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From: TSS ()
Subject: June 2005 Update on Feed Enforcement Activities to Limit the Spread of BSE and TSE surveillance update in the USA
Date: June 26, 2005 at 4:49 pm PST

June 20, 2005

June 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 June 11, 2005. As of June 11, 2005, FDA had received over 37,000 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 – 263

Number of active firms handling materials prohibited from use in ruminant feed – 176 (67% of those active firms inspected)

Of the 176 active firms handling prohibited materials, their most recent inspection revealed that:

2 firms (1.1%) were classified as OAI

8 firms (4.5%) 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 – 1,069

Number of active firms handling materials prohibited from use in ruminant feed – 411 (38% of those active firms inspected)

Of the 411 active firms handling prohibited materials, their most recent inspection revealed that:

1 firm (0.2%) was classified as OAI

7 firms (1.7%) 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 – 5,145

Number of active firms handling materials prohibited from use in ruminant feed – 1,920 (37% of those active firms inspected)

Of the 1,920 active firms handling prohibited materials, their most recent inspection revealed that:

2 firms (0.1%) were classified as OAI

27 firms (1.4%) 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 -- 329

Number of active firms handling materials prohibited from use in ruminant feed – 117 (36% of those active firms inspected)

Of the 117 active firms handling prohibited materials, their most recent inspection revealed that:

0 firms (0%) were classified as OAI

3 firms (2.6%) 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 – 6,550

Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 553 (8.4% of those active firms inspected)

Of the 553 of active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that:

5 firms (0.9%) were classified as OAI

20 firms (3.6%) 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 – 12,575

Number of active firms handling materials prohibited from use in ruminant feed – 3,288 (26% of those active firms inspected)

Of the 3,288 active firms handling prohibited materials, their most recent inspection revealed that:

8 firms (0.2%) were classified as OAI

90 firms (2.7%) 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 – 15,676

Number of active firms handling materials prohibited from use in ruminant feed – 4,093 (26% of those active firms inspected)

Of the 4,093 active firms handling prohibited materials, their most recent inspection revealed that:

10 firms (0.2%) were classified as OAI

98 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

http://www.fda.gov/cvm/bse0605.htm

THOSE TRIPLE BSE MAD COW FIREWALLS are still leaking in June 2005. The 8/4/97 ruminant to ruminant feed ban was nothing more than ink on paper. Lets look at one year ago;

Of the 3,444 active firms handling prohibited materials, their most recent inspection revealed that:

16 firms (0.5%) were classified as OAI

89 firms (2.6%) were classified as VAI

http://www.fda.gov/cvm/bseup112304.htm

BSE/TSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts
[BBC radio 4 FARM news] (audio realplayer LISTEN)

http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram

THE TEXAS GONZALES/PURINA INCIDENT SHOWED THAT 5.5 GRAMS OF
RUMINANT PROTEIN WAS FED TO CATTLE ;

FOR IMMEDIATE RELEASE
P01-05
January 30, 2001
Print Media:
301-827-6242
Broadcast Media:
301-827-3434
Consumer Inquiries:
888-INFO-FDA

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

Risk of oral infection with bovine spongiform encephalopathy agent in primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.

Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa

06/09/05 BSE Roundtable Discussion Transcript


snip...

2 Based on our scientific knowledge

3 of the disease, we have taken several key

4 steps, some of which have been in place for a

5 number of years to safeguard the health of US

6 livestock and our food supply against BSE.

7 And we are fortunate that Canada shares our

8 commitment and overall approach to dealing

9 with the disease by taking comparable and

10 effective measures consistent with our own.

11 This is especially important given that

12 historically the North American cattle

13 industry has been highly integrated.

14 In 1997, long before finding the

15 first native born case in North America, both

16 Canada and the United states implemented feed

17 regulations banning, with some exceptions,

18 the feeding of ruminant protein back to other

19 ruminants. This critical action has helped

20 prevent an outbreak similar to those seen in

21 countries where feed bans were instituted

22 only after BSE cases were identified. Expert

Page 28

~4525779.txt

23 risk analyses have repeatedly shown that if

24 BSE were introduced into the US herd, the

25 feed ban, even if not perfectly enforced,

30

1 would prevent the disease from becoming

2 established and spread in the United States.

