the
control of the companies and entered
commercial distribution.
12/28/03 " USDA announces recalled product was
distributed in Washington State,
Oregon, California, Nevada, Montana,
Idaho, Alaska, Hawaii, and Guam.
12/29/03 " Food Safety and Inspection Service
determines that the recalled meat
products were distributed to 42
locations, with 80 percent of the
products distributed to stores in
Oregon and Washington State.
12/31/03 " FDA offers assistance to USDA to
complete recall verification checks.
1/6/04 " USDA determines recalled product
was only distributed in Washington
State, Oregon, California, Nevada,
Montana, and Idaho.
1/8/04 " FDA is notified by the renderer that
some of the rendered material on
hold from Renderer 1 was
inadvertently shipped to Asia.
Renderer 1 commits to isolate and
return the rendered material.
" Rendering company notifies FDA of
shipment of product on hold.
(Continued From Previous Page)
Date USDA recall actions FDA actions Company actions
Appendix II
Federal Actions Associated with the
Discovery of an Animal in the United States
Infected with BSE
Page 47 GAO-05-51 Food Recall Programs
Source: GAO analysis of USDA and FDA information.
1/12/04 " FDA advises Renderers 1 and 2 that
they may have rendered meat or trim
subject to recall from retail stores.
" FDA requests Renderers 1 and 2 to
place all rendered material from
December 23 to January 9 on hold.
" FDA determines neither renderer had
shipped rendered material
manufactured after December 23,
2003.
2/9/04 " All rendered material was disposed of
in landfill, except material shipped to
Asia.
2/24/04 " Ship carrying rendered material
returns to U.S. port.
2/25/04 " Verification checks complete.
" USDA Boulder District Office
concludes recall is effective.
3/1/04 " Recall is closed.
3/2/04 " FDA observes disposal in landfill of
remaining rendered material...

snip...

REPORTS

1. Food Safety: USDA and FDA Need to Better Ensure Prompt and Complete
Recalls of Potentially Unsafe Food. GAO-05-51, October 7.tss
http://www.gao.gov/cgi-bin/getrpt?GAO-05-51
Highlights - http://www.gao.gov/highlights/d0551high.pdf


2004

U.S. Department of Agriculture

Office of Inspector General

Great Plains Region

Audit Report

Animal and Plant Health Inspection Service

and

Food Safety and Inspection Service

Bovine Spongiform Encephalopathy (BSE)

Surveillance Program - Phase I

Executive Summary

Report No. 50601-9-KC

August 2004

Animal and Plant Health Inspection Service and Food Safety and Inspection Service

Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase I

Results in Brief Since 1990, the U.S. Department of Agriculture’s (USDA) Animal and Plant

Health Inspection Service (APHIS) has led an interagency effort to monitor

Bovine Spongiform Encephalopathy (BSE), widely known as “mad cow

disease.” Central to this effort was the testing of cattle in a high-risk

category—those that exhibited a disorder in their central nervous systems

(CNS), such as difficulty standing, walking, etc., and cattle that died on the

farm from unclear causes. With the discovery of a BSE-infected animal in

December 2003, APHIS determined to expand its surveillance program to

test a larger number of high-risk animals. The goal of the program before

2004 had been to test 12,500 animals per year; under the expanded program,

the goal extends to over 200,000 animals to be tested in a 12 to 18 month

period.

The objectives of our audit were to determine whether the surveillance

program in place at the time of the December 2003 discovery of BSE was

adequately implemented and whether the expanded program will accomplish

its stated goal—to determine if “…BSE is actually present in the population

and if so, at what level.”

This is the first in a series of reports we are planning to issue on our

evaluation of USDA’s BSE surveillance activities. We could not fully

evaluate the first objective due to the absence of adequate documentation (see

General Comments Section) to support the basis for USDA’s BSE

surveillance plan prior to the discovery of the BSE-infected cow. Our

evaluation of the second objective was limited because the design and

implementation of the BSE surveillance program is still in a state of flux.

However, where possible, we assessed documents provided to us and

interviewed USDA personnel so that we could provide USDA with

recommendations on potential concerns and issues as it moves forward with

implementation.

USDA’s expanded surveillance program is based largely on a broadened plan

of sampling. This sampling plan has been announced as scientifically based

and representative of the population of U.S. cattle as a whole. However, we

concluded that several limitations inherent in the sampling plan need to be

clarified so that industry, the public, and U.S. trading partners understand

what the results of the testing actually imply.

• Sampling is not truly random because participation in the program is

voluntary. The BSE sampling plan, as designed, assumes each animal

USDA/OIG-A/50601-9-KC Page ii

has the same chance of being selected for BSE testing, which will not be

true if testing is voluntary. APHIS has the authority to collect samples,

but it has chosen not to exercise this authority, except at

federally-inspected slaughter facilities.

• Discovery of BSE cases will result in a statistical projection with either a

significantly lower confidence level or a significantly higher maximum

BSE prevalence level. By not discussing this, the plan’s statistical

statements may inadvertently overemphasize the implied “best-case

scenario.”

• As the plan is currently designed, APHIS cannot obtain a statistically

appropriate geographical representation of the U.S. cattle population.

Because the program is voluntary and the universe of high-risk cattle is

difficult to identify, obtain, and test, the surveillance plan needs to be

clarified and its conclusions relating to the prevalence of BSE may need

to be qualified.

• APHIS’ sampling plan assumes BSE is confined to the high-risk cattle

population; other studies show that healthy-looking animals may also

have BSE.

• APHIS’ plan to test 20,000 clinically normal cattle may give the incorrect

impression that these few tests will suggest a level of assurance higher

than warranted about the 45 million adult cattle in the United States.1

• APHIS cannot easily identify, obtain, or test cattle in its high-risk

population; therefore, the chances of detecting BSE, if it exists, may be

reduced and the projected maximum BSE prevalence rate may be

unreliable.

APHIS needs to fully disclose the assumptions that it made in designing its

sampling plan, and it needs to clarify the limitations that exist in the data it

will collect. Beyond its sampling design, however, lie significant challenges

for APHIS in its goal to determine if BSE exists in the United States at a

prevalence of at least one case per 10 million adult cattle. These

challenges—in identifying and testing the high-risk population of cattle—

were inherent in the operations of the surveillance program as it had been

conducted prior to June 2004, and still exist under the expanded program.

Cattle condemned at slaughter plants for CNS symptoms were not

always tested for BSE. This occurred because of confusion in testing

requirements and lack of coordination between APHIS and the agency

1 National Agricultural Statistics Service, Agricultural Statistics 2003, per Table 7-2 for 2002, 44,474,000

(equals 33,118,000 beef cows plus 9,112,000 milk cows plus 2,244,000 bulls).

USDA/OIG-A/50601-9-KC Page iii

that condemns cattle at slaughtering plants, the Food Safety and

Inspection Service (FSIS). Of the 680 cattle FSIS condemned for CNS

symptoms between fiscal years (FY) 2002 and 2004 (through

February 2004), we could validate that only 162 were tested for BSE.

USDA needs to increase testing of rabies-negative brain samples.

Rabies cases exhibit clinical signs not inconsistent with BSE, and a

negative rabies test means the cause of the cow’s disorder has not been

diagnosed. Nevertheless, this high priority population has not been

adequately pursued for BSE testing. Public health and State veterinary

diagnostic laboratories did not always submit rabies-negative samples for

BSE testing because there was no formal mechanism in place to ensure

the submissions.

A process for obtaining samples from animals that “died on the

farm” has not been developed. These samples are important because the

high-risk animals that die on the farm comprise the largest component of

the targeted high-risk population and the most difficult to identify,

obtain, and test. Identifying truly high-risk cattle that die on the farm

may be complicated by the reluctance of producers to submit them for

testing and the motivation to mischaracterize low-risk carcasses as “high

risk” since only the latter may qualify for reimbursement.

The age requirement for BSE testing should be standardized to prevent

confusion. Current testing guidance contains inconsistent age criteria for

testing cattle for BSE. Some documents emphasize testing of livestock

at 20 months of age, some at 24 months of age, and at least one—the

APHIS Surveillance Plan of March 2004—over 30 months of age. This

confusion has created and will continue to create a potential that some

cattle may not be subject to BSE testing.

We are recommending that APHIS implement management controls to

ensure that all high-risk animals, including those that test negative for rabies,

those condemned for CNS symptoms, and those that die on the farm from

unknown causes are sampled and tested in accordance with USDA policy and

the 2004 Surveillance Plan.

In reviewing APHIS’ management of the BSE surveillance program, we also

noted some areas of concern in program administration. Most critically, we

found that stronger controls were needed over the collection of test samples

and the recording of test information. We found cases in which test samplers

submitted nonviable samples and provided inaccurate or incomplete

information on their submission forms. We found other cases in which some

animals that had been tested for such non-high-risk symptoms as diarrhea and

inner ear infection were included in APHIS’ count of samples for the purpose

of meeting surveillance goals. Some information maintained in the

USDA/OIG-A/50601-9-KC Page iv

surveillance program’s database was the result of misentries. This database

was the source of APHIS’ reports on surveillance achievements.

We are recommending that APHIS expedite its development of a new

management information system to track and report its accomplishments

under the expanded surveillance program. We are also recommending that

APHIS implement performance measures and a continuous risk assessment to

enhance its management of the surveillance program and better assess the

program’s effectiveness.

Finally, we noted that, prior to June 1, 2004, APHIS did not have standard

written agreements in place to ensure consistent performance from

non-Federal laboratories and reasonable arrangements and charges from meat

plants and contractors who provide sampling services. Use of these entities

will increase as the 2004 surveillance program expands. Past arrangements

with meat plants and sampling contractors were made on a regional basis,

were sometimes informal, and resulted in costs ranging from $0 to $100 per

sample taken. We concluded that APHIS should impose a standardized

contract specifying the quality of work required and the costs the

Government is willing to incur for it.

The problems disclosed during our review, if not corrected, may negatively

impact the effectiveness of USDA’s overall BSE surveillance program,

impair its ability to perform risk assessments and program evaluations, and

reduce the credibility of any assertion regarding the prevalence of BSE in the

United States. These are complex challenges USDA needs to address as it

moves forward with implementation of its expanded BSE surveillance

program.

This audit was coordinated with the Office of Inspector General’s (OIG)

Investigations Division. OIG conducted two investigations to determine

whether employees of USDA and/or of the slaughter establishment misled or

provided false information concerning the identification of the BSE-positive

cow. In addition, OIG verified the procedures used by USDA and the

slaughter establishment to maintain the integrity of the brain tissue sample

from the slaughter establishment through delivery to the National Veterinary

Services Laboratories (NVSL) in Ames, Iowa. OIG also investigated the

circumstances surrounding the animal displaying possible CNS symptoms

that had not been tested in Texas. The results of these investigations will be

reported under separate cover.

Recommendations

In Brief We are recommending that APHIS fully disclose the assumptions that it

made in designing its sampling plan, and that it clarify the limitations that

exist in the data it will collect. We are also recommending that APHIS

implement management controls to ensure that all high-risk animals,

USDA/OIG-A/50601-9-KC Page v

snip...full text

http://www.usda.gov/oig/webdocs/50601-9-final.pdf

Audit Report

Animal and Plant Health Inspection Service

Oversight of the Importation

of Beef Products from Canada

Report No. 33601-01-Hy February 2005 UNITED STATES DEPARTMENT OF AGRICULTURE OFFICE OF INSPECTOR GENERAL Washington D.C. 20250

DATE: February 14, 2005

REPLY TO

ATTN OF: 33601-01-Hy

SUBJECT: Oversight of the Importation of Beef Products from Canada

TO: W. Ron DeHaven

Administrator

Animal and Plant Health Inspection Service

Barbara J. Masters

Acting Administrator

Food Safety and Inspection Service

ATTN: William J. Hudnall

Deputy Administrator

Marketing and Regulatory Programs – Business Services

Ronald F. Hicks

Assistant Administrator

Office of Program Evaluation, Enforcement and Review

This report presents the results of our audit of oversight of the importation of beef products from Canada. Your response to the draft, dated February 9, 2005, is included as exhibit A. Excerpts of your response and the Office of Inspector General’s (OIG) position are incorporated into the Findings and Recommendations section of the report. Based on your response, management decision has been reached on all recommendations except No. 3. Please follow your agency’s internal procedures in forwarding documentation for final action to the Office of the Chief Financial Officer. Management decisions for the remaining recommendation can be reached once you have provided the additional information outlined in the report section OIG Position.

