• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

JAPAN- New Case of BSE

Help Support Ranchers.net:

A

Anonymous

Guest
Japan confirms 21st case of mad cow disease
Sun Dec 11, 2005 1:58 AM ET


TOKYO (Reuters) - Japan has confirmed its 21st case of mad cow disease in a 69-month-old Holstein cow on the northernmost main island of Hokkaido, the Farm Ministry said.

The meat and intestines from the slaughtered cow will be destroyed and will not enter the food supply, the ministry said in a statement dated December 10.

The cow was born in February 2000, which is before Japan banned the use of meat-and-bone (MBM) meal as feed for all animals, the ministry said. MBM is thought to cause mad cow disease.

Japan adopted a policy of testing all cattle for mad cow in October 2001 after it discovered its first BSE case in a domestic herd.

Although the government dropped the universal testing policy in August, local governments continue to test all cattle.

The latest BSE case in Japan comes just ahead of a widely expected decision by Tokyo to lift a two-year ban on U.S. beef imports that was imposed after the discovery of a BSE case in the United States.

Japanese media have reported that Japan would officially announce an easing of the ban on Monday.
 
##################### Bovine Spongiform Encephalopathy #####################


Subject: Secretary Mike Johanns and United States Trade Representative, Ambassador Rob Portman - Washington, D.C. Dec 9, 2005 more BSeee
Date: December 10, 2005 at 9:21 am PST


Transcript of News Conference with Agriculture Secretary Mike Johanns and United States Trade Representative, Ambassador Rob Portman - Washington, D.C. - December 9, 2005

AUDIO: Agriculture Secretary Mike Johanns And US Trade Representative Rob Portman Hold Press Availability On Trade

AMBASSADOR PORTMAN: My voice is a little scratchy today but I don't think we need four bottles of water up here.

SEC. JOHANNS: Maybe they were anticipating really tough questions.

AMB. PORTMAN: Yes. So we may need all four by the end of this.

Thank you all very much for coming on a holiday Friday here locally, and I imagine I'll get to see some of you all over the next 10 days in Hong Kong.

Mike Johanns, Secretary of Agriculture, and I are leaving tomorrow morning along with the U.S. delegation made up of several agencies. We'll be flying directly from Washington to Hong Kong. We'll then be spending about 10 days in Hong Kong working through these WTO issues hoping that we can make progress toward a successful completion of the Doha Development Agenda by the end of 2006.

I am hopeful that in Hong Kong we can make incremental progress in a number of areas. One would certainly be a package for being sure that the least developed countries are assured that in this round they will receive very specific benefits to help them integrate fully into the global trading system and to be able to take advantage of the market opening opportunities that will arise from a successful Doha Round.

We've got a lot of work to do. Hong Kong will not be a time for us to make some major breakthroughs that the United States had hoped for, but we do hope that we can make incremental progress and establish building blocks that would go toward even more progress early in the new year.

In Hong Kong we will be stressing that improving market access is again the key to achieving the goals of the Doha round. We've said this many times, but it bears repeating-- the best way to promote development, expand economic opportunities and alleviate poverty in all countries is through expanded trade. And the only way to expand trade is for countries to open their markets in meaningful ways.

This is particularly true in agriculture, which from the start has been at the core of the Doha Round. It's a tough issue. It's always a tough political issue back home. It's one reason that agriculture has not been part of previous rounds with the exception of the Uruguay Round. The previous seven didn't include agriculture. But it's in agriculture where you find the highest tariffs and you find the highest trade-distorting subsidies.

It's also an area where many developing countries see that they have a comparative advantage. They have the ability to sell their products overseas and they're looking for a more level playing field.

That's why it I support Doha. The broad development goals of the Doha Round depend on progress in agriculture, and increasing market access in agriculture will benefit farmers everywhere. The World Bank has studied this and indicated that 93 percent of the gain in agriculture will come from gains in market access.

This is particularly true though among farmers in the developing world who confront an average world tariff of 62 percent in agriculture.

We must also reduce trade-distorting domestic supports. And the United States has taken the lead in putting a proposal on the table. It reduces trade-distorting supports here, in Europe, in Japan, and other countries that provide support -- and eventually under the U.S. proposal, eliminating trade-distorting support.




snip...


In Hong Kong though I think we need to make progress to get there in two fronts. One is, again to give the least developed countries more assurance as to what they will get from the round, and that is basically the trade capacity help to be able to take advantage of the trade openings.

And second, we need to make incremental progress in all three of these areas: agriculture, manufacturing and services.

QUESTION: (unclear)

SEC. JOHANNS: U.S. inspection programs are really beyond a doubt safe. And I'll offer a couple thoughts on that. The analysis or report you referenced there, if you'd asked me a question where you said, Mike, your inspectors found zero problems, I'd say, wait a minute, that sounds rather remarkable; I wonder what's going on out there.

But the report actually indicates they're doing their job. They're identifying the issues that we need to deal with and then demanding that those issues be fixed.

The other thing I would tell you about Japan, and this is really unique to Japan -- as you know we've agreed in this first phase with Japan to start at meat from animals 20 months and under. And you're just not going to find BSE there. It's just not there. So from a number of standpoints, I can safely assure the Japanese consumer that beef is safe.

But probably the best assurance I can give them is as you know the Japanese process over the last two years has been enormously meticulously carried out, painstakingly so. At times we couldn't even detect progress. I mean that's how thorough and comprehensive this process was. And at every stage of the process the conclusion was reached that U.S. beef is safe as Japanese beef.