3 Additional safeguards in place,

4 both in the United States and Canada include

5 comparable and effective import restrictions,

6 slaughter restrictions, the rendering process

7 and removal of specified risk materials from

8 the human food supply. Given these

9 safeguards and the fact that BSE can be

10 transmitted only under very specific

11 conditions and not through casual contact

12 between animals, the risk of BSE transmission

13 in the United States and Canada remains

14 extremely low. ...

snip...

http://www.aphis.usda.gov/lpa/issues/bse/BSE_roundtable_6_9_05.pdf

Release No. 0066.05
Contact:
Ed Loyd (202) 720-4623
Jim Rogers (202) 690-4755




USDA RELEASES TECHNICAL ASSESSMENT ON THE IMPLEMENTATION OF THE CANADIAN FEED BAN

WASHINGTON, Feb. 25, 2005


snip...

>>> USDA assembled a team of technical experts that arrived in Canada on Jan. 24 to gather all relevant information to do an in-depth assessment on Canada's ruminant-to-ruminant feed ban and their feed ban inspection program. USDA took this additional step to ensure compliance with Canada's feed ban control measures. The feed ban has been determined to be an important BSE risk mitigation measure to protect animal health.

The inspection team's report states that "Canada has a robust inspection program, that overall compliance with the feed ban is good and that the feed ban is reducing the risk of transmission of bovine spongiform encephalopathy in the Canadian cattle population." <<<

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/02/0066.xml

HOLY MAD COW, this is like the blind leading the blind. the total lack of BSE protocol here again shows that the USDA/APHIS et al should NOT be giving any expert BSE advise to anyone. ...TSS


Questions and Answers on BSE
(Items 14-22 added on May 18, 2005)

[Overall BSE measures/firewalls]


Are all cattle inspected prior to slaughter?
Why isn't USDA testing all cattle slaughtered in the United States?
Do you think you will find more cases of BSE? (APHIS)
[SRM]

Are all SRMs properly removed? What is the procedure? How is SRM-removal and prevention of cross-contamination ensured?
Isn't Advanced Meat Recovery (AMR) still being used?
[Feed Ban]

Feed ban: The United States claims that it has been implementing a ban on feeding mammalian proteins to ruminants since 1997, but it still is primarily a ruminant-to-ruminant feed ban. How can you prevent bovine-derived poultry feed, for example, from commingling with cattle feed?
[Compliance]

What was the rate of compliance of the U.S. feed ban in the initial stages of its implementation?
Please provide an update on the investigation into the recent labor union allegation of problems with the implementation/compliance of the SRM regulation.
[About A40]

What is A Maturity?
How can A40 assure that animals are younger than 21 months old?
How can you verify that each inspector correctly and consistently performs the maturity grading? Do you have any monitoring system in place to assure the accuracy of the inspector?
[Other]

What is vCJD? How many vCJD cases have been found in the United States? What about the alleged cases in New Jersey?
With respect to trade between the United States and Canada, now that Canada has found 3 BSE cases (4 including the one found in Washington state), how will the United States ensure that no BSE-infected animals will enter the United States when the U.S.-Canadian border opens?
[Added May 18, 2005]


snip...

Q6. The United States claims that it has been implementing a ban on feeding mammalian proteins to ruminants since 1997, but it still is primarily a ruminant-to-ruminant feed ban. How can you prevent bovine-derived poultry feed, for example, from commingling with cattle feed?

A6. There is a scientific consensus that BSE cannot be transmitted through the use of mammalian origin meat-and-bone meal (MBM) tp swine, poultry, or other non-ruminant species. However, firms that handle or produce feed for ruminants and non-ruminants are required to have separate equipment or facilities or have an adequate cleanout process in order to prevent cross-contamination.

The feed ban's restrictions on the use of mammalian protein apply only to its use in ruminant feed and not to feed for other species. Therefore, mammalian origin meat-and-bone meal (MBM) may be used in feed for swine, poultry, and other non-ruminant species. However, firms that handle material prohibited for ruminants (but allowed for non-ruminants) and also produce ruminant feed are required to have separate equipment or facilities or else have cleanout procedures adequate to prevent cross-contamination. This requirement applies to firms at all levels, from rendering to on-farm mixing. They also are required to clearly label prohibited material as not to be fed to ruminants. Guidance on preventing cross-contamination is available through FDA's Center for Veterinary Medicine.

Q7. What was the rate of compliance of the U.S. feed ban in the initial stages of its implementation?