In accordance with Departmental Regulation 1720-1, please furnish a reply within 60 days describing the corrective actions taken or planned, and the timeframes for implementation of the remaining recommendation. Please note that the regulation requires management decision to be reached on all recommendations within 6 months of report issuance

/s/

ROBERT W. YOUNG

Assistant Inspector General

for Audit

USDA/OIG-A/33601-01-Hy Page i

Executive Summary

Animal and Plant Health Inspection Service’s Oversight of the Importation of Beef Products from Canada (Audit Report No. 33601-01-Hy)


Results in Brief This report presents the results of the Office of Inspector General’s (OIG) audit of the Animal and Plant Health Inspection Service’s (APHIS) oversight of the importation of beef products from Canada following the detection of a Canadian cow with bovine spongiform encephalopathy (BSE) in May 2003. In June 2004, we initiated several actions in response to concerns raised by four U.S. Senators that the U.S. Department of Agriculture (USDA) did not follow appropriate safety measures, beginning sometime in the fall of 2003, in allowing expanded Canadian beef imports into the United States. We reviewed USDA’s actions pertaining to the importation of Canadian products, including the use of risk mitigation1 measures.

On May 20, 2003, the Secretary halted imports of live cattle, other live ruminants, beef, and other ruminant products from Canada after a cow in Alberta was found to have BSE. Prior to this time, there was a free flow of trade between the United States and Canada for live cattle and beef. Due to the serious impact on trade, USDA officials sought a method to allow limited imports from Canada and determined to use the APHIS permit process as a vehicle to facilitate trade. At that time, APHIS did not have a history of issuing permits for the importation of edible meat and meat products. Veterinary import permits were generally issued for items derived from animals, such as blood, cells or cell lines, hormones, and microorganisms including bacteria, viruses, protozoa, and fungi.

On August 8, 2003, the Secretary of Agriculture (Secretary) announced a list of low-risk products, including boneless beef from cattle less than 30 months of age and veal meat from calves less than 36 weeks of age, which would be allowed into the United States from Canada, under certain predetermined conditions. In November 2003, USDA published a proposed rule in the Federal Register to create a low-risk category for countries with BSE, to place Canada on that list, and to allow imports of, among other things, low-risk beef products and live cattle under 30 months of age to resume. This rule for live animals and processed meat products was issued January 4, 2005.

The Secretary’s announcement on August 8, 2003, regarding low-risk products followed USDA’s review of the results of Canada’s epidemiological investigation into the detection of BSE in that country. Based on the results

1 Risk mitigations include such actions as certificates indicating the product is pure liver, Canadian Food Inspection Agency (CFIA) verification that calves were 36 weeks of age or less when slaughtered, and CFIA verification that animals are not known to have been fed prohibited products during their lifetime.

USDA/OIG-A/33601-01-Hy Page ii

of the investigation, as well as international guidelines2 that indicated that products derived from young animals do not pose a risk to human health, USDA issued permits to allow these low-risk products into the United States.

Subsequent to the Secretary’s announcement, APHIS issued 1,155 permits3 allowing the import of a variety of products from Canada, to include many items that had been included in the Secretary’s announcement as well as other items that were not initially identified as allowable low-risk products. In April 2004, a lawsuit was filed in U.S. District Court in Montana, which resulted in a temporary restraining order that identified the specific low-risk Canadian products that were eligible for import into the United States. The list of low-risk products was the same as the list posted on August 15, 2003, by APHIS on its website as a clarification of the Secretary’s August 8, 2003, announcement. On May 5, 2004, the District Court converted the temporary restraining order into a preliminary injunction. Among other things, the preliminary injunction included an exhibit listing the specific Canadian products that would be considered low-risk and details of required risk mitigations.

To accomplish our review of USDA’s actions pertaining to the importation of Canadian products, we interviewed officials from APHIS, the Food Safety and Inspection Service (FSIS), and the Office of the General Counsel (OGC). We analyzed APHIS records relating to the oversight of imported Canadian product, to include a review of the 1,155 import permits and associated documentation. We met with personnel from the U.S. Department of Homeland Security’s Customs and Border Protection (CBP) in Detroit, Michigan and Sweetgrass, Montana to understand their actions to enforce restrictions on the importation of ruminant products from Canada. We also visited FSIS import reinspection facilities located in Buffalo, New York; Detroit, Michigan; and Sweetgrass, Montana. At these facilities, we analyzed documentation on file for 12,427 shipments of ruminant products to determine whether the product imported from Canada met APHIS requirements. These facilities reinspected more than 646 million of the 802 million pounds of Canadian product presented for entry into the United States between September 2003 and September 2004.

From August 2003 to April 2004, APHIS officials allowed a gradual expansion in the types of Canadian beef products approved for import into the United States. The expansions in product type included processed products, bone-in product, and edible bovine tongues, hearts, kidneys, and lips. In October 2003, APHIS allowed bovine tongues despite the APHIS Transmissible Spongiform Encephalopathy (TSE) Working Group4

2 The International Office of Epizootics, the international standard-setting organization for animal health, established these guidelines.

3 As of September 16, 2004.

4 Created by APHIS to analyze risks of BSE to the United States, disseminate accurate information about TSEs, and act as a reference source for responding to questions about TSEs.

USDA/OIG-A/33601-01-Hy Page iii

conclusion in June 2003 that fresh or frozen bovine tongues were "moderate risk" products,5 even when the required risk mitigations were in place. Thus, bovine tongues, one of the items for which APHIS approved import permits, were deemed as posing a "moderate risk," and not a "low risk" by the APHIS TSE Working Group.

The Chairperson of the TSE Working Group explained that the risk status for bovine tongues changed from moderate to low some time between June and November 2003, although the change was not documented prior to the November 2003 issuance of APHIS’ "Risk Analysis: BSE Risk from Importation of Designated Ruminants and Ruminant Products from Canada into the United States." The risk analysis categorized bovine tongues as eligible product when Canadian inspection officials verify the risk mitigation, which is that tonsils are removed.

Additionally, APHIS allowed an expansion in the type of Canadian facilities that would be allowed to produce items for export to the United States. The gradual expansion occurred because the agency employees tasked with administering the permit process did not consider the initial announcement made by the Secretary to exclude products similar to those on the published list of low-risk products, if APHIS had concluded that the products posed similar risk levels. However, APHIS did not develop documentation to support the agency’s conclusions that the additional products were low-risk products. APHIS also did not have a review structure or other monitoring process in place to identify discrepancies between publicly stated policy and agency practice. According to APHIS officials, they considered the initial announcement made by the Secretary to be part of an effort to demonstrate to the world that such trade with Canada was safe and appropriate. Accordingly, they allowed the import of products they considered low risk in an attempt to further that greater effort. However, APHIS did not document the process it used to determine the additional products were low risk.

As a result of the "permit creep" that occurred between August 2003 and April 2004, APHIS issued permits for the import of beef tongue as well as other permits for products with questionable eligibility. Further, the agency allowed the import of products from Canadian facilities that produced both eligible and ineligible products, thus increasing the possibility that higher-risk product could be inadvertently exported to the United States. This practice contrasted with APHIS’ publicly stated policy that only Canadian facilities that limited production to eligible products would be allowed to ship to the United States. In addition, APHIS did not

5 "Recommendations of APHIS TSE Working Group for allowing certain commodities from Canada to be imported into the United States," dated June 16, 2003. When required risk mitigation measures are in place, to include various CFIA verifications, removal of tonsils, and random sample analysis by USDA of any suspicious tissue to confirm absence of specified risk materials, fresh and frozen bovine tongues have a "moderate" risk.

USDA/OIG-A/33601-01-Hy Page iv

communicate its decisions to all interested parties and USDA was criticized by segments of the public, the cattle industry, and the U.S. Congress.

APHIS issued permits to allow the import of beef cheek meat with questionable eligibility because the agency did not establish a clear working definition for the general term "boneless beef." Instead of coordinating with FSIS, APHIS reviewers relied upon their own understanding of the term. Some APHIS reviewers considered the term "boneless beef" broadly, to mean any bovine meat that did not contain a bone. Thus, some applicants who requested permits to import beef cheek meat and other products received permits allowing the import of "boneless beef or boneless beef trim." As a result, over 63,000 pounds of beef cheek meat with questionable eligibility entered U.S. commerce from Canada.

Further, we found that FSIS did not always communicate effectively about the eligibility status of beef cheek meat. FSIS distributed information to its import inspectors by way of a series of numbered memoranda, titled Part 4, Canada, BSE Restrictions, Revision 2 through Revision 11. Some of the issuances were supplemented by additional guidance, in the form of supplemental memoranda. However, in our opinion, FSIS managers did not ensure consistent interpretation of the provisions of the various memoranda, a factor that contributed to the entry of the previously mentioned 63,000 pounds of beef cheek meat with questionable eligibility. Because APHIS changed its instructions to FSIS frequently and did not document the direction provided to FSIS,6 it was even more difficult for FSIS to keep its field staff fully apprised of the status of product eligibility.

FSIS officials did not agree that the import inspectors misinterpreted the instructions in the numbered memoranda. Furthermore, FSIS officials asserted that the 63,000 pounds of beef cheek meat was eligible for import when it was imported from April to June 2004. However, they agreed that controls should be strengthened to better communicate the eligibility of product that frequently changed as beef cheeks did from August 2003 to July 2004. Two FSIS import inspectors we interviewed advised us that beef cheeks had been "going back and forth" regarding eligibility. APHIS notified FSIS that effective July 20, 2004, beef cheek meat was not an eligible product for import into the United States. According to APHIS direction, beef cheek meat has not been eligible for import since July 20, 2004. As of the date of this report, it is still not eligible for import. Some FSIS officials assert that the beef cheek meat was eligible product. In contrast, the APHIS National Incident Commander for BSE Enhanced Surveillance stated in an August 18, 2004 interview, that further discussion was still required with respect to the import of cheek meat and that no new

6 We found that APHIS did not document its direction to FSIS prior to April 2004 when the Ranchers-Cattlemen Action Legal Fund (R-CALF) filed a lawsuit against USDA in U.S. District Court in Montana.

scientific information on this topic had been considered by APHIS. Given the importance of the issues, ongoing litigation, and differences in scientific opinion, it would have been prudent for APHIS to write down its decisions about the eligibility status of beef cheek meat at points in time. However, the agency did not do so; or did not retain such documentation for our review.

In January 2005, FSIS assessed the shipments of beef check meat and concluded, "FSIS has no reason to believe that these four shipments7 of beef cheek meat are injurious to health." In its assessment, FSIS explained that in January 2004, the agency implemented interim final rules that prohibited the use of specified risk materials for human food. On the matter of beef cheek meat, the FSIS rule maintained that beef cheeks are not part of the skull, which is a specified risk material. The FSIS rule continued to allow the use of beef cheek meat for human food, provided that the meat is not contaminated with specified risk materials. FSIS further supported its conclusion on the basis that Canada had a pre-existing equivalent specified risk material system in place. However, as previously noted, beef cheek meat is not a product that is currently eligible to be imported into the United States.

APHIS issued 1,155 permits for the importation of ruminant products from Canada without ensuring that the agency had an appropriate system of internal controls to manage the process. The APHIS permit system was originally designed to allow for the import of research quantities (generally small amounts) of material into the United States. According to APHIS officials, this permit system handled approximately 400 permit requests annually. The procedures that APHIS had developed for handling permit requests for small amounts of product were not adequate to deal with the high volume of requests for large quantities of commercial use beef. The agency did not implement or finalize standard operating procedures for processing the large volume of permits. For example, APHIS did not establish controls to ensure that risk mitigation measures were consistently applied. We found that 8 of the 83 permits issued for bovine liver did not include the risk mitigation measure that the livers be from animals slaughtered after August 8, 2003.8 We also found that APHIS did not implement requirements to perform onsite monitoring of permit holders, Canadian facilities, or inspection personnel9 at U.S. ports of entry. As a result, there was reduced assurance that Canadian beef entering the United States was low-risk. Some product with questionable eligibility, as described above, entered U.S. commerce. ...snip...full text;

http://www.usda.gov/oig/webdocs/33601-01-HY.pdf

February 2005

MAD COW DISEASE

FDA’s Management of the Feed Ban Has

Improved, but Oversight Weaknesses

Continue to Limit Program Effectiveness

FDA has made needed improvements to its management and oversight of the

feed-ban rule in response to GAO’s 2002 report, but program weaknesses

continue to limit the effectiveness of the ban and place U.S. cattle at risk of

spreading BSE. Improvements made include FDA establishing a uniform

method of conducting compliance inspections and training FDA inspectors,

as well as state inspectors who carry out inspections under agreements with

FDA, on the new method. FDA also implemented new data-entry procedures

that are designed to more reliably track feed-ban inspection results.

Consequently, FDA has a better management tool for overseeing compliance

with the feed-ban rule and a data system that better conforms to standard

database management practices. However, various program weaknesses

continue to undermine the nation’s firewall against BSE. For example:

• FDA acknowledges that there are more feed manufacturers and

transporters, on-farm mixers, and other feed industry businesses that are

subject to the feed ban than the approximately 14,800 firms inspected to

date; however, it has no uniform approach for identifying additional

firms.