Then you do a comparison of the countries. We have a herd size of about 90 million. We process about 30 million animals a year, thereabouts, probably a little bit more than that. We've been able to identify since the enhanced surveillance started one case that was actually so difficult to find we had to test and test and test to find it even.

Japan is familiar with BSE. They've now identified their 20th case of BSE. So in working with the Japanese government and with food safety people it was not like we were working with people who had never had any exposure to BSE issues. So when you factor it all in, all the things we've done, I can assure the Japanese consumer beyond a shadow of a doubt that beef is safe. And we're very anxious to return it to their marketplace.

And we'll work with the consumers. We know that it's been a very long process and we have work to do with the consumers. We're going to do everything we can to accomplish confidence in U.S. beef. And I'm very, very confident that we will achieve that.

AMB. PORTMAN: All the way in the back corner?

QUESTION: (off-mike)


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/3/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2005%2F12%2F0543.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_parentnav=TRANSCRIPTS_SPEECHES&PC_7_2_5JM_navid=TRANSCRIPT#7_2_5JM



>>>The other thing I would tell you about Japan, and this is really unique to Japan -- as you know we've agreed in this first phase with Japan to start at meat from animals 20 months and under. And you're just not going to find BSE there. It's just not there. So from a number of standpoints, I can safely assure the Japanese consumer that beef is safe. <<<


r i g h t! kinda like the WMD issue and gitmo, no lies here either.


the myth that cattle under 30 months of age are free from BSE/TSE is just that, a myth, and it's a false myth !


the youngest age of BSE case to date is 20 months old; As at: 31 May
2003 Year of onset Age youngest case (mnths) Age 2nd youngest case
(mnths) Age 2nd oldest case (yrs.mnths) Age oldest case (yrs.mnths) 1986
30 33 5.03 5.07 1987 30 31 9.09 10.00 1988 24 27 10.02 11.01(2) 1989 21
24(4) 12.00(2) 15.04 1990 24(2) 26 13.03 14.00 1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02 1993 29 30(3) 14.10 18.10 1994 30(2) 31(2) 14.05
16.07 1995 24 32 14.09 15.05 1996 29 30 15.07 17.02 1997 37(7) 38(3)
14.09 15.01 1998 34 36 14.07 15.05 1999 39(2) 41 13.07 13.10 2000 40 42
17.08 19.09 2001 48(2) 56 14.10 14.11 2002 51 52 15.08 15.09(2) 2003 50
62 11.11 14.11

http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html

http://www.defra.gov.uk/animalh/bse/index.html

The implications of the Swiss result for Britain, which has had the most
BSE, are complex. Only cattle aged 30 months or younger are eaten in
Britain, on the assumption, based on feeding trials, that cattle of that
age, even if they were infected as calves, have not yet accumulated
enough prions to be infectious. But the youngest cow to develop BSE on
record in Britain was 20 months old, showing some are fast incubators.
Models predict that 200-300 cattle under 30 months per year are infected
with BSE and enter the food chain currently in Britain. Of these 3-5
could be fast incubators and carrying detectable quantities of prion.

http://www.sare.org/htdocs/hypermail/html-home/28-html/0359.html

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


SO, with GWs BSE MRR policy, like i said, it is nothing more than a legal tool to trade ALL STRAINS of this mad cow agent around the globe. WE know of atypical TSE in USA via Marsh et al, and we know when USA scrapie is transmitted to USA cow, it does not look like UK BSE. BUT what about Japans beef brought into USA? seems they have atypical TSE in Japan cattle that is in very young cattle and evidently, there TSE agent has even been detected in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve), so why would USA want to import that into USA$ With our much superior BSE/TSE surveillance system in USA cattle and the fact we have had this fabulous ruminant to ruminant mad cow feed ban in effect since 8/4/97, where no cattle have been fed ruminant protein since then;-), why should we risk this new phenotype of TSE to the USA, since we have all the other TSEs here in the USA under control:-(not)$


Muscle tissue has recently been detected with PrPSc
in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve) of the 11th BSE
cow in Japan (Yoshifumi Iwamaru et al). also recently, Aguzzi et al Letter to the Editor
Vet Pathol 42:107-108 (2005), Prusiner et al CDI test is another example of detection
of the TSE agent in muscle in sCJD, Herbert Budka et al CJD and inclusion body myositis:
Abundant Disease-Associated Prion Protein in Muscle, and older studies from Watson
Meldrum et al Scrapie agent in muscle - Pattison I A (1990), references as follow ;


PrPSc distribution of a natural case of bovine
spongiform encephalopathy

Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori-
kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa

Priori Disease Research Center, National Institute of Animal Health, 3-1-5
Kannondai, Tsukuba 305-0856 Japan [email protected]

Abstract

Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes
progressive neurodegeneration of the central nervous system. Infectivity
of BSE agent is accompanied with an abnormal isoform of prion protein
(PrPSc).

The specified risk materials (SRM) are tissues potentially carrying BSE
infectivity. The following tissues are designated as SRM in Japan: the
skull including the brain and eyes but excluding the glossa and the masse-
ter muscle, the vertebral column excluding the vertebrae of the tail, spinal
cord, distal illeum. For a risk management step, the use of SRM in both
animal feed or human food has been prohibited. However, detailed
PrPSc distribution remains obscure in BSE cattle and it has caused con-
troversies about definitions of SRM. Therefore we have examined PrPSc
distribution in a BSE cattle by Western blotting to reassess definitions of
SRM.