A7. FDA initiated a feed ban in August 1997. Compliance rates for the first year showed higher than anticipated for a new program with 50-85 percent of the renderers and feed manufacturers in compliance with all aspects of the regulation. The majority of problems were minor, relating to noncompliance of simple documentation requirements as opposed to serious concerns such as the presence of prohibited material. As of July 2004, conditions or practices warranting regulatory sanctions had been found in less than one percent of inspected facilities. Inspection results are posted in a searchable online database. In August, 2005, the U.S. will have had an effective feed ban in place for 8 years, the time period recommended by OIE to effectively mitigate the spread or introduction of BSE within a domestic herd.

Q14. A recent Government Accountability Office (GAO) report found that 19 percent of the feed industry has not been re-inspected in the past five years. How can the FDA ensure the Japanese people that U.S. cattle are not consuming meat-and-bone meal?

A14. To maximize enforcement of the ruminant feed ban, FDA inspects firms (renderers, feed mills, etc.) considered to be of highest risk more frequently than low risk firms. High-risk firms are those which manufacture, or process feeds or feed ingredients containing prohibited meat-and-bone meal (which is allowed for non-ruminants). High-risk firms are inspected at least once every year to ensure their compliance with FDA requirements preventing cross contamination.

Low risk firms are those that purchase feed or feed ingredients from high-risk firms, but do not further process or re-manufacture the feed or feed ingredients. For most of these firms there is no commercial handling of meat-and-bone meal since they are handling only packaged products like pet food. As a result, it would be highly unlikely that cattle would have access to any of these products.

Once FDA has established through inspection that these firms do not manufacture or process feeds containing meat-and-bone meal, the frequency of re-inspection is reduced so that greater enforcement activities can be focused on the high-risk firms. The 19 percent of the feed industry cited in the GAO report consist entirely of low risk firms.

snip...

Q22. What is the U.S. response to the EU's classification of the U.S. as having a risk level III in its geographical bovine encephalopathy risk assessment (GBR)?

A22. The U.S. has expressed its disappointment to the EU over this determination, which was based on unsubstantiated assumptions and uses worst-case scenarios without proper justification. In fact, we feel that the U.S. has learned many lessons over the past 15 years from GBR III countries with demonstrated risks (as in Europe). We used this information to develop a strong BSE control program that ensures that the risk to consumers in the U.S. is negligible.

More specifically, we implemented BSE control measures such as an import ban and a feed ban long before the 1st case of BSE was discovered in Canada. As a result, despite extensive surveillance, BSE has never been disclosed in an animal born in the United States. Also the U.S. and Canada both implemented multiple BSE controls to prevent the spread of BSE in North America. That is why the U.S. has had no domestic cases of BSE except for one Canadian cow, and why Canada has had only 4 cases confined to a small geographical area. ...

http://tokyo.usembassy.gov/e/p/tp-20050304-71.html#14

National Renderers Association Public Response to USDA-APHIS
ANPR “Risk Reduction Strategies for Potential BSE Pathways Involving Downer Cattle and Dead Sock of Cattle and Other Species”


Docket No. 01-68-1, Federal Register, Vol.68, No.13: 2703 – 2711, 01/21/2003

http://www.rendermagazine.com/news/USDA-ANPRDownersApendices.doc

SCRAPIE USA UPDATE MAY 2005

SCRAPIE has increased drastically since the report i posted in March 2005, with additional case in a goat;

SCRAPIE USA MONTHLY REPORT 2005

AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure 3). There were 11 new infected and source flocks reported in March (Figure 4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 39 (Figure 6), with 1 flock released in March. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN addition, as of March 31, 2005, 225 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat cases was reported in January 2005. New infected flocks, source flocks, and flocks released or put on clean-up plans for FY 2005 are depicted in Figure 10. ...

FULL TEXT ;

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

SCRAPIE USA MAY 2005

AS OF MAY 31, 2005, there were 104 scrapie infected and source flocks (Figure 3). There were 20 new infected and source flocks reported in May (Figure 4) with a total of 104 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 63 (Figure 6), with 16 flocks released in May. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.61 : 1. In addition, as of May 31, 2005, 367 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 85 were RSSS cases (Figure 7). This includes 75 NEWLY confirmed cases in May 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...