• FDA has not reinspected approximately 2,800, or about 19 percent, of

those businesses, in 5 or more years; several hundred are potentially

high risk. FDA does not know whether those businesses now use

prohibited material in their feed.

• FDA’s feed-ban inspection guidance does not include instructions to

routinely sample cattle feed to test for potentially prohibited material as

part of the compliance inspection. Instead, it includes guidance for

inspectors to visually examine facilities and equipment and review

invoices and other documents.

• Feed intended for export is not required to carry a caution label “Do not

feed to cattle or other ruminants,” when the label would be required if

the feed were sold domestically. Without that statement, feed containing

prohibited material could be inadvertently or intentionally diverted back

to U.S. cattle or given to foreign cattle.

• FDA has not always alerted USDA and states when it learned that cattle

may have been given feed that contained prohibited material. This lapse

has been occurring even though FDA’s guidance calls for such

communication.

• Although research suggests that cattle can get BSE from ingesting even a

small amount of infected material, inspectors do not routinely inspect or

review cleanout procedures for vehicles used to haul cattle feed.

http://www.gao.gov/highlights/d05101high.pdf

FULL TEXT;

http://www.gao.gov/new.items/d05101.pdf

HERE's what old stan the man had to say about it in Congressional Testimony

''DAMNING TESTIMONY'' ...TSS


Senator Michael Machado from California

''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''

Stanley Prusiner

''nobody has ever ask us to comment''

''they don't want us to comment''

''they never ask''

i tried to see Venemon, after Candian cow was discovered with BSE.
went to see lyle. after talking with him... absolute ignorance... then
thought i
should see Venemon... it was clear his entire policy was to get cattle
bonless beef prods
across the border... nothing else mattered...
his aids confirmed this... 5 times i tried to see Venemon, never worked...
eventually met with carl rove the political... he is the one that
arranged meeting
with Venemon... just trying to give you a sense of the distance... healh
public safety...
was never contacted...
yes i believe that prions are bad to eat and you can die from them...END

Dr. Stan bashing Ann Veneman - 3 minutes

http://maddeer.org/video/embedded/08snip.ram

Senator Michael Machado from California

''USDA does not know what's going on''.
''USDA is protecting the industry''.
''SHOULD the state of California step in''

http://maddeer.org/video/embedded/machado.html

OPERATOR: "Next question comes from Dan Goldstein. Your line is open."

REPORTER: "Yeah. Hi. It's Dan Goldstein. Two questions, one for Dr. Clifford and one for the Secretary. Mr. Secretary, first of all, does this somewhat do you think may shake the confidence of the international community, one, in the ability of the Ames Laboratory and, two, also the efficacy of the IHC test?

"And then also for Dr. Clifford, what does this mean in terms of the protocols? Will you now have to go back and perhaps test more animals with Western Blot tests?"

SEC. JOHANNS: "Let me address the question about the Ames Laboratory, and I'm sure the doctor will want to offer a thought also.

"One of the things we are very, very proud of is that Ames laboratory. They do great work there, and again I remind everybody that the IHC test is an internationally accepted test. And that comes from the OIE, and like I said even amongst scientists you would get debate about the test.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/06/0207.xml

I had to throw this in before going further, kind like the infamous "Brownie, you're doing a heck of a job" speech.

Stanley Prusiner - Discoverer of Prions

"THE BEEF IN JAPAN IS SAFER THAN USA BEEF"

"UNDER/OVER 30 MONTH RULE IS STUPID ... ARBITRARY NUMBER"

1 TO A MAXIMUM OF 5 sCJD per million in stans push for the spontaneous theory (patent cdi test$).

90% of CJD is spontaneous, without route and source. (i do not agree, he got the prize, i have no Phds).

stan does mention the atypical TSE in Italian cows and almost goes to sCJD being caused by meat, but

his patent could not bring his heart to do that$ this theory is wrong in the sense of 85% of all

sCJD cases are spontaneous. i have asked him to clarify what figures he thinks of the 85%+ of sCJD

he thinks is spontaneous and what % is from one of the many proven routes and sources of TSE,

and stan has failed to reply to that question. also, the spontaneous theory of TSE has not been proven,

in a sense of producing a TSE that is identical to any field TSE documented to date. IN FACT,

the latest science is proving the UK/BSE/nvCJD only theory is being proven to be false.


Stanley Prusiner - Discoverer of Prions

http://maddeer.org/video/embedded/prusiner.html

-------- Original Message --------
Subject: Strain-specified characteristics of mouse synthetic prions
Date: Tue, 8 Feb 2005 12:58:36 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


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

Published online before print January 25, 2005, 10.1073/pnas.0409079102
PNAS | February 8, 2005 | vol. 102 | no. 6 | 2168-2173

NEUROSCIENCE
Strain-specified characteristics of mouse synthetic prions

Giuseppe Legname *, {dagger} {ddagger} , Hoang-Oanh B. Nguyen *, Ilia
V. Baskakov * § , Fred E. Cohen *, ¶, ||, Stephen J.
DeArmond * {ddagger} , ** and Stanley B. Prusiner *, {dagger} {ddagger}
, ||, {dagger} {dagger}

*Institute for Neurodegenerative Diseases and Departments of {dagger}
Neurology, ¶Cellular and Molecular Pharmacology, ||Biochemistry and
Biophysics, and **Pathology, University of California, San Francisco, CA
94143

Contributed by Stanley B. Prusiner, December 6, 2004

Synthetic prions were produced in our laboratory by using recombinant
mouse prion protein (MoPrP) composed of residues 89-230. The first mouse
synthetic prion strain (MoSP1) was inoculated into transgenic (Tg) 9949
mice expressing N-terminally truncated MoPrP({Delta} 23-88) and WT FVB
mice expressing full-length MoPrP. On first and second passage in Tg9949
mice, MoSP1 prions caused disease in 516 ± 27 and 258 ± 25 days,
respectively; numerous, large vacuoles were found in the brainstem and
gray matter of the cerebellum. MoSP1 prions passaged in Tg9949 mice were
inoculated into FVB mice; on first and second passage, the FVB mice
exhibited incubation times of 154 ± 4 and 130 ± 3 days, respectively. In
FVB mice, vacuolation was less intense but more widely distributed, with
numerous lesions in the hippocampus and cerebellar white matter. This
constellation of widespread neuropatho-logic changes was similar to that
found in FVB mice inoculated with Rocky Mountain Laboratory (RML)
prions, a strain derived from a sheep with scrapie. Conformational
stability studies showed that the half-maximal GdnHCl (Gdn1/2)
concentration for denaturation of MoSP1 prions passaged in Tg9949 mice
was {approx} 4.2 M; passage in FVB mice reduced the Gdn1/2 value to
{approx} 1.7 M. RML prions passaged in either Tg9949 or FVB mice
exhibited Gdn1/2 values of {approx} 1.8 M. The incubation times,
neuropathological lesion profiles, and Gdn1/2 values indicate that MoSP1
prions differ from RML and many other prion strains derived from sheep
with scrapie and cattle with bovine spongiform encephalopathy.

neurodegeneration

------------------------------------------------------------------------
Author contributions: G.L., I.V.B., F.E.C., and S.B.P. designed
research; H.-O.B.N. and S.J.D. performed research; G.L., S.J.D., and
S.B.P. analyzed data; S.B.P. contributed new reagents/analytic tools;
and G.L., S.J.D., and S.B.P. wrote the paper.

Abbreviations: PrP, prion protein; MoPrP, mouse PrP; PrPSc,
disease-causing isoform of PrP; MoSP1, mouse synthetic prion1; rec,
recombinant; Tg, transgenic; RML, Rocky Mountain Laboratory; Gdn1/2,
half-maximal GdnHCl; HuM, human-mouse; PK, proteinase K.

{ddagger} G.L., S.J.D., and S.B.P. have a financial interest in InPro
Biotechnology, Inc.

§ Present address: Medical Biotechnology Center, University of Maryland
Biotechnology Institute, Baltimore, MD 21201.

{dagger} {dagger} To whom correspondence should be addressed. E-mail:
stanley@ind.ucsf.edu .

© 2005 by The National Academy of Sciences
of the USA


http://www.pnas.org/cgi/content/abstract/102/6/2168?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=prion&searchid=1107887303603_6112&stored_search=&FIRSTINDEX=0&volume=102&issue=6&journalcode=pnas


Greetings list members,


> The incubation times, neuropathological lesion profiles, and Gdn1/2
> values indicate that MoSP1 prions differ from RML and many other prion
> strains derived from sheep with scrapie and cattle with bovine
> spongiform encephalopathy.


THIS is what i was most curious about when everyone (well not everybody)
jumped on the ''spontaneous sCJD/TSE bandwagon again''. i wanted to know
if the synthetic TSE (which stan produced) was infectious. HERE we
find it is, BUT, it does not seem to match other TSEs. SO the myth
or theory that 85%+ of all sporadic CJD (or CJDs) just happen
spontaneously (without any route or source of agent) from a misfolding
prion
is pretty much put to rest. i never believed it anyway. there was never
any science
to back it up.


> SPONTANEOUS PRION DISEASES
> The discovery that a small change in the condition of a cell can cause
> the development of a prion offers an explanation, says Prusiner, for
> the sporadic form of Creutzfeldt Jakob disease (CJD), which is
> responsible for 85 percent of cases of prion disease in humans
> (occurring in 1 or 2 people per million) and is believed to develop
> spontaneously. It also supports his belief, he says, that sporadic
> forms of prion disease are caused by prion strains that are different
> from the one causing bovine spongiform encephalopathy (BSE) in cattle
> in Britain. He says he thinks that sporadic BSE will be found in one
> to five cattle per million and predicts such numbers will be found
> with increased testing for BSE.


http://www.mnbeef.org/BSE/prion_finding_offers_insight_int.htm


THIS was total BSeee and everybody knew it...

OH, and by the way, see the increase in sporadic CJD over the
last decade or so here (excluding N. America).

http://www.eurocjd.ed.ac.uk/sporadic.htm

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

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

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology, University College, Queen Square, London WC1N 3BG, UK 1
Corresponding author e-mail: j.collinge@prion.ucl.ac.uk


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

Abstract


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

http://embojournal.npgjournals.com/cgi/content/full/21/23/6358

THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease


http://www.pnas.org/cgi/content/abstract/0305777101v1


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

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

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

Sarah E. Lloyd, Jacqueline M. Linehan, Melanie Desbruslais,
Susan Joiner, Jennifer Buckell, Sebastian Brandner,
Jonathan D. F. Wadsworth and John Collinge

Correspondence
John Collinge
j.collinge@prion.ucl.ac.uk

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of
Neurology,
University College, London WC1N 3BG, UK
Received 9 December 2003
Accepted 27 April 2004

Distinct prion strains can be distinguished by differences in incubation
period, neuropathology
and biochemical properties of disease-associated prion protein (PrPSc)
in inoculated mice.
Reliable comparisons of mouse prion strain properties can only be
achieved after passage in
genetically identical mice, as host prion protein sequence and genetic
background are known
to modulate prion disease phenotypes. While multiple prion strains have
been identified in
sheep scrapie and CreutzfeldtJakob disease, bovine spongiform
encephalopathy (BSE) is
thought to be caused by a single prion strain. Primary passage of BSE
prions to different lines
of inbred mice resulted in the propagation of two distinct PrPSc types,
suggesting that two
prion strains may have been isolated. To investigate this further, these
isolates were
subpassaged in a single line of inbred mice (SJL) and it was confirmed
that two distinct prion
strains had been identified. MRC1 was characterized by a short
incubation time (110±3 days),
a mono-glycosylated-dominant PrPSc type and a generalized diffuse
pattern of PrP-immunoreactive
deposits, while MRC2 displayed a much longer incubation time (155±1 days),
a di-glycosylated-dominant PrPSc type and a distinct pattern of
PrP-immunoreactive deposits
and neuronal loss. These data indicate a crucial involvement of the host
genome in modulating
prion strain selection and propagation in mice. It is possible that
multiple disease phenotypes
may also be possible in BSE prion infection in humans and other animals.

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


REPORTS

Human Prion Protein with
Valine 129 Prevents Expression
of Variant CJD Phenotype

Jonathan D. F. Wadsworth, Emmanuel A. Asante,
Melanie Desbruslais, Jacqueline M. Linehan, Susan Joiner,
Ian Gowland, Julie Welch, Lisa Stone, Sarah E. Lloyd,
Andrew F. Hill,* Sebastian Brandner, John Collinge

Variant Creutzfeldt-Jakob disease (vCJD) is a unique and highly distinctive
clinicopathological and molecular phenotype of human prion disease
associated with infection with bovine spongiform encephalopathy (BSE)-like
prions. Here, we found that generation of this phenotype in transgenic mice
required expression of human prion protein (PrP) with methionine 129.
Expression of human PrP with valine 129 resulted in a distinct phenotype
and,
remarkably, persistence of a barrier to transmission of BSE-derived
prions on
subpassage. Polymorphic residue 129 of human PrP dictated propagation of
distinct prion strains after BSE prion infection. Thus, primary and
secondary
human infection with BSE-derived prions may result in sporadic CJD-like or
novel phenotypes in addition to vCJD, depending on the genotype of the
prion
source and the recipient.

snip...