The 11th BSE case in Japan was detected in fallen stock surveillance.
The carcass was stocked in the refrigerator. For the detection of PrPSc,
200 mg of tissue samples were homogenized. Following collagenase
treatment, samples were digested with proteinase K. After digestion,
PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets
were subjected to Western blotting using the standard procedure.
Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish
peroxidase was used for the detection of PrPSc.

PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal
ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected
in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve).

Our results suggest that the currently accepted definitions of SRM in
BSE cattle may need to be reexamined. ...

179

T. Kitamoto (Ed.)
PRIONS
Food and Drug Safety
================


ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to
November 2, 2004;


Bovine spongiform encephalopathy (BSE) in Japan


snip...


"Furthermore, current studies into transmission of cases of BSE that are
atypical or that develop in young cattle are expected to amplify the BSE
prion"


NO. Date conf. Farm Birth place and Date Age at diagnosis


8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23


9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21


Test results


# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology
negative


b = atypical BSE case


c = case of BSE in a young animal


b,c, No PrPSc on IHC, and no spongiform change on histology


International Symposium of Prion Diseases held in Sendai, October 31, to
November 2, 2004.

The hardback book title is 'PRIONS' Food and Drug Safety
T. Kitamoto (Ed.)


Tetsuyuki Kitamoto
Professor and Chairman
Department of Prion Research
Tohoku University School of Medicine
2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN
TEL +81-22-717-8147 FAX +81-22-717-8148
e-mail; [email protected]
Symposium Secretariat
Kyomi Sasaki
TEL +81-22-717-8233 FAX +81-22-717-7656
e-mail: [email protected]


snip...end


THIS brings up about another 9,200 points of concern. IF you look above at these two atypical TSE cows from Japan, (of which we could very well export more just like it), please notice the testing protocol;


>>># 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology
negative <<<


9,200 points of mad cow concern is the fact the USDA et al DID NOT use rapid TSE test OR WB test to test for BSE/TSE on 9,200 cattle, they used the least likely to find the agent only, the IHC, of which, DID NOT show up on two of those very young atypical positive Japanese cows, PLUS, like the one TEXAS cow they did finally confirm after 7+ months of trying to cover up. besides this, we have some 500,000 bse/tse test, the infamous June 2004 enhanced BSE/TSE surveillance (cover-up) program, where here the testing protocol was terribly flawwed on all these cows, where only IHC and rapid testing was used, no WB. Dr. Detwiler warned of this problem way back;


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


National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary

The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative. ...


http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html


APHIS et al forgets to add here that on that one additional non-definitive test of July 27, 2005, here again they could not use WB due to samples being preserved. Here in 2005 we have still not gotten the proper BSE/TSE testing protocol done correctly, after being told that we did since 1997.


hey, but its not about 'sound science' or 'human health'. GWs enhanced SRM program was nothing more than commodities and futures in action;


Our analysis suggests that if all slaughter animals are tested, but

there is no increase in access to either the Japanese or

South Korean markets, the result would be a net loss of

$17.50 (the estimated cost of testing) per head. Alternatively,

if full access to the Japanese and South Korean

markets is regained without implementing a broad

based BSE testing program, the potential revenue gain

ranges from about $45 to $66 per head (Figure 1).


http://www.oznet.ksu.edu/library/agec2/MF2679.pdf


GW seems to get his cake and eat it too $

nothing like 'sound science' in this administration, to hell with human health.


>>>Then you do a comparison of the countries. We have a herd size of about 90 million. We process about 30 million animals a year, thereabouts, probably a little bit more than that. We've been able to identify since the enhanced surveillance started one case that was actually so difficult to find we had to test and test and test to find it even. <<<


IN TEXAS we feed our cattle 5.5 grams of potentially BSE/TSE tainted protein, and that's o.k. per the FDA;


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


WE know what happens to most stumbling and staggering suspect mad cows in TEXAS too. THERE tissue samples either sit up on a shelf for 7+ months waiting for everyone to forget about, OR ;


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


WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;


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.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula


Published online January 27, 2005

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

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise that it

could take as little of 1 gram of brain to cause BSE by the oral route within the

same species. This information did not become available until the "attack rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to ensure

that the actual result was within both a lower and an upper limit within the study

and the designing scientists would not have expected all the dose levels to trigger

infection. The dose ranges chosen by the most informed scientists at that time

ranged from 1 gram to three times one hundred grams. It is clear that the designing

scientists must have also shared Mr Bradley's surprise at the results because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

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

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


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD COW DISEASE FEED



GAO


GAO-06-157R FDA Feed Testing Program

October 11, 2005


SNIP...FULL TEXT 29 PAGES ;


http://www.gao.gov/new.items/d06157r.pdf


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


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


http://www.fda.gov/cvm/5580.htm


[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. [[email protected]]

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

To: [email protected].

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. [[email protected]] 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


still disgusted in cold cold Bacliff, Texas, dreaming of the warm Caribbean Isands. take us away...


TSS

#################### https://lists.aegee.org/bse-l.html ####################
 
Release No. 0546.05
Contact:
Suzan Holl (301) 734 6464
Jerry Redding (202) 720 6959

Printable version
USDA AMENDS REGULATIONS GOVERNING THE IMPORTATION OF WHOLE CUTS OF BONELESS
BEEF FROM JAPAN

Questions and Answers: The Importation of Boneless Beef from Japan

WASHINGTON, Dec. 12, 2005- The U.S. Department of Agriculture's Animal and
Plant Health Inspection Service today announced that it is amending
regulations governing the importation of meat and other edible animal
products to reestablish, under certain conditions, the importation of whole
cuts of boneless beef from Japan. This final rule will continue to safeguard
the United States against the introduction of bovine spongiform
encephalopathy (BSE).