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

CWD USA UPDATE

http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html

Press Releases
5/13/2005: More Negatives for Chronic Wasting Disease in Captive Heards Learn More

5/9/2005: Negative Results for Chronic Wasting Disease in Captive Herd Learn More

5/4/2005: DEC Announces Sampling Results for Chronic Wasting Disease Learn More

4/29/2005: DEC Issues Emergency Regulations in Response to Discovery of Chronic Wasting Disease. Learn More

4/27/2005: Chronic Wasting Disease Found in Oneida County Deer. Learn More.

4/21/2005: DEC Releases Results of Tests for Chronic Wasting Disease. Learn More.

4/13/2005: DEC to Test For Chronic Wasting Disease in Hamilton County. Learn More.

4/8/2005: Chronic Wasting Disease Update: Test Results Reveal Three Additional Positives From Index Herd. Learn More.

4/5/2005: Chronic Wasting Disease Update. Learn More.

4/2/2005: Second Case of CWD Found in Oneida County Deer. Learn More.

3/31/2005: Positive Case of CWD Found in Oneida County Deer. Learn More.

Transcript from March 31 Press Conference Regarding First Case of CWD in NewYork State

If you have difficulty opening the PDF files, please contact the Department of Agriculture & Markets.

http://www.agmkt.state.ny.us/AI/cwd.html

TME USA UPDATE

Transmissible Mink Encephalopathy
Veterinary Services

February 2002

Transmissible mink encephalopathy (TME) is a rare illness that affects the central nervous system of ranch-raised mink. It was first detected in the United States in 1947. Since then, TME outbreaks have been reported in numerous locations worldwide, including the United States, Canada, Finland, Germany, and the republics of the former Soviet Union.

Related Diseases

TME is classified as a transmissible spongiform encephalopathy (TSE). Different TSE's are caused by similar as-yet uncharacterized agents that produce spongiform changes in the brain. Other TSE's include scrapie, which affects sheep and goats; bovine spongiform encephalopathy (BSE); feline spongiform encephalopathy; chronic wasting disease of deer and elk; and five rare diseases in humans, kuru, both classical and variant Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia. TSE's have also been reported in Europe in captive wild ruminants, cats, and monkeys. The occurrence of TSE's in captive wild animals is believed to have resulted from BSE-contaminated feed.

These rare, progressively degenerative central nervous system diseases are characterized by a very long incubation period, a short clinical course, and a 100 percent mortality rate. The infectious agent responsible for TME is smaller than the smallest known virus and has not been characterized to date. There are three main theories on the nature of this agent: (1) the agent is a virus with unusual characteristics, (2) the agent is a prionóan exclusively host-coded protein that is modified to a protease-resistant form after infection, or (3) the agent is a virinoóa small, noncoding regulatory nucleic acid coated with a host-derived protective protein. The TME agent is extremely resistant to heat and to normal sterilization processes. It also does not evoke any detectable immune response or inflammatory reaction in host animals.

Public interest surrounding TSE's soared when the United Kingdom announced in March 1996 that BSE may be linked to a variant form of CJD. BSE, widely referred to as "mad cow disease," has devastated the cattle industry in the United Kingdom. The fear of this disease prompted countries around the world to step up measures to ensure that they remain free of BSE. BSE has not been detected in the United States, and the U.S. Department of Agriculture (USDA) works proactively to keep it that way. USDA's Animal and Plant Health Inspection Service (APHIS) and Food Safety and Inspection Service take aggressive measures in prevention, education, surveillance, and response.

Clinical Signs

TME has an average incubation period of more than 7 months before the onset of clinical signs. These signs can last from 3 days to 6 weeks. Early clinical signs, which can be quite subtle, include an increase in nest soiling and dispersal of droppings throughout the cage. In addition, mink may step into their food often or eat with difficulty. As the disease progresses, an infected animal becomes increasingly excited, arching its tail over its back like a squirrel. TME-infected animals may exhibit severe incoordination, difficulty walking, and pronounced jerkiness of hind limbs. In advanced cases, signs include rapid circling, compulsive chewing of the tail, and clenching of the jaw. Seizures rarely occur. Near death, affected mink become sleepy and unresponsive.

Diagnosis

TME produces no changes in the body that are visible upon necropsy examination. However, microscopic examination shows that the disease is limited to the central nervous system, causing distinct spongelike changes in specific areas of the brain.

Currently, there are no validated tests to detect TSE's in a live animal. Veterinary pathologists confirm disease by microscopic examination of brain tissue or by the detection of the prion protein.
Epidemiology

Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old.