In conclusion, we have demonstrated
that BSE and vCJD prion infection in
transgenic mice can result in the propaga-
tion of distinct molecular and neuropatho-
logical phenotypes dependent on host PrP
residue 129 and possibly other, as yet
unidentified, disease modifying loci (10).
These data predict a critical role for PRNP
codon 129 in governing the thermodynamic
permissibility of human PrPSc conformation
that can be interpreted within a conforma-
tional selection model of prion transmission
barriers (17-19) (SOM text) and suggest
that there is no overlapping preferred
conformation for Val129 and Met129 human
PrP that can be generated as a result of
exposure to the vCJD/BSE prion strain.
Biophysical measurements suggest that this
powerful effect of residue 129 on prion
strain selection is likely to be mediated by
means of its effect on the conformation of
PrPSc or its precursors or on the kinetics of
their formation, as it has no measurable
effect on the folding, dynamics, or stability
of the normal cellular prion protein PrPC
(20).

Although caution must be exercised in
extrapolating from animal models, even
where, as here, faithful recapitulation of
molecular and pathological phenotypes is
possible, our findings argue that primary
human BSE prion infection, as well as sec-
ondary infection with vCJD prions by iatro-
genic routes, may not be restricted to a single
disease phenotype. These data, together with
the recent recognition of probable iatrogenic
transmission of vCJD prions to recipients of
blood {21, 22), including a PRNP codon 129
Met/Val heterozygous individual (22), re-
iterate the need to stratify all human prion
disease patients by PrPSc type. This surveil-
lance will facilitate rapid recognition of novel
PrPSc types and of any change in relative
frequencies of particular PrPSc subtypes in
relation to either BSE exposure patterns or
iatrogenic sources of vCJD prions.

References and Notes

snip...end

To whom correspondence should be addressed.
E-mail: j.collinge@prion.ucl.ac.uk

www.sciencemag.org SCIENCE VOL 306 3 DECEMBER 2004


Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions

Mathias Heikenwalder,1* Nicolas Zeller,1* Harald Seeger,1* Marco
Prinz,1* Peter-Christian Klöhn,2 Petra
Schwarz,1 Nancy H. Ruddle,3 Charles Weissmann,2 Adriano Aguzzi1!

1Institute of Neuropathology, University Hospital of ZĂĽrich, CH-8091
ZĂĽrich, Switzerland. 2Medical Research Council Prion
Unit, Department of Neurodegenerative Diseases, Institute of Neurology,
Queen Square, London WC1N 3BG, UK. 3Department
of Epidemiology and Public Health and Section of Immunobiology, Yale
University School of Medicine, New Haven, CT
06520, USA.

*These authors contributed equally to this work.
Present address: Institute of Neuropathology, Georg-August-Universität,
D-37073 Göttingen, Germany.
!To whom correspondence should be addressed. E-mail:
adriano@pathol.unizh.ch

Prions typically accumulate in nervous and lymphoid
tissues. Because proinflammatory cytokines and immune
cells are required for lymphoid prion replication, we
tested whether inflammatory conditions affect prion
pathogenesis. We administered prions to mice with five
inflammatory diseases of kidney, pancreas or liver. In all
cases, chronic lymphocytic inflammation enabled prion
accumulation in otherwise prion-free organs.
Inflammatory foci consistently correlated with
lymphotoxin upregulation and ectopic induction of PrPCexpressing
FDC-M1+ cells, whereas inflamed organs of
mice lacking lymphotoxin-? or its receptor did not
accumulate PrPSc nor infectivity upon prion inoculation.
By expanding the tissue distribution of prions, chronic
inflammatory conditions may act as modifiers of natural
and iatrogenic prion transmission.

snip...

The above results indicate that chronic follicular
inflammation, induced by a variety of causes, specifies prion
tropism for otherwise prion-free organs. In most instances
infectivity tended to rise with time, suggesting local prion
replication. Organ-specific expression of one single proinflammatory
cytokine (LT?) or chemokine (SLC) sufficed to
establish unexpected prion reservoirs, suggesting
differentiation of ubiquitous stromal constituents into prionreplication
competent cells. In several instances, prion
concentration in individual inflamed organs approached that
of spleen long before any clinical manifestation of scrapie.
Inflamed non-lymphoid organs not only accumulated PrPSc,
but transmitted bona fide prion disease when inoculated into
healthy recipient mice.

Knowledge of the distribution of prions within infected
hosts is fundamental to consumer protection and prevention
of iatrogenic accidents. Based on the failure to transmit BSE
infectivity from any tissue but central nervous system,
intestinal, and lymphoid tissue (35), the risk to humans of
contracting prion infection from other organs has been
deemed small even in countries with endemic BSE. It may be
important now to test whether superimposed viral, microbial
or autoimmune pathologies of farm animals trigger
unexpected shifts in the organ tropism of prions. Conversely,
the lack of infectivity in burned out postinflammatory
pancreases suggests that anti-inflammatory regimens may
abolish ectopic prion reservoirs.

References and Notes ............snip...........end

/ www.sciencexpress.org / 20 January 2005 / Page 5 /
10.1126/science.1106460TSS


kind regards,
terry


######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########


Medical Sciences
Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease

Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy


Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.

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

C.C. and G.Z. contributed equally to this work.

||To whom correspondence should be addressed.

E-mail: salvatore.monaco@mail.univr.it .
www.pnas.org/cgi/doi/10.1073/pnas.0305777101


Discussion

In natural and experimental TSEs, PrPSc deposition represents

an early event that occurs weeks to months before the development

of spongiform changes (20, 21). As a consequence, the

detection of PrPSc by Western immunoblot provides a unique

opportunity in the diagnosis of BSE early in the incubation

period and, therefore, in presymptomatic animals. The identification

of the present cattle by postmortem biochemical tests, in

the absence of clear neurological involvement, suggests that the

disorder was detected at early stages, and this may also explain

the lack of widespread vacuolar changes.

Previous pathological studies in clinically suspect cases of BSE

in Great Britain have provided evidence for a uniform pattern

in the severity and distribution of vacuolar lesions in affected

animals, with medulla oblongata nuclei being the most involved

(22). While confirming that the BSE epidemic has been sustained

by a single agent, these studies have assessed the validity

of statutory criteria for the diagnosis of BSE, which is currently

based on both histopathological and immunobiochemical exam-

3068  www.pnas.orgcgidoi10.1073pnas.0305777101 Casalone et al.

ination of the medulla. However, the prevailing involvement of

cortical regions in the cattle with amyloid deposition suggests

that postmortem brain sampling should not be limited to the

obex. In addition, a careful analysis of PrPSc glycoform profiles

at the confirmatory Western immunoblot may provide a molecular

means of identifying atypical cases of bovine TSE.

Bovine Amyloidotic Spongiform Encephalopathy (BASE): A Second

Bovine TSE. The present findings show that a previously undescribed

pathological and immunohistochemical phenotype, associated

with cattle TSE, is related to the presence of a PrPSc type

with biochemical properties, including the gel mobility of the

protease-resistant fragment and glycoform ratios, different from

those encountered in cattle BSE. Brain deposition of this

pathological isoform of cattle PrP correlates with the formation

of PrP-amyloid plaques, as opposed to typical BSE cases. Although

in several natural and experimental recipients of the

BSE agent, including humans (13), neuropathological changes

are characterized by the presence of PrP-positive amyloid

deposits with surrounding vacuolation, cattle BSE is not associated

with PrP-amyloid plaque formation. On the basis of the

above features, we propose to name the disease described here

BASE. Although observed in only two cattle, the BASE phenotype

could be more common than expected. In previous

studies, amyloid congophilic plaques were found in 1 of 20 BSE

cases examined systematically for amyloid (23), and it was reported

that focal cerebral amyloidosis is present in a small proportion of

BSE cases (24). Although no biochemical analysis of PrPSc glycotype

is available for these animals with ‘‘atypical BSE phenotype,’’

our present results underscore the importance of performing

a strain-typing in bovine TSE with amyloid deposition.

In sCJD, the neuropathological phenotype largely correlates

with the molecular type of PrPSc and distinct polymorphic sites

of PRNP (9, 19). This is in contrast with the situation in cattle,

where different genotypes have been reported based on the

variable numbers of octapeptide repeats in each allele, but no

evidence for single-codon polymorphisms in the PrP gene has

been established (25, 26). Because the present animals shared a

similar genetic background and breed, differences in disease

phenotypes between cattle with BSE and BASE can be tentatively

related only to distinct PrPSc types or alternative routes of

infection and spread of prion pathology. Accordingly, the lack of

involvement of the motor dorsal nucleus of the vagus and the

slight involvement of the brainstem in BASE, suggests a route for

spreading of the agent other than the alimentary tract. Therefore,

unless the BASE agent propagates throughout the olfactory

pathway or other peripheral routes, it is possible that this

disorder represents a sporadic form of cattle TSE, which would

also explain the difference in ages between the two groups of

affected animals.

Phenotypic Similarities Between BASE and sCJD. The transmissibility

of CJD brains was initially demonstrated in primates (27), and

classification of atypical cases as CJD was based on this property

(28). To date, no systematic studies of strain typing in sCJD have

been provided, and classification of different subtypes is based

on clinical, neuropathological, and molecular features (the polymorphic

PRNP codon 129 and the PrPSc glycotype) (8, 9, 15, 19).

The importance of molecular PrPSc characterization in assessing

the identity of TSE strains is underscored by several studies,

showing that the stability of given disease-specific PrPSc types is

maintained upon experimental propagation of sCJD, familial

CJD, and vCJD isolates in transgenic PrP-humanized mice (8,

29). Similarly, biochemical properties of BSE- and vCJDassociated

PrPSc molecules remain stable after passage to mice

expressing bovine PrP (30). Recently, however, it has been

reported that PrP-humanized mice inoculated with BSE tissues

may also propagate a distinctive PrPSc type, with a ‘‘monoglycosylated-

dominant’’ pattern and electrophoretic mobility of the

unglycosylated fragment slower than that of vCJD and BSE (31).

Strikingly, this PrPSc type shares its molecular properties with the

a PrPSc molecule found in classical sCJD. This observation is at

variance with the PrPSc type found in MV2 sCJD cases and in

cattle BASE, showing a monoglycosylated-dominant pattern but

faster electrophoretic mobility of the protease-resistant fragment

as compared with BSE. In addition to molecular properties

of PrPSc, BASE and MV2 sCJD share a distinctive pattern of

intracerebral PrP deposition, which occurs as plaque-like and

amyloid-kuru plaques. Differences were, however, observed in

the regional distribution of PrPSc. While inMV2 sCJD cases the

largest amounts of PrPSc were detected in the cerebellum,

brainstem, and striatum, in cattle BASE these areas were less

involved and the highest levels of PrPSc were recovered from the

thalamus and olfactory regions.

In conclusion, decoding the biochemical PrPSc signature of

individual human and animal TSE strains may allow the identification

of potential risk factors for human disorders with

unknown etiology, such as sCJD. However, although BASE and

sCJD share several characteristics, caution is dictated in assessing

a link between conditions affecting two different mammalian

species, based on convergent biochemical properties of diseaseassociated

PrPSc types. Strains of TSE agents may be better

characterized upon passage to transgenic mice. In the interim

until this is accomplished, our present findings suggest a strict

epidemiological surveillance of cattle TSE and sCJD based on

molecular criteria.

We are grateful to Giuseppe Ru (Centro di Referenza Nazionale per le

Encefalopatie Animali, Istituto Zooprofilattico Sperimentale di Torino)

for the provision of surveillance data. We also thank Diana Bazan for

preparing material for transmission electron microscopy, and Ines

Fig. 4. Electrophoretic analysis of PrPSc in cattle TSE and sCJD. (a) Western

blot detection of PrPSc in brains of group 1 animals (lanes 1 and 5); subject with

sCJD and type 1 PrPSc, methioninemethionine at codon 129 (lane 2); subject

with sCJD and type 2 PrPSc, methioninevaline at codon 129 (lane 3); and group

2 cattle (lane 4). (b) Relative proportions of the three PrPSc glycoforms in group

1 and group 2 cattle compared with glycoform profiles obtained in nine sCJD

patients, methioninevaline at codon 129 and with type 2 PrPSc. Mean 

standard deviation is shown. Upper band, diglycosylated form; middle band,

monoglycosylated form; and lower band, unglycosylated form.