In September 2001, APHIS prohibited the importation of ruminants and most
ruminant products from Japan following the confirmation of BSE in a
native-born cow in that country. Recently, Japan requested that APHIS
consider resuming the importation of beef from Japan to the United States.
In a Federal Register notice published Aug. 18, 2005, APHIS proposed to
amend the import regulations by allowing the importation of whole cuts of
boneless beef from Japan under specified conditions. The regulations will be
amended under this final rule.

After conducting a thorough risk analysis, APHIS has determined that such
beef can be safely imported to the United States from Japan under the
following conditions:

* The beef is prepared in an establishment that is eligible to have its
products imported to the United States under the Federal Meat Inspection
Act. This includes provisions that specified-risk materials (SRMs) must be
removed under appropriate conditions and it also prohibits the use of
air-injection stunning devices.
* The beef must be derived from cattle that are not subjected to a pithing
process at slaughter.
* The mitigation measures must be certified on an original certificate
issued by an authorized veterinary official of the Japanese government.

Research has demonstrated that only a limited number of tissues from cattle
may harbor infectious levels of BSE. These are primarily the central nervous
system tissues, such as the brain and spinal cord. Requirements for the
removal of these tissues, commonly referred to as SRMs, would prevent them
from entering the human food supply and are an important safeguard to
protect public health. Research has not demonstrated that bovine muscle
meat, which would be the sole product eligible for importation under the
final rule, harbors BSE. The import conditions in the final rule including
the removal of SRMs, are based on scientific research and in combination
allow for the safe importation of whole cuts of boneless beef from Japan.

This final rule is scheduled for publication in the Dec. 14, 2005 Federal
Register and becomes effective at 11:30 a.m. EST on Dec. 12, 2005.


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retriev
econtent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/2/_th/J_2_9D/_s.7_0_A/7_0_1OB?
PC_7_2_5JM_contentid=2005%2F12%2F0546.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_p
arentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM


Release No. 0545.05
Contact:
USDA Press Office (202) 720-4623

Printable version
AUDIO: AGRICULTURE SECRETARY MIKE JOHANNS REMARKS REGARDING RESUMPTION OF
BEEF TRADE WITH JAPAN

USDA_1 MP3

* ACTUALITY: JAPANESE CONSUMERS TO SOON ENJOY U.S. BEEF 00:00:34 - Secretary
of Agriculture Mike Johanns saying that Japanese consumers will soon enjoy
U.S. beef.

USDA_2 MP3

* ACTUALITY: U.S. WILL BEGIN IMPORTING KOBE BEEF SOON 00:00:53 - Agriculture
Secretary Mike Johanns announcing U.S. will accept Kobe beef soon.

USDA_3 MP3

* ACTUALITY: U.S. TO BEGIN EXPORTING BEEF TO JAPAN 00:00:18 -Secretary of
Agriculture Mike Johanns makes announcement that U.S. will begin exporting
U.S. beef almost immediately.

USDA_4 MP3

* ACTUALITY: U.S. TO ACCEPT KOBE BEEF 00:01:02 - Agriculture Secretary Mike
Johanns saying U.S. will be able to supply enough beef.


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retriev
econtent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/2/_th/J_2_9D/_s.7_0_A/7_0_1OB?
PC_7_2_5JM_contentid=2005%2F12%2F0545.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_p
arentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM


Release No. 0544.05
Contact:
USDA Press Office (202) 720-4623

Printable version
STATEMENT BY AGRICULTURE SECRETARY MIKE JOHANNS REGARDING THE OPENING OF THE
JAPANESE MARKET TO U.S. BEEF

Clarification noted in bold 3rd paragraph and last paragraph, number of
countries

December 11, 2005

"I'm very pleased to announce that the Japanese market is now open to U.S.
beef products. Resuming beef trade with Japan is great news for American
producers and Japanese consumers, as well as an important step toward
normalized trade based on scientifically sound, internationally recognized
standards.

"Reopening the Japanese market to U.S. beef has been a top priority for me
since becoming Secretary, and I want to thank the many people and
organizations who have been instrumental in this success. First and
foremost, my thanks to President Bush for being personally and directly
engaged in this effort. I want to thank my colleagues in the President's
cabinet, Secretaries Rice, Snow, Gutierrez and Ambassador Portman, as well
as Ambassadors Baker and Schieffer, for making this issue a centerpiece of
their discussions with Japan. I also extend my thanks to Chairmen Goodlatte
and Chambliss, the entire American meat industry, and all of the USDA staff
involved with the many meetings, site visits, reports and other
consultations with Japan's food safety officials to confirm the safety of
U.S. beef.

"Japan's action today provides sets an excellent example for other countries
in Asia whose markets remain closed. Now is the time for Taiwan, South
Korea, Hong Kong, China, Singapore and others to open their markets to U.S.
beef. I urge all countries to take a science-based approach and adopt OIE
standards for allowing beef trade. Building bridges of understanding and
collaboration between nations is an important part of ensuring food safety.
American producers are proud of our safe, high-quality beef products and we
greatly value the opportunity to promote the safety of our products to
consumers in Japan and around the world. As I have said many times
throughout this process, our goal is the resumption of normal beef trade
throughout the world and we will continue to aggressively work toward that
objective."