The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.

The 1985 Stetsonville Outbreak

The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died.

The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME.

The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE's, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from "downer cattle" and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted.

Although Marsh's hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS' National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.
Additional Information

Veterinarians and livestock and poultry owners who suspect an animal may be affected with a TSE should immediately contact State or Federal animal health authorities.

For further information, contact
USDA, APHIS, Veterinary Services
Emergency Programs
4700 River Road, Unit 41
Riverdale, MD 20737-1231
Telephone: (301) 734-8073
Fax: (301) 734-7817


http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahtme.html


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

Title: Transmission of Transmissible Mink Encephalopathy (Tme) to Raccoons (Procyon Lotor) by Intracerebral Inoculation

Authors

Hamir, Amirali
Miller, Janice
O'Rourke, Katherine
Bartz, Jason - CREIGHTON UNIVERSITY
Stack, Mick - VLA, WEYBRIDGE, UK
Chaplin, Melanie - VLA, WEYBRIDGE, UK


Submitted to: Journal Of Veterinary Diagnostic Investigation
Publication Acceptance Date: January 21, 2003
Publication Date: January 1, 2004
Citation: Hamir, A.N., Miller, J.M., O'Rourke, K.I., Bartz, J.C., Stack, M.J., Chaplin, M.J. 2004. Transmission Of Transmissible Mink Encephalopathy (Tme) To Raccoons (Procyon Lotor) By Intracerebral Inoculation. Journal Of Veterinary Diagnostic Investigation. 16(1):57-63.

Interpretive Summary: To determine the transmissibility of transmissible mink encephalopathy (TME) agent to raccoons and to provide information about clinical course, lesions and suitability of currently used diagnostic tests for detection of TSEs in raccoons, 4 raccoon kits were inoculated in the brain with a brain suspension from mink experimentally infected with TME. One uninoculated raccoon kit served as a control. All 4 animals in the TME-inoculated group became sick and were euthanized between 21 and 23 weeks post inoculations (PI). Necropsy examinations revealed no gross lesions. However, laboratory tests were positive for the disease (spongiform encephalopathy). These findings further confirm that TME is transmissible to raccoons and that tests currently used for transmissible spongiform encephalopathy (TSE) in livestock detects the disease (prion protein) in raccoon tissues. According to previously published data, the incubation period of sheep scrapie in raccoons is 2 years, whereas chronic wasting disease (CWD) had not shown transmission after 3 years of observation. Further studies, such as the incubation periods of bovine spongiform encephalopathy (BSE, mad cow disease) and other TSE isolates in raccoons are needed before the raccoon model can be recommended for differentiation of TSE agents. IMPACT: Since incubation periods for the 3 US TSEs (scrapie, TME and CWD) in raccoons appear to be markedly different, it may be possible to use raccoons for differentiating unknown TSE agents.
Technical Abstract: To determine the transmissibility of transmissible mink encephalopathy (TME) agent to raccoons and to provide information about clinical course, lesions and suitability of currently used diagnostic procedures for detection of TSEs in raccoons, 4 raccoon kits were inoculated intracerebrally with a brain suspension from mink experimentally infected with TME. One uninoculated raccoon kit served as a control. All 4 animals in the TME-inoculated group became sick and were euthanized between 21 and 23 weeks post inoculations (PI). Necropsy examinations revealed no gross lesions. Spongiform encephalopathy was observed by light microscopy and the presence of protease-resistant prion protein (PrPres) was detected by immunohistochemistry and Western blot techniques. Scrapie associated fibrils (SAF) were observed by negative stain electron microscopy in the brains of 3/4 inoculated raccoons. These findings further confirm that TME is transmissible to raccoons and that diagnostic techniques currently used for transmissible spongiform encephalopathy (TSE) in livestock detects prion protein in raccoon tissue. According to previously published data, the incubation period of sheep scrapie in raccoons is 2 years, whereas chronic wasting disease (CWD) had not shown transmission after 3 years of observation. Since incubation periods for the 3 US TSEs (scrapie, TME and CWD) in raccoons appear to be markedly different, it may be possible to use raccoons for differentiating unknown TSE agents. However, further studies, such as the incubation periods of bovine spongiform encephalopathy (BSE) and other TSE isolates in raccoons, as well as characterization of the raccoon PrP gene and information concerning PrP polymorphisms are needed before the model can be further characterized for differentiation of TSE agents.