Casalone et al. PNAS  March 2, 2004  vol. 101 


http://www.pnas.org/cgi/reprint/0305777101v1


Characterization of two distinct prion strains derived from bovine spongiform encephalopathy transmissions to inbred mice
Sarah E. Lloyd, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Jennifer Buckell, Sebastian Brandner, Jonathan D. F. Wadsworth and John Collinge


MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, London WC1N 3BG, UK


Correspondence
John Collinge
j.collinge@prion.ucl.ac.uk

Distinct prion strains can be distinguished by differences in incubation period, neuropathology and biochemical properties of disease-associated prion protein (PrPSc) in inoculated mice. Reliable comparisons of mouse prion strain properties can only be achieved after passage in genetically identical mice, as host prion protein sequence and genetic background are known to modulate prion disease phenotypes. While multiple prion strains have been identified in sheep scrapie and Creutzfeldt–Jakob disease, bovine spongiform encephalopathy (BSE) is thought to be caused by a single prion strain. Primary passage of BSE prions to different lines of inbred mice resulted in the propagation of two distinct PrPSc types, suggesting that two prion strains may have been isolated. To investigate this further, these isolates were subpassaged in a single line of inbred mice (SJL) and it was confirmed that two distinct prion strains had been identified. MRC1 was characterized by a short incubation time (110±3 days), a mono-glycosylated-dominant PrPSc type and a generalized diffuse pattern of PrP-immunoreactive deposits, while MRC2 displayed a much longer incubation time (155±1 days), a di-glycosylated-dominant PrPSc type and a distinct pattern of PrP-immunoreactive deposits and neuronal loss. These data indicate a crucial involvement of the host genome in modulating prion strain selection and propagation in mice. It is possible that multiple disease phenotypes may also be possible in BSE prion infection in humans and other animals.


http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471


Asante/Collinge et al findings 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;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'flounder@wt.net'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.


I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.


Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm

Subject: Federal Veterinarian Volume 61 Number 10 October 2004 (TSE report)
Date: November 9, 2004 at 2:14 pm PST


-------- Original Message --------
Subject: Federal Veterinarian Volume 61 Number 10 October 2004 (TSE report)
Date: Tue, 9 Nov 2004 16:14:36 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE


snip...


http://www.vegsource.com/talk/madcow/messages/93490.html


Detecting Mad Cow Disease By Stanley B. Prusiner July 2004


http://www.google.com/search?svnum=30&as_scoring=d&hl=en&ie=UTF-8&edition=us&q=spontaneous+bse+soto+tss&as_drrb=q&as_qdr=d&btnmeta%3Dsearch%3Dsearch=Search+the+Web


-------- Original Message --------
Subject: FIVE POSSIBLE SOURCES OF BSE IN NORTH AMERICAN CATTLE
Date: Fri, 24 Sep 2004 08:58:36 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy


Science, Vol 305, Issue 5692, 1918-1921 , 24 September 2004
[HELP with high resolution image viewing] [Return to Article]


Five possible sources of BSE in North American cattle. Sheep, deer, and
elk could spread prion diseases (TSEs) to cattle through direct animal
contact or contamination
of pastures. Endemic BSE has not been proven to exist anywhere in the
world, but it is difficult to exclude this possibility because of the
inefficient spread of BSE infectivity
between individual animals (2). BSE caused by spontaneous misfolding of
the prion protein has not been proven.


Science, Vol 305, Issue 5692, 1918-1921 , 24 September 2004
[DOI: 10.1126/science.1103581]


BIOMEDICINE:
A Fresh Look at BSE

Bruce Chesebro*

Mad cow disease, or bovine spongiform encephalopathy (BSE), is the cattle
form of a family of progressive brain diseases. These
diseases include scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in
humans, and chronic wasting disease (CWD) in deer and elk.
They are also known as either "prion diseases" because of the association
of a misfolded cellular prion protein in pathogenesis or
"transmissible spongiform encephalopathies" (TSEs) because of the
spongelike nature of the damaged brain tissue (1).

The recent discovery of two BSE-infected cows, one in Canada and one in
the United States, has dramatically increased concern in
North America among meat producers and consumers alike over the extent to
which BSE poses a threat to humans as well as to
domestic and wild animals. The European BSE epidemic of the late-1980s
seems to have been initiated a decade earlier in the United
Kingdom by changes in the production of meat and bone meal (MBM) from
rendered livestock, which led to contamination of MBM with
the BSE infectious agent. Furthermore, the fact that UK farmers fed this
rendered MBM to younger animals and that this MBM was
distributed to many countries may have contributed to the ensuing BSE
epidemic in the United Kingdom and internationally (2).

Despite extensive knowledge about the spread of BSE through contaminated
MBM, the source of BSE in Europe remains an unsolved
mystery (2). It has been proposed that BSE could be derived from a
cross-species infection, perhaps through contamination of MBM by
scrapie-infected sheep tissues (see the
figure). Alternatively, BSE may have been an endemic disease in cattle
that went unnoticed because of its low level of horizontal transmission.
Lastly, BSE might have originated
by "spontaneous" misfolding of the normal cellular prion protein into the
disease-associated abnormal isoform (3), which is postulated to be the
infectious agent or "prion."


Five possible sources
of BSE in North American cattle. Sheep, deer, and elk could spread prion
diseases
(TSEs) to cattle
through direct animal contact or contamination of pastures. Endemic BSE has
not been proven to
exist anywhere in the
world, but it is difficult to exclude this possibility because of the
inefficient spread of BSE
infectivity between
individual animals (2). BSE caused by spontaneous misfolding of the prion
protein has not been
proven.

CREDIT: KATHARINE
SUTLIFF/SCIENCE


Spontaneous protein misfolding is not a new phenomenon as proteins are
known to sometimes misfold after synthesis. Cells in turn have devised
ingenious ways to deal with this
problem. These include molecular chaperone proteins that bind to
misfolded proteins and help them to unfold, and organelles called
proteosomes that degrade misfolded or
unwanted proteins. However, although misfolded prion proteins have been
generated in test tubes as well as in cultured cells, it has been difficult
to demonstrate that such
misfolded abnormal prion proteins are infectious (4, 5). Even the most
recent data do not prove conclusively that infectivity has been generated
in vitro because misfolded
synthetic prion proteins were not able to transfer disease directly to
wild-type mice (6). To obtain infectivity and subsequent prion disease, the
misfolded proteins had to be
inoculated and incubated for 1 to 2 years in transgenic mice that
overexpressed a mutant version of the prion protein. Previous data from
this group showed that transgenic mice
expressing high amounts of prion protein developed neurological disease
without inoculation of misfolded prion protein (7). Thus, at the
biochemical level, the critical attributes
of the misfolded prion protein required for infectivity are not known,
and misfolding of prion protein alone may not be sufficient to generate an
infectious agent (8).

Nevertheless, the idea that BSE might originate due to the spontaneous
misfolding of prion proteins has received renewed interest in the wake of
reports suggesting the occurrence
of atypical BSE (9-11). These results imply that new strains of cattle
BSE might have originated separately from the main UK outbreak. Where and
how might such strains have
originated? Although such rare events cannot be studied directly, any
number of sources of the original BSE strain could also explain the
discovery of additional BSE strains in
cattle (see the figure). However, it would be worrisome if spontaneous
BSE were really a valid etiology because such a mechanism would be
impossible to prevent--unlike other
possible scenarios that could be controlled by large-scale eradication of
TSE-positive animals.

Another way to look at this problem is to examine evidence for possible
spontaneous TSE disease in other animals besides cattle. Spontaneous BSE
would be extremely difficult to
detect in cattle, where horizontal spread is minimal. However, in the
case of the sheep TSE disease, scrapie, which spreads from ewes to lambs at
birth as well as between adults,
spontaneous disease should be detectable as new foci of clinical
infection. In the early 1950s scrapie was eradicated in both Australia and
New Zealand, and the mainland of both
these countries has remained scrapie-free ever since. This scrapie-free
status is not the result of selection of sheep resistant to scrapie because
sheep from New Zealand are as
susceptible as their UK counterparts to experimental scrapie infection
(12). These experiments of man and nature appear to indicate that
spontaneous clinical scrapie does not
occur in sheep. Similarly, because CWD is known to spread horizontally,
the lack of CWD in the deer or elk of eastern North America but its
presence in western regions would
also argue against a spontaneous disease mechanism. This is particularly
noteworthy in New Zealand, where there are large numbers of deer and elk
farms and yet no evidence of
spontaneous CWD. If spontaneous scrapie does not occur in sheep or deer,
this would suggest that spontaneous forms of BSE and sporadic
Creutzfeldt-Jakob disease (sCJD) are
unlikely to be found in cattle or humans. The main caveat to this notion
is that spontaneous disease may arise in some animal species but not
others. In humans, sCJD--which is
considered by some researchers to begin by spontaneous misfolding of the
prion protein--usually takes more than 50 years to appear. Thus, in animals
with a shorter life-span,
such as sheep, deer, and cattle, an analogous disease mechanism might not
have time to develop.

What can we conclude so far about BSE in North America? Is the BSE
detected in two North American cows sporadic or spontaneous or both?
"Sporadic" pertains to the rarity of
disease occurrence. "Spontaneous" pertains to a possible mechanism of
origin of the disease. These are not equivalent terms. The rarity of BSE in
North America qualifies it as a
sporadic disease, but this low incidence does not provide information
about cause. For the two reported North American BSE cases, exposure to
contaminated MBM remains the
most likely culprit. However, other mechanisms are still possible,
including cross-infection by sheep with scrapie or cervids with CWD,
horizontal transmission from cattle
with endemic BSE, and spontaneous disease in individual cattle. Based on
our understanding of other TSEs, the spontaneous mechanism is probably the
least likely. Thus,
"idiopathic" BSE--that is, BSE of unknown etiology--might be a better
term to describe the origin of this malady.

What does all this imply about testing cattle for BSE in North America?
Current testing in the United States indicates that BSE is rare (one
positive result in 40,000 cattle
tested). However, additional testing of 200,000 head of slaughtered
cattle over the next 1 to 2 years, as recently proposed by the U.S.
Department of Agriculture (USDA), should
tell us the incidence more precisely. Nevertheless, if any rare cases are
detected, we may still not know their origin. If evidence arises of a focal
occurrence of BSE, we might
gain important insight into unexpected sources of contamination. However,
because current tests do not seem to be able to detect BSE in infected
animals less than 30 months of
age, even more extensive testing will not completely guarantee the
negative status of younger animals in the food chain. Therefore, the
alternative option of testing all slaughtered
cattle, as implemented in some countries such as Japan, would appear to
provide little additional benefit. This fact has been acknowledged as the
basis for a new agreement between
the United States and Japan aimed at reestablishing the beef trade
between the two countries.

One problem with the current U.S. testing program was the announcement a
few months ago of unconfirmed positive BSE tests in two additional North
American animals that were
subsequently found to be negative when tested with the more accurate
method of Western blotting. The public release of information about
unconfirmed positive tests detected by
the rapid test used for mass screening may be a good idea in the interest
of openness, but it has the potential to create unwarranted anxiety. If
unconfirmed positives are a
frequent occurrence, it would seem reasonable to follow a more cautious
approach and wait until confirmatory testing is complete before publicly
announcing the details.

Based on the experience of many European countries, the mainstays of
controlling BSE in cattle and avoiding spread to humans are threefold:
first, eliminate feeding of ruminant
tissues to ruminants; second, remove high-risk cattle tissues from human
food; and third, continue to test for BSE in cattle in order to monitor
progress with the elimination of
the disease on a local and national basis. In the next 12 months, after
extensive USDA test results are available, the extent of any possible BSE
spread in the United States will be
better documented. But, in fact, the United States and Canada have
already instituted the most important steps to prevent the spread of cattle
BSE in advance of the results--that
is, a ban on feeding ruminant MBM to other ruminants and removal of
high-risk tissues from meat for human consumption. It is hoped that the new
data will not deviate enough
from previous predictions to require further measures for management of
this problem. The most important line of defense against any possible
spread of BSE will be to maintain
strict vigilance in the implementation of the current regulations.

References

1.S. B. Prusiner, Proc. Natl. Acad. Sci. U.S.A 95, 13363 (1998)
[Medline].
2.P. G. Smith, R. Bradley, Br. Med. Bull. 66, 185 (2003) [Medline].
3.C. Weissmann, A. Aguzzi, Curr. Opin. Neurobiol. 7, 695 (1997)
[Medline].
4.A. F. Hill et al., J. Gen. Virol. 80, 11 (1999) [Medline].
5.R. Chiesa et al., J. Virol. 77, 7611 (2003) [Medline].
6.G. Legname et al., Science 305, 673 (2004).
7.D. Westaway et al., Cell 76, 117 (1994) [Medline].
8.B. Chesebro, Science 279, 42 (1998).
9.A. G. Biacabe et al., EMBO Rep. 5, 110 (2004) [Medline].
10.Y. Yamakawa et al., Jpn. J. Infect. Dis. 56, 221 (2003) [Medline].
11.C. Casalone et al., Proc. Natl. Acad. Sci. U.S.A. 101, 3065 (2004)
[Medline].
12.E. F. Houston et al., J. Gen. Virol. 83, 1247 (2002) [Medline].