Under the agreement announced today, the United States is able to export
beef from cattle 20 months of age and younger to Japan. More than 94 percent
of total U.S. ruminant and ruminant products, with a total export value of
$1.7 billion in 2003, are now eligible for export to Japan. In 2003, the
United States exported $1.4 billion worth of beef and beef products to
Japan. Prior to the December 2003 discovery of the first BSE-infected cow in
the United States, the U.S. exported beef and beef products to 119
countries. With the opening of Japan, 67 countries have now established
trade to at least selected U.S. beef and beef products.

http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retriev
econtent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/2/_th/J_2_9D/_s.7_0_A/7_0_1OB?
PC_7_2_5JM_contentid=2005%2F12%2F0544.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_p
arentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM


JAPANESE BORDER OPENS TO CANADIAN BEEF

OTTAWA, December 11, 2005 – The Canadian Food Inspection Agency (CFIA) today
announced that Japan has agreed to reopen its border to Canadian beef and
selected beef products from cattle aged 20 months and younger.

The restoration of trade with Japan is the product of over two years of
extensive engagement at all levels of government, including technical
discussions, information sharing and industry endorsement. During this
period, Canadian food safety, public and animal health experts presented
detailed reports of Canada's response to mitigate bovine spongiform
encephalopathy (BSE) risks. Japanese officials visited Canadian feed lots,
farms, feed mills and slaughter facilities to observe these safeguards at
work.

Japan was one of a number of countries that closed their borders to Canadian
beef after the 2003 detection of BSE in Canada. Prior to suspending trade,
Japan was the third largest importer of Canadian beef and beef products.
Canada exported more than $81 million worth of product to Japan in 2002.
Canada's top two importers, the United States and Mexico, reopened their
borders to a range of products in 2003.

Regaining access to Japan marks a significant milestone in Canada's ongoing
efforts to fully restore trade to pre-BSE levels. Canadian officials will
continue to work closely with their counterparts in Japan and other
international markets to demonstrate the scope and effectiveness of
safeguards in place to protect human and animal health as the basis for
expanded safe trade opportunities. These efforts will pursue access for all
commodities deemed eligible for export in accordance with the science-based
standards of the World Organization for Animal Health.

In addition to meeting the age requirement, beef products destined for Japan
must be processed in accordance with a range of conditions. Additional
details are available through regional CFIA offices.

- 30 -

For information:

Canadian Food Inspection Agency
Media Relations: (613) 228-6682

http://www.inspection.gc.ca/english/corpaffr/newcom/2005/20051211e.shtml

BSE import policy for bovine animals and their products

APHD-DSAE-IE-2005-9-1
Printer-friendly PDF Version

December, 2005

Main Page - BSE
1. Bovine animals

For the purpose of this policy, bovine animals consist of cattle and bison.
Taxonomically they are classified as members of the Subfamily Bovinae1 from
the genus Bos, which includes cattle (Bos taurus and Bos indicus) and bison
(Bos bison).
2. Importing commodities into Canada

Depending on the nature of the commodity, certain BSE related restrictions
may be applicable. Those commodities listed in section 3 may be generally
imported into or transit Canada regardless of the BSE status of a country
while commodities listed in sections 4 and 5 may be subjected to certain
restrictions depending on the BSE status of the country, which is determined
on the basis of a risk assessment as detailed in Appendix 1. However, before
undertaking a risk assessment for a particular country it is important to
determine the range of commodities for which a country is seeking market
access. In many cases it is likely that a risk assessment will not be
required. For example, if a country that has reported BSE cases within the
preceding seven years is interested in just exporting meat and meat
products, cell lines and veterinary biologics to Canada, a risk assessment
would not be necessary as the measures for these commodities are the same
regardless of whether it would be classified as Category 2 (controlled
BSE-risk) or Category 3 (undetermined BSE-risk). On the other hand, a risk
assessment would be required before a country, that has not reported BSE,
could export these commodities without BSE related restrictions to determine
if it qualifies for Category 1 (negligible BSE-risk).

If a risk assessment has not been undertaken for a particular country the
applicable measures are those prescribed for countries as having an
undetermined BSE-risk (Category 3). It is important to note that before a
particular commodity can be imported other conditions must still be met. For
example, before meat and meat products can be imported, the Canadian Food
inspection Agency (CFIA) must evaluate and approve the meat inspection
system of a country and specific measures for other diseases of concern must
also be met. In addition, there may be other restrictions impacting on the
end use of the product within Canada, for example, restrictions governing
the end use of bovine blood and blood products in the preparation of drugs
(including pharmaceuticals, and natural health care products), which are
under the mandate of Health Canada. It is the responsibility of the importer
to ensure compliance with the specific requirements of the Canadian
regulatory authority responsible for the end use of imported products.

Table 1 summarises the list of commodities covered by this import policy in
sections 3-5 and their associated BSE-related restrictions detailed in
section 6. Commodities not included in this table will be assessed on a case
by case basis taking into account the nature of the product, the methods of
production and proposed use with applicable conditions developed on the
basis of a risk assessment.