Page Modified: 06/26/2005


http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=140042

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

Statement By Agriculture Secretary Mike Johanns Regarding The Passage Of S.J.Res. 4 By The United States Senate

March 3, 2005

"I am very disappointed in today's vote by the United States Senate to disapprove the rule submitted by the U.S. Department of Agriculture to establish minimal risk regions and resume trade in Canadian beef and cattle under 30 months of age.

"Today's action undermines the U.S. efforts to promote science-based regulations, complicates U.S. negotiations to reopen foreign markets to U.S. beef and would perpetuate the economic disruption of the beef and cattle industry.

"USDA remains confident that the requirements of the minimal-risk rule, in combination with the animal and public health measures already in place in the United States and Canada, provide the utmost protection to both U.S. consumers and livestock. We also remain fully confident in the underlying risk assessment, developed in accordance with the OIE guidelines, which determined Canada to be a minimal risk region.

"I will now work with the U.S. House of Representatives to prevent passage of this resolution, which is strongly opposed by the Bush Administration, and continue our aggressive efforts to reopen international markets to U.S. beef."


Last Modified: 03/04/2005


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/03/0074.xml

THIS MMR POLICY THAT JOHANNS AND GW HAVE SHOVED DOWN THE THROAT OF MILLIONS, well, in doing so they also have shoved TSEs down the throat of millions and millions have needlessly become exposed. ALL the OIE did in approving this was give the green light for the legal trading of all strains of TSEs globally. IT was an assinine move on all parties involved, it was a move based on nothing more than greed (commodities and futures), there was no science involved. with the many strains of TSE in North America in cattle, sheep, goats, deer, elk, mink, humans, we have a very unique and dangerous situation with all these different strains of TSEs being rendered and fed back to humans and animals for human consumption. for this administration to continue to base it's BSE/TSE mad cow protocols and policy solely on commodities and futures will continue to further expose this deadly agent needlessly to millions of animals and humans, thus the accumulation will continue, the agent will amplify and spread in feed, the hospital surgical arena, tissue and blood, cosmetics, supplements, in short a multitude of proven routes and sources. Johanns statement about BSE mad cow disease and walking across the street to the store to buy beef, and the chances of being run over by a car greater, than dying from beef, might hold true for some. there are many out there though, this did NOT hold true to. course, the sporadic CJD does not count, kinda like that 3 postive test they did not announce on the Texas inconclusive did not count. but science and transmission studies speak for themselves;

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


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

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

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


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

IN light of 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


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


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

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

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

PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)
Publication date: 20 August 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)

Report

Summary
Summary of the Scientific Report

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

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

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

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


http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/573_en.html



From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]

Greetings FDA,

snip...

PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions
or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry... but the transmission studies DO NOT lie, only the politicians and the industry do... and they are still lying to this day...TSS


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


>> Differences in tissue distribution could require new regulations
>> regarding specific risk material (SRM) removal.

snip...end

full text ;

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


It was, however, performed in the USA in 1979, when it was shown that cattle
inoculated with the scrapie agent endemic in the flock of Suffolk sheep at
the United States Department of Agriculture in Mission, Texas, developed a
TSE quite unlike BSE. 32

http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543


The findings of the initial transmission, though not of the clinical or
neurohistological examination, were communicated in October 1988 to Dr
Watson, Director of the CVL, following a visit by Dr Wrathall, one of the
project leaders in the Pathology Department of the CVL, to the United States
Department of Agriculture. 33


http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546


The results were not published at this point, since the attempted
transmission to mice from the experimental cow brain had been inconclusive.
The results of the clinical and histological differences between
scrapie-affected sheep and cattle were published in 1995. Similar studies in
which cattle were inoculated intracerebrally with scrapie inocula derived
from a number of scrapie-affected sheep of different breeds and from
different States, were carried out at the US National Animal Disease Centre.
34

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

Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy BSE-L

http://vegancowboy.org/TSS-part1of8.htm

Moms death from hvCJD (Heidenhain Variant Creutzfeldt Jakob Disease)

http://www.vegsource.com/talk/madcow/messages/7252.html

'MOMS AUTOPSY REPORT'

http://www.vegsource.com/talk/madcow/messages/7548.html


Terry S. Singeltary Sr.

P.O. BOX 42

Bacliff, Texas USA 77518




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