The author is in the Laboratory of Persistent Virus Diseases, Rocky
Mountain Laboratories, National Institute of Allergy and Infectious
Diseases, Hamilton, MT 59840, USA.
E-mail: bschesebro@nih.gov 10.1126/science.1103581


Volume 305, Number 5692, Issue of 24 Sep 2004, pp. 1918-1921.
Copyright © 2004 by The American Association for the Advancement of
Science. All rights reserved.


http://www.sciencemag.org/cgi/content/full/305/5692/1918


TSS


Terry S. Singeltary Sr.

Steven DeArmond - Professor of Neuropathology


http://maddeer.org/video/embedded/dearmond.html

Entire 5 hour hearing - The California Channel

(scroll down to "022404 Senate Info-Hearing")

http://www.calchannel.com/february2004.htm

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.

####

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

9

B. Investigation of Handling of CNS-Suspect Cow in San Angelo, Texas

Overview

On May 4, 2004, the FSIS Acting Regional Director in Dallas, Texas reported that a cow identified as having Central Nervous System (CNS) symptoms by an FSIS veterinarian at Lone Star Beef Processors (Lone Star Beef), a beef processing facility in San Angelo, Texas was not tested for BSE after it had been slaughtered. The initial decision by the FSIS Veterinary Medical Officer (VMO) on-site at Lone Star Beef to have the cow tested for BSE was overturned by a senior APHIS official and the cow’s carcass was sent to a rendering plant. FSIS regulations at the time of the incident required VMOs to contact the APHIS Assistant Area Veterinarian in Charge (AAVIC) to allow APHIS to collect a BSE surveillance sample from suspect cattle.

OIG initiated an investigation to determine if the AAVIC in Austin, Texas, provided a false statement to USDA FSIS investigators during their inquiry of his decision not to test the animal at Lone Star Beef. To conduct our investigation, OIG reviewed previously obtained statements, various documents and USDA regulations, and interviewed APHIS, FSIS, beef processing facility, and rendering company personnel.

Summary of OIG Findings

The OIG investigation found no substantive evidence that the USDA official(s) responsible for the decision not to take brain tissue samples from the cow for BSE testing, or any other USDA personnel, provided false information or engaged in intentional misconduct. We determined that a misjudgment was made by at least one USDA veterinary official in the handling of the suspect cow. Sworn statements provided by the two responsible USDA veterinary officials involved differ as to whether both concurred in this decision.

The suspect cow’s carcass was sent to a rendering plant in San Angelo on April 27, 2004 for processing as inedible by-product. APHIS then utilized its "Indemnity Plan"

10

procedures to purchase the by-products as a preventative safety measure, and disposed of it at a local landfill in accordance with applicable environmental standards.

Evidence shows that at the time of this incident, communication problems occurred between the APHIS and FSIS employees involved. Taken together, the statements of both APHIS and FSIS personnel and other evidence indicate inconsistencies in their understanding of procedures for BSE tissue sampling of CNS suspect cattle in certain circumstances, and the handling of the carcass pending test results. It is apparent from the sworn statements provided to OIG that APHIS and FSIS personnel and Lone Star Beef officials could not resolve how best to proceed, and that confusion existed about how to properly handle the CNS-suspect carcass.

On May 5, 2004, FSIS and APHIS Veterinary Services announced a new joint policy regarding BSE sampling of condemned cattle at slaughter plants. The policy establishes protocols for the agencies’ responsibilities to obtain samples from condemned cattle exhibiting signs of CNS disorders, regardless of age. The policy provides that FSIS will henceforth do all sampling at Federally-inspected slaughter facilities. For any condemned cattle that APHIS samples for BSE at other facilities, the protocols request (though not require) that the carcass not go to inedible rendering until the sample comes back negative.

Description of Key Events

At approximately 8 a.m. on April 27, 2004, the cow that later became the subject of controversy was delivered to Lone Star Beef in San Angelo, Texas. The cow’s owner informed OIG investigators that it had injured itself some months earlier and, subsequently, experienced difficulty in walking. Upon its arrival at Lone Star Beef, an FSIS VMO and a Lone Star Beef employee saw the cow stagger, fall, and then get up. The VMO condemned the cow for exhibiting CNS disorder symptoms. The cow was then immediately killed and injected with dye by Lone Star Beef workers, to mark the carcass as unusable for human consumption. These actions by Lone Star Beef

11

employees were premature because, at that time, APHIS’s regional BSE protocol called for CNS-suspect cattle to be transported live to Texas A&M University for observation, tissue sampling, and disposal.

The FSIS VMO notified an APHIS Animal Health Technician that he had condemned a cow at Lone Star Beef for CNS symptoms, and the Technician arrived at the facility to take a brain tissue sample for BSE testing. Before a tissue sample was taken, the FSIS VMO and APHIS Technician spoke to Lone Star Beef officials about what to do with the cow’s carcass during the period in which the BSE testing of the tissue would be performed. The USDA personnel and Lone Star Beef officials could not reach agreement on proper retention of the carcass; company officials did not want to keep a decomposing carcass on site, since they believed that a local landfill would refuse to take the carcass.

Seeking a resolution to the dispute, Lone Star Beef’s vice president placed a phone call to the AAVIC at the regional office in Austin, Texas. In the sworn statement he provided to OIG investigators, Lone Star Beef’s vice president said he informed the AAVIC that, based upon an employee’s description of the cow’s condition before it was killed, the vice president believed the cow was possibly experiencing wheat poisoning, not CNS disorders. The vice president informed the AAVIC that he rejected the recommendations of the USDA personnel on-site to preserve the carcass at the facility, or transport it to a landfill, for the reasons stated above. The vice president said the AAVIC then told him APHIS would not require a brain tissue sample for BSE testing from the carcass, and that it could be sent to a rendering facility.

The most senior facility official on site, the president of Lone Star Beef, said he was present at the meeting where this phone call to APHIS took place, and that his vice president informed him that the AAVIC said APHIS was not going to take a tissue sample.

The APHIS Technician who had arrived on site intending to perform the tissue sample extraction from the carcass provided a sworn statement to OIG. She stated that in a

12

phone call subsequent to that between the Lone Star Beef vice president and the AAVIC (described above), she was directed by the AAVIC not to take a brain tissue sample. The FSIS VMO who had condemned the cow told OIG investigators that upon being handed a cell phone by the Technician, he spoke with an unidentified person at APHIS who said, "We have decided not to take a sample."1 The VMO assumed this to mean that APHIS had determined no sample for BSE testing was necessary. However, the VMO told OIG investigators that he never changed his original diagnosis of CNS. This phone conversation between the APHIS AAVIC and the FSIS VMO was the determining action that prevented BSE testing of the CNS suspect carcass.

The AAVIC’s sworn statement differs with the FSIS VMO’s description of what substantively transpired during the phone call. The AAVIC said that when he received the earlier call from the Lone Star Beef vice president about the problem of handling the carcass, the vice president said the following: the "FSIS" at the facility (namely, the VMO who condemned the cow) had improperly handled the cow; he believed the cow likely had wheat poisoning, not a CNS disorder; and that his facility did not have a place to hold the carcass during any BSE test analysis period. The AAVIC said he then followed up this conversation with a call to the FSIS VMO on site.

The AAVIC states that he and the VMO then discussed the suspect cow’s condition before it had been slaughtered. He said the VMO advised that the only problem observed with the cow was that it had fallen and could not get up. The AAVIC said the VMO never said the suspect cow had ever staggered. The AAVIC said that during this conversation, he and the VMO agreed on the following points: many things could have caused the animal to fall and not be able to arise, therefore it need not be sampled for BSE or classified as a CNS condemnation; and due to the lack of CNS symptoms, the carcass could be sent to a rendering facility. At approximately 2:45 p.m., the carcass was picked up by San Angelo Services, and taken to its rendering facility.

1 The individual was the AAVIC. The AAVIC states in his sworn statement to OIG that he spoke on the phone with the VMO.

13

At the conclusion of this phone call with the FSIS VMO, the AAVIC said he called Lone Star Beef’s vice president to inform him that he (AAVIC) and the VMO agreed the carcass could be sent to the rendering facility. The AAVIC then directed the APHIS Technician on-site not to take any tissue samples from the carcass. When questioned about this decision by OIG investigators, the AAVIC said the decision made on this particular animal was not out of the ordinary, and that as an AAVIC, he made such decisions on a regular basis.

This concludes the summary of OIG’s investigations into the conduct of USDA personnel involved in BSE-related incidents in Washington State and San Angelo, Texas. We found no criminal conduct or intentional misconduct by USDA personnel. However, the cases are significant for illustrating some of the difficulties USDA faces in establishing and implementing an effective BSE surveillance plan. Our investigative findings demonstrate the need for the Department to issue clear regulations and policies for BSE inspection and testing, and to provide APHIS and FSIS field personnel with the training and guidance to effectively implement them.

http://www.usda.gov/oig/webdocs/Testimony7-2004.pdf

UNITED STATES DEPARTMENT OF AGRICULTURE

OFFICE OF INSPECTOR GENERAL

STATEMENT OF THE HONORABLE PHYLLIS K. FONG

INSPECTOR GENERAL

Before the

HOUSE APPROPRIATIONS SUBCOMMITTEE

ON

AGRICULTURE, RURAL DEVELOPMENT, FOOD AND DRUG ADMINISTRATION,

AND

RELATED AGENCIES

February 17, 2005

http://www.usda.gov/oig/webdocs/TestimonyFeb1705.pdf

A Review of the USDA’s Expanded BSE Cattle Surveillance Program

Testimony of The Honorable Phyllis K. Fong

Inspector General

U.S. Department of Agriculture

Before a Joint Hearing of the

House Committee on Government Reform

and House Committee on Agriculture

United States House of Representatives

July 14, 2004

http://www.usda.gov/oig/webdocs/Testimony7-2004.pdf

suppressed peer review of Harvard study October 31, 2002

http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf

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

Release No. 0217.05
Contact:
Office of Communication (202) 720-4623

Printable version
Statement by Agriculture Secretary Mike Johanns Regarding the Sample Sent
to Weybridge, England for Further Testing June 16, 2005
"We find ourselves in a situation where we have two internationally accepted
tests that have produced conflicting results. I believe in this situation we
have an obligation to be thorough. We've consulted with our top scientists
at USDA and with internationally recognized experts to determine our best
course in this unique case. We have agreed upon a protocol that includes
additional testing both here at USDA and at an international reference
laboratory in Weybridge, England. When we have all of the final results we
will share them very publicly.

"We know there is absolutely no risk to animal or human health related to
this case. Our safeguards worked exactly as they were designed to work.
Because they worked, we now have the opportunity to learn more about this
sample, knowing it could advance the science behind our testing efforts."


Last Modified: 06/16/2005


http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/06/0217.xml

USDA 2003

We have to be careful that we don't get so set in the way we do things that we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.
Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip.............


Dr. Detwiler: It seems a good idea, but I'm not aware of it.
Another important thing to get across to the public is that the negatives
do not guarantee absence of infectivity. The animal could be early in the
disease and the incubation period. Even sample collection is so important.
If you're not collecting the right area of the brain in sheep, or if
collecting lymphoreticular tissue, and you don't get a good biopsy, you
could miss the area with the PRP in it and come up with a negative test.
There's a new, unusual form of Scrapie that's been detected in Norway. We
have to be careful that we don't get so set in the way we do things that we
forget to look for different emerging variations of disease. We've gotten
away from collecting the whole brain in our systems. We're using the brain
stem and we're looking in only one area. In Norway, they were doing a
project and looking at cases of Scrapie, and they found this where they did
not find lesions or PRP in the area of the obex. They found it in the
cerebellum and the cerebrum. It's a good lesson for us. Ames had to go
back and change the procedure for looking at Scrapie samples. In the USDA,
we had routinely looked at all the sections of the brain, and then we got
away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an
'official' test result as recognized by APHIS
.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't
they still asking for the brain? But even on the slaughter, they're looking
only at the brainstem. We may be missing certain things if we confine
ourselves to one area.


snip...