In developing measures necessary to protect human or animal life or health
World Trade Organization Members have certain rights and obligations, which
are detailed in the Agreement on the Application of Sanitary and
Phytosanitary Measures (SPS Agreement) as well as the SPS provisions of the
North American Free Trade Agreement (NAFTA). One important obligation
relates to the concept of equivalence, which is the capability of different
sanitary measures to achieve the same outcome. In applying this policy,
provided a trading partner can objectively demonstrate that its measures
achieve the same level of protection as those required by Canada, it is the
Government of Canada's intention that the trading partner's measures be
accepted as equivalent.

Table 1: BSE-related restrictions for certain commodities derived from
bovine animals or containing material of bovine origin. Note that this table
provides a general summary. For a complete description of the applicable
conditions refer to the relevant section in the text.
Commodity Category 1 country
(negligible BSE-risk) Category 2 country
(controlled BSE-risk) Category 3 country
(undetermined BSE-risk)
a) milk and milk products

b) semen and in vivo derived bovine embryos

c) hides and skins

d) gelatin and collagen prepared exclusively from hides and skins (excluding
hides and skins from the head)

e) protein-free tallow (maximum level of insoluble impurities of 0.15% in
weight) and derivatives made from this tallow;

f) dicalcium phosphate (with no trace of protein or fat)

g) deboned skeletal muscle meat (excluding mechanically separated meat) from
bovine animals 30 months of age or less, which were not subjected to a
stunning process, prior to slaughter, with a device injecting compressed air
or gas into the cranial cavity, or to a pithing process, and which were
subject to ante-mortem and post-mortem inspections and were not suspect or
confirmed BSE cases, and which has been prepared in a manner to avoid
contamination with SRM

h) blood and blood by-products, from bovine animals which were not subjected
to a stunning process, prior to slaughter, with a device injecting
compressed air or gas into the cranial cavity, or to a pithing process, and
which were subject to ante-mortem and post-mortem inspections and were not
suspect or confirmed BSE cases, and which has been prepared in a manner to
avoid contamination with SRM
no BSE restrictions related to country status no BSE restrictions related to
country status no BSE restrictions related to country status
i) live animals; Permanent ID; born after a feed ban; etc. Prohibited
j) ruminant derived meat-and-bone meal or greaves, or any commodities
containing such products Prohibited
k) meat and meat products other than deboned skeletal muscle meat as defined
in (g) air injection stunning and pithing prohibited; SRM excluded
l) gelatin and collagen prepared from bones not prepared from SRM; subjected
to certain processing steps
m) tallow (non protein-free) air injection stunning and pithing prohibited;
not prepared from SRM Prohibited
n) tallow derivatives made from non protein free tallow air injection
stunning and pithing prohibited; SRM excluded; produced by hydrolysis,
saponification or transesterification using high temperature and pressure
o) dicalcium phosphate containing protein or fat air injection stunning and
pithing prohibited; not prepared from SRM Prohibited
p) products produced by subjecting bones to rigorous processes of extraction
and purification such as ossein, bone ash, bone charcoal and bone oil no BSE
restrictions related to country status not prepared from SRM
q) products and by-products that have been subjected to rigorous processes
of extraction and purification such as animal glue, oleosterin,
triglycerides, glycerol, sorbitan esters not prepared from SRM
r) commercially prepared pet food and finished pet chews, such as dried
processed ears, pizzles, hooves or tendons not prepared from SRM
s) cell lines Not prepared from SRM imported from a Category 2 or 3 country
air injection stunning and pithing prohibited; not prepared from SRM
t) veterinary biologics
3. Commodities that can be imported into or transit Canada regardless of the
BSE status of an exporting country

The following commodities derived from bovine animals can be imported into
or transit Canada regardless of the BSE status of an exporting country:

* milk and milk products;
* semen and in vivo derived bovine embryos collected and handled in
accordance with the recommendations of the International Embryo Transfer
Society;
* hides and skins;
* gelatin and collagen prepared exclusively from hides and skins (excluding
hides and skins from the head);
* protein-free tallow (maximum level of insoluble impurities of 0.15% in
weight) and derivatives made from this tallow2;
* dicalcium phosphate (with no trace of protein or fat)2;
* deboned skeletal muscle meat (excluding mechanically separated meat) from
bovine animals 30 months of age or less, which were not subjected to a
stunning process, prior to slaughter, with a device injecting compressed air
or gas into the cranial cavity, or to a pithing process, and which were
subject to ante-mortem and post-mortem inspections and were not suspect or
confirmed BSE cases, and which has been prepared in a manner to avoid
contamination with SRM;
* blood and blood by-products, from bovine animals which were not subjected
to a stunning process, prior to slaughter, with a device injecting
compressed air or gas into the cranial cavity, or to a pithing process, or
to a pithing process, and which were subject to ante-mortem and post-mortem
inspections and were not suspect or confirmed BSE cases, and which has been
prepared in a manner to avoid contamination with SRM.

4. Commodities prohibited from importation into Canada

Ruminant derived meat-and-bone meal or greaves, or any commodities
containing such products are specifically prohibited from importation into
Canada unless a risk assessment has been undertaken and the country is
classified as Category 1 (negligible BSE-risk).