FULL TEXT;


Completely Edited Version
PRION ROUNDTABLE


Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

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

From: TSS ()
Subject: JOHANN MAD ABOUT FONG, FOR UNCOVERING THE USA MAD COW COVER-UP (JOHANNS MUST GO!!!)
Date: July 6, 2005 at 9:28 am PST

The Honorable Phyliss Fong is now on the hot seat for doing the right thing. SHE did what no one else could do,
tell the truth about BSE in the USA. NOW, she is in GWs hot seat. Johanns must be fired for his roll in exposing every American to the BSE/TSE agent, then lying about it.
HE must be fired!

THE HONORABLE PHYLISS FONG FOR PRESIDENT!!!
No Sacred Cows: Phyllis Fong Takes on the Beltway and Mad Cow Disease

Asian Week, News Report, AsianWeek Staff Report, Jul 06, 2005

Newly appointed Agriculture Secretary Mike Johanns appears to be headed for a showdown with veteran Inspector General Phyllis K. Fong for ordering new tests for mad cow disease in the nation’s beef supply.


Since the tests Fong ordered have returned positive, several countries have once again stopped buying U.S. beef, provoking uproar in the cattle industry.


Reacting to industry pressure, Johanns now claims Fong requested the tests without his knowledge or approval and added: “It caught me by surprise, to be very honest with you. I believe the secretary should be involved in all decisions of this significance.”


Fong, the senior officer of the Inspector General’s office of the USDA was sworn in on December 2, 2002 after serving as Inspector General for the Small Business Administration. Like Johanns, she is appointed by the president and confirmed by the Senate. The Inspector General’s office is an independent arm of the department that performs audits and investigations.


When she ordered the re-testing of the latest case, she issued a statement saying she was also probing “the performance of [laboratories] in complying with procedures for conducting tests.” With the cow that was suspected of having the disease, she reported: “Auditors noted an unusual pattern of conflicting test results on one sample.”


The Veterinary Laboratories Agency in Weybridge, England, an outside testing agency, confirmed that a sample from an animal in November 2004 tested positive for bovine spongiform encephalopathy, or mad cow disease.


Yet Johanns, who took the reins of the Agriculture Department early this year in a Bush cabinet shake-up, insists that Fong has overstepped her bounds. “I was asked by the Senate and the president to operate the department,” Johanns said. “She could recommend; she could strongly urge. But then the question is whether it’s an operational decision.”


He reportedly learned of Fong’s order from his chief of staff after the new testing was already under way. He charges that it’s up for debate whether Fong had the authority to order the new tests, and asserts: “It’s my domain.”


This is not the first time Fong has found herself in the eye of the storm.


After allegations of misconduct arose in the handling of the first cow with mad cow disease, Fong launched a criminal investigation.


“Currently we are investigating allegations surrounding the actual state of the diseased cow before it went to slaughter,” Fong testified last year before the House subcommittee on agriculture appropriations. “So that’s a criminal investigation that’s open, ongoing, active and it’s focused on that issue.”


Fong’s investigation concluded that there was no criminal negligence, but in July she released an audit of the USDA’s testing program and concluded it had serious flaws that could undermine its credibility and lead to questionable estimates of how widespread the disease is in America.


Fong recently re-opened investigations started during the administration of Johanns’ predecessor, Ann Veneman. Veneman began a reform push on testing U.S. beef, but her efforts eventually ran aground amid battles between competing interests, including the beef industry, scientists and consumer activists.


The two behind-the-scenes audits follow complaints by several cow-state senators over policies and procedures in testing for mad cow disease.


Fong said in a statement that “our field work is ongoing” with results expected “late this summer.”


USDA’s Top Cop


As a young girl, Phyllis Fong had a hankering for the law. Those interests began in her childhood, kindled by her father.


“When I was growing up, I remember searching, as all kids do, for a career path that matched my talents,” she said in an article for the USDA. “And my father said to me, at one point in high school, that he really thought law school would be right for me, that I would be a tremendous lawyer. I had never thought about that as an option.”


Fong’s family had emigrated from Hawai‘i to China generations before, in the mid-1800s. Unlike a lot of APA families who insist that the children follow in the family business, Fong recalls, “He was a doctor and yet he did not suggest I go into medical school. I think he was tired of my arguing with him about everything!”


“I had a wonderful experience growing up. They call Hawai‘i a melting pot because of its multi-racial and multi-cultural society. I always felt that everyone there had the opportunity to become anything. It didn’t matter what color, what sex, what race, what ethnic heritage you were, if you were interested in something you could pursue it,” she said.


An unusual route led to her toward the senior job as USDA’s Inspector General. After studying Asian studies and finishing her law degree, she intended to become an international lawyer specializing in trade and immigration.


But when Fong arrived in Washington, D.C., she got a job with the U.S. Civil Rights Commission, which at the time was studying immigration policy. One thing led to another, and a colleague who was the Inspector General at the U.S. Small Business Administration asked her to become her special assistant


“I realized this was a good opportunity. Who can be against going after fraud and abuse? Who can be against economy and efficiency in government?” Fong has been in the field ever since, and oversees about 600 employees divided almost evenly between investigators and auditors.


Name: Phyllis K. Fong


Salary: $136,900


Position: Inspector General, USDA. She’s responsible for conducting and supervising audits and evaluations, as well as investigations and law enforcement efforts.


Birthplace: Philadelphia, Pennsylvania


Family: Married, two daughters, ages 4 and 7


Education: BA degree in Asian Studies, Pomona College; Juris Doctorate, Vanderbilt University School of Law


Past Experience: She was Inspector General of the U.S. Small Business Administration from 1999-2002 after holding several positions with the SBA, including Assistant Inspector General for Management and Legal Counsel and Assistant Inspector General for Management and Policy. In the early 1980s, she had served as assistant general counsel for the Legal Services Corporation and, before that, as an attorney with the U.S. Commission on Civil Rights.


Hobbies/Interests: Needlepoint


Priorities: “To instill the message within USDA that OIG’s mission is not just to audit and investigate. Our mission is to work in partnership with the Department to manage programs more effectively and deal with fraud and abuse.”

The Associated Press and USDA contributed to this report.


http://news.ncmonline.com/news/view_article.html?article_id=67ea9860e23ed4d55409d8d845e3b40b


----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Wednesday, November 09, 2005 3:21 PM
Subject: Re: Hydrolyzed Feather Meal, 50 lb. bags, Recall # V-109-5 "Do not feed to cattle or other ruminants" USA


> ##################### Bovine Spongiform Encephalopathy #####################
>
> Greetings,
>
>
> > i am still concerned that the FDA et al seems to have stopped posting
>
> > updates on ruminant feed ban violations???
>
>
> well, seems the GAO answered that question. i knew something was up.
> just more of the same old BSeee. ...
>
>
> Mad Cow Disease: An Evaluation of a Small Feed Testing Program FDA
> Implemented in 2003 With Recommendations for Making the Program a Better
> Oversight Tool. GAO-06-157R, October 11
>
> http://www.gao.gov/cgi-bin/getrpt?GAO-06-157R
>
>
>
> TSS
>
>
>
>
> ----- Original Message -----
> From: "Terry S. Singeltary Sr."
> To:
> Sent: Friday, October 28, 2005 9:36 AM
> Subject: Hydrolyzed Feather Meal, 50 lb. bags, Recall # V-109-5 "Do not feed
> to cattle or other ruminants" USA
>
>
> ##################### Bovine Spongiform Encephalopathy
> #####################
>
> From: TSS ()
> Subject: Hydrolyzed Feather Meal, 50 lb. bags, Recall # V-109-5 "Do not feed
> to cattle or other ruminants" USA
> Date: October 27, 2005 at 7:33 pm PST
>
>
> RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
> ______________________________
> PRODUCT
> Hydrolyzed Feather Meal, 50 lb. bags, Recall # V-109-5
> CODE
> Lot number: 11579
> RECALLING FIRM/MANUFACTURER
> Recalling Firm: Griffin Industries, Inc., Cold Springs, KY, by telephone on
> September 2, 2005.
> Manufacturer: Griffin Industries, Inc., Henderson, KY. Firm initiated recall
> is ongoing.
> REASON
> Product may contain prohibited material and is not identified with the
> cautionary statement: "Do not feed to cattle or other ruminants".
> VOLUME OF PRODUCT IN COMMERCE
> 863/50 lb. bags
> DISTRIBUTION
> IN
>
> END OF ENFORCEMENT REPORT FOR SEPTEMBER 28, 2005
>
> ###
>
>
> http://www.fda.gov/bbs/topics/enforce/2005/ENF00919.html
>
>
>
> RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
> ______________________________
> PRODUCT
> Triple Play Blocks with Rumensin, medicated feed blocks for beef animals,
> sheep and goats, Recall # V-106-5
> CODE
> No product labeling or lot coding
> RECALLING FIRM/MANUFACTURER
> A-C Feed Ltd, Winters, TX, by telephone and by letter beginning June 2,
> 2005. Firm initiated recall is complete.
> REASON
> Distribution of a medicated free choice feed block for which there is no New
> Animal Drug Application on file.
> VOLUME OF PRODUCT IN COMMERCE
> 70.41 tons of Triple Play Blocks and 704.1 pounds of Rumensin 80
> DISTRIBUTION
> TX
>
> ______________________________
> PRODUCT
> a) Procaine Penicillin - 10, Type B Medicated Feed,
> containing penicillin (from 10 g/lb. procaine
> penicillin), 6.0 g/lb., packaged in 50-lb. bags.
> Recall # V-107-5;
> b) Deccox 10X, Type B Medicated Feed, containing
> decoquinate, 2,271 mg/lb., packaged in 10-lb.
> and 50-lb. bags. Recall # V-108-5
> CODE
> a) All product that is not labeled with the warning;
> b) All product that does not include sheep (as well as
> cows and goats) producing milk for food in the
> warning statement
> RECALLING FIRM/MANUFACTURER
> International Nutrition, Inc., Omaha, NB, by telephone on August 3, 2005 and
> by fax on August 4, 2005. Firm initiated recall is ongoing.
> REASON
> a) Labels lacked required warning to not feed to
> chickens or turkeys producing eggs for human consumption;
> b) Labels lacked required warning to not feed to sheep
> producing milk for food. Cows and goats were properly
> listed on the label.
> VOLUME OF PRODUCT IN COMMERCE
> 111/50-lb. bags Procaine Penicillin -- 10;
> 19887/50-lb. bags and 3,710/10-lb.s Deccox 10X
> DISTRIBUTION
> KS, NE, MN, IA, CO, MO, and AZ
>
> END OF ENFORCEMENT REPORT FOR SEPTEMBER 14, 2005
>
> ###
>
>
> http://www.fda.gov/bbs/topics/enforce/2005/ENF00917.html
>
>
> Greetings,
>
>
>
> i am still concerned that the FDA et al seems to have stopped posting
> updates on ruminant feed ban violations??? here are the last ones posted;
>
>
>
> BSE -- CVM Updates
>
> June 2005 Update on Feed Enforcement Activities to Limit the Spread of
> BSE (June 20, 2005)
>
> March 2005 Update on Feed Enforcement Activities to Limit the Spread
> of BSE (March 17, 2005)
>
> November 2004 Update on Ruminant Feed (BSE) Enforcement Activities
> (November 23, 2004)
>
> FDA Evaluates Test Kits to Detect Animal Proteins in Animal Feed
> (November 4, 2004)
>
> July 2004 Update on Ruminant Feed (BSE) Enforcement Activities (July
> 29, 2004)
>
> FDA and USDA Request Comments and Scientific Information on Possible
> New BSE Safeguards (July 9, 2004)
>
> April 2004 Update on Ruminant Feed (BSE) Enforcement Activities (April
> 22, 2004)
>
> Update on Ruminant Feed (BSE) Enforcement Activities (February 6,
> 2004)
>
> Guidance for Investigators on Ruminant Feed (BSE) Inspections
> Available (November 10, 2003)
>
> Information about Ruminant Feed (BSE) Inspections Available (October
> 10, 2003)
>
> Update On Ruminant Feed (BSE) Enforcement Activities (September 30,
> 2003)
>
> NEW VERSION OF BSE INSPECTION CHECKLIST RELEASED (April 22, 2002)
>
> RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES (April 15, 2002)
>
> RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES (October 30, 2001)
>
> FDA HOLDING PUBLIC HEARING ON RUMINANT FEED (BSE) RULES (October 10,
> 2001 )
>
> BSE INSPECTION CHECKLIST AVAILABLE ON THE CVM INTERNET HOME PAGE
> (September 25, 2001)
>
> RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES (July 7, 2001 )
>
> CVM PROVIDES INFORMATION ABOUT RUMINANT FEED (BSE) INSPECTIONS (April
> 19, 2001 )
>
> RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES (March 23, 2001 )
>
> UPDATE ON RUMINANT FEED (BSE) ENFORCEMENT ACTIVITIES (January 10,
> 2001 )
>
> BSE FEED REGULATION TEAM TO RECEIVE VICE PRESIDENTIAL AWARD (May 13,
> 1999 )
>
> FDA GUIDANCE ON BSE FEED REGULATION AVAILABLE (July 14, 1998 )
>
> SATELLITE TELECONFERENCE ON FEED RULES ANNOUNCED (May 15, 1998 )
>
> FDA GUIDANCE ON RUMINANT FEED RULES AVAILABLE (March 26, 1998)
>
> INFORMATION FOR DAIRY AND BEEF PRODUCERS -- PROTEIN FEED RULES
> (January 22, 1998)
>
> DEADLINE FOR RUMINANT FEED RULE (October 9, 1997)
>
> REQUEST FOR COMMENT ON RUMINANT FEED DRAFT RULE -- MAMMALIAN PROTEINS
> PROHIBITED IN RUMINANT FEED (April 15, 1997)
>
> FDA PROPOSES PRECAUTIONARY BAN AGAINST RUMINANT-TO-RUMINANT FEEDING
> (January 2, 1997)
>
> BSE "Fact Sheet"
>
>
>
> Web Page Updated by mdt - June 21, 2005, 9:20 AM ET
>
>
>
> http://www.fda.gov/cvm/bse_updates.htm
>
>
>
> TSS
>
> #################### https://lists.aegee.org/bse-l.html
> ####################
>
> #################### https://lists.aegee.org/bse-l.html ####################
>

From: TSS ()
Subject: CVM/TSS Update November 2005 Update on Feed Enforcement Activities
to Limit the Spread of BSE
Date: December 6, 2005 at 8:01 am PST

CVM Update
November 2005 Update on Feed Enforcement Activities to Limit the Spread of
BSE

To help prevent the establishment and amplification of BSE through feed in
the United States, FDA implemented a final rule that prohibits the use of
most mammalian protein in feeds for ruminant animals. This rule, Title 21
Part 589.2000 of the Code of Federal Regulations, here called the Ruminant
Feed Ban, became effective on August 4, 1997.