An exemption from this prohibition may be considered on a case-by-case basis
if the materials used in the production of ruminant derived meat-and-bone
meal or greaves, or any commodities containing such products have undergone
a treatment or process to eliminate the BSE-agent equivalent to that applied
in Canada. Details of the treatment or process deemed to be equivalent
together with supporting data and references as appropriate should be
provided to CFIA for approval.
5. Commodities that can be imported into or transit Canada subject to
certain BSE-related measures

The following commodities derived from bovine animals or containing material
of bovine origin are subject to certain BSE-related measures before they can
be imported into or transit Canada:

* live animals;
* meat and meat products other than deboned skeletal muscle meat as defined
in section 3 (g);
* gelatin and collagen prepared from bones intended for food, animal food,
fertilisers, veterinary biologics, or as unprocessed material for the
preparation of cosmetics, drugs (including pharmaceuticals and natural
health products) or medical devices;
* tallow and tallow derivatives, and dicalcium phosphate, other than
protein-free tallow and dicalcium phosphate (with no trace of protein or
fat) as defined in section 3 (e) intended for food, animal food,
fertilisers, veterinary biologics, or as unprocessed material for the
preparation of cosmetics, drugs (including pharmaceuticals and natural
health products) or medical devices;
* Products derived from bovine animals by subjecting bones to rigorous
processes of extraction and purification such as ossein, bone ash, bone
charcoal and bone oil and intended for food, animal food, fertilisers, or as
unprocessed material for the preparation of cosmetics, drugs (including
pharmaceuticals and natural health products), medical devices or veterinary
biologics;
* Products and by-products derived from bovine animals that have been
subjected to rigorous processes of extraction and purification such as
animal glue, oleosterin, triglycerides, glycerol, sorbitan esters and
intended for food, animal food, fertilisers, or as unprocessed material for
the preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics;
* Commercially prepared pet food and finished pet chews, such as dried
processed ears, pizzles, hooves or tendons;
* cell lines;
* veterinary biologics (vaccines, antibody products and diagnostic kits).

The types of measures that are applicable are dependant on the BSE-risk
category of the exporting country, which is determined by a risk assessment
as outlined in Appendix 1. The relevant measures are set down in section 6
for each of the three BSE-risk categories:

* Category 1. negligible BSE-risk
* Category 2. controlled BSE-risk
* Category 3. undetermined BSE-risk

If a risk assessment has not been undertaken for a particular country the
applicable measures are those prescribed for a category 3 country
(undetermined BSE-risk). Commodities not included in this section will be
assessed on a case by case basis taking into account the nature of the
product, the methods of production and proposed end use with applicable
conditions developed on the basis of a risk assessment.
6. Risk management measures
6.1. Category 1 Countries (negligible BSE-risk)

6.1.1. Definition

Category 1 countries are those countries that:

*

a) have never reported a BSE-case, and where,
either:

the conclusion of risk assessment is that the likelihood that BSE exists in
the country is negligible,

or where:

the conclusion of the risk assessment indicates that the likelihood of the
bovine animal population having been exposed to a TSE-agent within the last
7 years is negligible and that the level of surveillance maintained during
at least the last 7 years should have detected BSE cases if they were
present.

Or:

*

b) have not reported BSE-cases in imported and/or indigenous animals for a
period of at least seven years and have satisfied each of the following
conditions throughout the same period:
o the likelihood of imported commodities being contaminated or infected with
a TSE-agent has remained negligible;
o the likelihood of bovine animals having been exposed to a TSE that exists
in the country's domestic or wild ruminant population has remained
negligible;
o the measures to eradicate BSE have been maintained;
o a level of surveillance capable of demonstrating the effectiveness of the
eradication measures has been maintained without the detection of any
BSE-cases.

The risk assessment for a country in this category must be reviewed
regularly to ensure that it continues to qualify as a Category 1 country.

6.1.2. General provisions

* BSE is compulsorily notifiable.
* The Veterinary Administration has authority over any animal suspected or
confirmed of having BSE. This is needed to ensure that a thorough
investigation is undertaken and that affected animals, when slaughtered or
at death, are completely destroyed.

6.1.3. Cell lines and Veterinary biologics (vaccines, antibody products and
diagnostic kits) containing material of bovine origin intended for use in
animals

Considering that cell lines and veterinary biologics often contain
ingredients from a variety of sources, some of which may have been imported
into the country, it is important to ensure that such ingredients do not
contain or are not contaminated with the BSE-agent. As a result,
certification is required for all cell lines and veterinary biologics that
they do not contain any imported ingredients from a country classified as
Category 2 (controlled BSE-risk) or Category 3 (undetermined BSE-risk) that
may have been:

* prepared from bovine animals subjected to a stunning process, prior to
slaughter, with a device injecting compressed air or gas into the cranial
cavity or to a pithing process (laceration, after stunning, of central
nervous tissue by means of an elongated rod-shaped instrument introduced
into the cranial cavity), or;
* prepared from or contain the following specified risk materials (SRM):
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all bovine animals aged 30 months or older;
o the small intestine and tonsils from bovine animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive.

An exemption from this requirement for cell lines and veterinary biologics
will be considered on a case-by-case basis considering the nature of the
product, the source of materials of bovine origin, the manufacturing methods
employed, and the intended use.

6.1.4. Commodities other than cell lines and Veterinary biologics

While specific measures for BSE are not necessary for all other commodities
derived from bovine animals, before a particular commodity can be imported
other relevant conditions must still be met, for example, the evaluation and
approval of the meat inspection system of a country and specific measures
for other diseases of concern.
6.2. Category 2 Countries (controlled BSE-risk)

6.2.1. Definition

Category 2 countries are those countries where:

* it is likely that imported commodities were contaminated or infected with
a TSE-agent, and/or;
* it is likely that a TSE exists in the country's domestic or wild ruminant
population, and;
* either indigenous BSE-cases have been reported, or it is likely that
indigenous bovine animals have been exposed to a TSE-agent, and;
* the measures in place are effectively controlling BSE and are likely to
lead to its eradication.