This is an update on FDA enforcement activities regarding the ruminant feed
regulation. FDA's CVM has assembled data from the inspections that have been
conducted AND whose final inspection report has been recorded in the FDA's
inspection database as of November 26, 2005. As of November 26, 2005, FDA
had received over 41,000 inspection reports. The majority of these
inspections (around 68%) were conducted by State officials under contract to
FDA, with the remainder conducted by FDA officials.

Inspections conducted by FDA or State investigators are classified to
reflect the compliance status at the time of the inspection based upon the
objectionable conditions documented. These inspection conclusions are
reported as Official Action Indicated (OAI), Voluntary Action Indicated
(VAI), or No Action Indicated (NAI).

An OAI inspection classification occurs when significant objectionable
conditions or practices were found and regulatory sanctions are warranted in
order to address the establishment's lack of compliance with the regulation.
An example of an OAI inspection classification would be findings of
manufacturing procedures insufficient to ensure that ruminant feed is not
contaminated with prohibited material. Inspections classified with OAI
violations will be promptly re-inspected following the regulatory sanctions
to determine whether adequate corrective actions have been implemented.

A VAI inspection classification occurs when objectionable conditions or
practices were found that do not meet the threshold of regulatory
significance, but do warrant advisory actions to inform the establishment of
findings that should be voluntarily corrected. Inspections classified with
VAI violations are more technical violations of the Ruminant Feed Ban. These
include provisions such as minor recordkeeping lapses and conditions
involving non-ruminant feeds.

An NAI inspection classification occurs when no objectionable conditions or
practices were found during the inspection or the significance of the
documented objectionable conditions found does not justify further actions.

The results to date are reported here both by “segment of industry” and “in
total”. NOTE – A single firm can operate as more than one firm type. As a
result, the categories of the different industry segments are not mutually
exclusive.

RENDERERS

These firms are the first to handle and process (i.e., render) animal
proteins and to send these processed materials to feed mills and/or protein
blenders for use as a feed ingredient.

Number of active firms whose initial inspection has been reported to FDA –
274

Number of active firms handling materials prohibited from use in ruminant
feed – 185 (68% of those active firms inspected)

Of the 185 active firms handling prohibited materials, their most recent
inspection revealed that:

1 firm (0.5%) was classified as OAI

11 firms (5.9%) were classified as VAI

LICENSED FEED MILLS

FDA licenses these feed mills to produce medicated feed products. The
license is required to manufacture and distribute feed using certain potent
drug products, usually those requiring some pre-slaughter withdrawal time.
This licensing has nothing to do with handling prohibited materials under
the feed ban regulation. A medicated feed license from FDA is not required
to handle materials prohibited under the Ruminant Feed Ban.

Number of active firms whose initial inspection has been reported to FDA –
1,079

Number of active firms handling materials prohibited from use in ruminant
feed – 426 (39% of those active firms inspected)

Of the 426 active firms handling prohibited materials, their most recent
inspection revealed that:

0 firm (0%) was classified as OAI

8 firms (1.9%) were classified as VAI

FEED MILLS NOT LICENSED BY FDA

These feed mills are not licensed by the FDA to produce medicated feeds.

Number of active firms whose initial inspection has been reported to FDA –
5,165

Number of active firms handling materials prohibited from use in ruminant
feed – 2,036 (39% of those active firms inspected)

Of the 2,036 active firms handling prohibited materials, their most recent
inspection revealed that:

2 firms (0.1%) were classified as OAI

24 firms (1.2%) were classified as VAI

PROTEIN BLENDERS

These firms blend rendered animal protein for the purpose of producing
quality feed ingredients that will be used by feed mills.

Number of active firms whose initial inspection has been reported to FDA --
340

Number of active firms handling materials prohibited from use in ruminant
feed – 147 (43% of those active firms inspected)

Of the 147 active firms handling prohibited materials, their most recent
inspection revealed that:

0 firms (0%) were classified as OAI

7 firms (4.8%) were classified as VAI

RENDERERS, FEED MILLS, AND PROTEIN BLENDERS

This category includes only those firms that actually use prohibited
material to manufacture, process, or blend animal feed or feed ingredients.

Number of active renderers, feed mills, and protein blenders whose initial
inspection has been reported to FDA – 6,576

Number of active renderers, feed mills, and protein blenders processing with
prohibited materials – 539 (8.2% of those active firms inspected)

Of the 539 of active renderers, feed mills, and protein blenders processing
with prohibited materials, their most recent inspection revealed that:

3 firms (0.6%) were classified as OAI

23 firms (4.3%) were classified as VAI

OTHER FIRMS INSPECTED

Examples of such firms include ruminant feeders, on-farm mixers, pet food
manufacturers, animal feed salvagers, distributors, retailers, and animal
feed transporters.

Number of active firms whose initial inspection has been reported to FDA –
13,477

Number of active firms handling materials prohibited from use in ruminant
feed – 3,748 (28% of those active firms inspected)

Of the 3,748 active firms handling prohibited materials, their most recent
inspection revealed that:

8 firms (0.2%) were classified as OAI

95 firms (2.5%) were classified as VAI

TOTAL FIRMS

Note that a single firm can be reported under more than one firm category;
therefore, the summation of the individual OAI/VAI firm categories will be
more than the actual total number of OAI/VAI firms, as presented below.

Number of active firms whose initial inspection has been reported to FDA –
16,476

Number of active firms handling materials prohibited from use in ruminant
feed – 4,553 (27% of those active firms inspected)

Of the 4,553 active firms handling prohibited materials, their most recent
inspection revealed that:

9 firms (0.2%) were classified as OAI

107 firms (2.4%) were classified as VAI


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

Issued by:
FDA, Center for Veterinary Medicine,
Communications Staff, HFV-12
7519 Standish Place, Rockville, MD 20855
Telephone: (240) 276-9300 FAX: (240) 276-9115
Internet Web Site: http://www.fda.gov/cvm

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

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

snip...

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...

snip...

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

snip...

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 thought
this was a fanatical incident to be _avoided_ in the US _at all costs_...

snip...

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

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

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

ABSTRACT
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
England.

INTRODUCTION

Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough
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 previous 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.

OBSERVATIONS AND RESULTS

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 behavioral 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 weeks, approximately 40% of
all the adult mink on the farm died from TME.
Since previous incidences of TME were associated with common or shared feeding
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.

DISCUSSION
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. Because (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.

ACKNOWLEDGEMENTS
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 acknowledge the help and
encouragement of Robert Hanson who died during the course of these investigations.

REFERENCES
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 cattle?
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 spongiform encephalopathy
in cattle. Vet. Rec. 121:419-420.

MARSH

http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

12/10/76
AGRICULTURAL RESEARCH COUNCIL
REPORT OF THE ADVISORY COMMITTE ON SCRAPIE
Office Note
CHAIRMAN: PROFESSOR PETER WILDY

snip...

A The Present Position with respect to Scrapie
A] The Problem

Scrapie is a natural disease of sheep and goats. It is a slow
and inexorably progressive degenerative disorder of the nervous system
and it ia fatal. It is enzootic in the United Kingdom but not in all
countries.

The field problem has been reviewed by a MAFF working group
(ARC 35/77). It is difficult to assess the incidence in Britain for
a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during
the five years 1971-1975. A further inestimable loss arises from the
closure of certain export markets, in particular those of the United
States, to British sheep.

It is clear that scrapie in sheep is important commercially and
for that reason alone effective measures to control it should be
devised as quickly as possible.

Recently the question has again been brought up as to whether
scrapie is transmissible to man. This has followed reports that the
disease has been transmitted to primates. One particularly lurid
speculation (Gajdusek 1977) conjectures that the agents of scrapie,
kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of
mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed
for human or animal food at slaughter or rendering plants" (ARC 84/77)"
The problem is emphasised by the finding that some strains of scrapie
produce lesions identical to the once which characterise the human
dementias"

Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety
of laboratory personnel requires prompt attention. Second, action
such as the "scorched meat" policy of USDA makes the solution of the
acrapie problem urgent if the sheep industry is not to suffer
grievously.

snip...

76/10.12/4.6

http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf


Infected and Source Flocks

As of August 31, 2005, there were 115 scrapie infected and source flocks (figure 3). There were 3 new infected and source flocks reported in August (Figure 4) with a total of 148 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 102 (Figure 6), with 5 flocks released in August. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.69 :
1. In addition, as of August 31, 2005, 574 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 122 were RSSS cases (Figure 7). This includes 55 newly confirmed cases in August 2005 (Figure 8). Fifteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat case was reported in May 2005.

snip...

full text ;

http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html


Coexistence of multiple PrPSc types in individuals with

Creutzfeldt-Jakob disease

Magdalini Polymenidou, Katharina Stoeck, Markus Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi

Summary

Background The molecular typing of sporadic Creutzfeldt-Jakob disease (CJD) is based on the size and glycoform

ratio of protease-resistant prion protein (PrPSc), and on PRNP haplotype. On digestion with proteinase K, type 1 and

type 2 PrPSc display unglycosylated core fragments of 21 kDa and 19 kDa, resulting from cleavage around amino

acids 82 and 97, respectively.

Methods We generated anti-PrP monoclonal antibodies to epitopes immediately preceding the differential proteinase

K cleavage sites. These antibodies, which were designated POM2 and POM12, recognise type 1, but not type 2, PrPSc.

Findings We studied 114 brain samples from 70 patients with sporadic CJD and three patients with variant CJD.

Every patient classified as CJD type 2, and all variant CJD patients, showed POM2/POM12 reactivity in the

cerebellum and other PrPSc-rich brain areas, with a typical PrPSc type 1 migration pattern.

Interpretation The regular coexistence of multiple PrPSc types in patients with CJD casts doubts on the validity of

electrophoretic PrPSc mobilities as surrogates for prion strains, and questions the rational basis of current CJD

classifications.


snip...


The above results set the existing CJD classifications

into debate and introduce interesting questions about

human CJD types. For example, do human prion types

exist in a dynamic equilibrium in the brains of affected

individuals? Do they coexist in most or even all CJD

cases? Is the biochemically identified PrPSc type simply

the dominant type, and not the only PrPSc species?


http://neurology.thelancet.com Published online October 31, 2005

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

03-025IFA
03-025IFA-2
Terry S. Singeltary


Page 1 of 17

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements

for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and

Requirements for the Disposition of Non-Ambulatory Disabled Cattle

THE BSE/TSE SUB CLINICAL Non-Ambulatory Disabled Cattle

Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;

snip...FULL TEXT ;


http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION


http://docket.epa.gov/edkfed/do/EDKStaffItemDetailView?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808

http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007d48096b40d

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

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

OLD TSS SUBMISSIONS;

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument


Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL
IMPORTS FROM CANADA


https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


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 ...


http://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, ...

http://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. ...


http://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 ...
http://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

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

01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3

http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm

Send Post-Publication Peer Review to journal:


Re: 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


''sound science''

TSS




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