The risk assessment for a country in this category must be reviewed
regularly to ensure that it continues to qualify as a Category 2 country.

6.2.2. General provisions

* The feeding of ruminants with meat-and-bone meal and greaves derived from
ruminants has been banned and the ban has been effectively enforced in the
whole country;
* BSE is compulsorily notifiable;
* The Veterinary Administration has authority over any animal suspected or
confirmed of having BSE. This is needed to ensure that a thorough
investigation is undertaken and that affected animals, when slaughtered or
at death, are completely destroyed.

6.2.3. Live bovine animals

Certification by the Veterinary Administration that the animal:

* is identified by a permanent identification system enabling it to be
traced back to its dam and herd of origin;
* was born after the implementation of the feed ban;
* was not fed ruminant proteins prohibited under the feed ban during its
lifetime;
* is not the progeny of a BSE suspect or confirmed female;
* was not reared during its first year of life with a BSE suspect or
confirmed case;
* was not born in the same herd and within 12 months of the birth of a BSE
suspect or confirmed case.

An exemption from these requirements for live bovine animals will be
considered on a case-by-case basis considering the intended use of the
animals, for example, animals imported for a temporary stay; animals for
immediate slaughter; animals imported for medical use, scientific research
or zoological collections; bulls destined for semen production centers.

6.2.4. Meat and meat products from bovine animals other than deboned
skeletal muscle meat as defined in section 3 (g)

Certification by the Veterinary Administration that:

* ante-mortem and post-mortem inspection is carried out on all bovine
animals from which the meat or meat products originate;
* where the meat or meat products are destined for human consumption they
have been passed as fit for human consumption in the country of origin;
* the facility in which the animals are slaughtered and processed is
approved and inspected by the Veterinary Administration;
* the animals from which the meat or meat products destined for export
originate were not subjected to a stunning process, prior to slaughter, with
a device injecting; compressed air or gas into the cranial cavity or to a
pithing process (laceration, after stunning, of central nervous tissue by
means of an elongated rod-shaped instrument introduced into the cranial
cavity);
* the meat and meat products destined for export do not contain:
o the following specified risk materials (SRM):
+ the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column, excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum, from all bovine animals aged 30 months or older;
+ the small intestine and tonsils from bovine animals of all ages;
o mechanically separated meat from the skull and vertebral column from
animals aged 30 months or older;
* the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive.

6.2.5. Gelatin and collagen prepared from the bones of bovine animals and
intended for food, animal food, fertilisers, or as unprocessed material for
the preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics

Certification by the Veterinary Administration that the bones:

* do not include skulls and vertebrae (excluding the vertebrae of the tail)
from all animals aged 30 months or older;
* have been subjected to a process which includes all the following steps:
o pressure washing (degreasing);
o acid demineralisation;
o prolonged alkaline treatment;
o filtration;
o sterilisation at >138°C for a minimum of 4 seconds;
o or, to an equivalent process in terms of infectivity reduction3.

6.2.6. Tallow (other than protein-free tallow as defined in section 3) and
dicalcium phosphate (other than protein or fat free dicalcium phosphate as
defined in section 3) derived from bovine animals and intended for food,
animal food, fertilisers, or as unprocessed material for the preparation of
cosmetics, drugs (including pharmaceuticals and natural health products),
medical devices or veterinary biologics

Certification by the Veterinary Administration that the tallow or dicalcium
phosphate:

* originates from bovine animals:
o that have been subjected to an ante-mortem and post mortem inspection;
o were not subjected to a stunning process, prior to slaughter, with a
device injecting compressed air or gas into the cranial cavity or to a
pithing process (laceration, after stunning, of central nervous tissue by
means of an elongated rod-shaped instrument introduced into the cranial
cavity);
* has not been prepared using the following SRM or any protein products
derived from them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all animals aged 30 months or older;
o the small intestine and tonsils from animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive.

6.2.7. For tallow derivatives (other than those made from protein-free
tallow as defined in section 3) derived from bovine animals and intended for
food, animal food, fertilisers, or as unprocessed material for the
preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics

Certification by the Veterinary Administration that the tallow derivatives:

* originate from bovine animals:
o that have been subjected to an ante-mortem and post mortem inspection;
o were not subjected to a stunning process, prior to slaughter, with a
device injecting compressed air or gas into the cranial cavity or to a
pithing process (laceration, after stunning, of central nervous tissue by
means of an elongated rod-shaped instrument introduced into the cranial
cavity);
* have not been prepared using the following SRM or any protein products
derived from them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all animals aged 30 months or older;
o the small intestine and tonsils from animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive;
* have been produced by hydrolysis, saponification or transesterification
using high temperature and pressure.

6.2.8. Products derived from bovine animals by subjecting bones to rigorous
processes of extraction and purification such as ossein, bone ash, bone
charcoal and bone oil and intended for food, animal food, fertilisers, or as
unprocessed material for the preparation of cosmetics, drugs (including
pharmaceuticals and natural health products), medical devices or veterinary
biologics.

Certification by the Veterinary Administration that the products were not
derived from:

* skulls and vertebrae (excluding the vertebrae of the tail) from all
animals aged 30 months or older;
* have been subjected to a rigorous process of extraction or purification
approved by CFIA.

6.2.9. Products and by-products derived from bovine animals that have been
subjected to rigorous processes of extraction and purification such as
animal glue, oleosterin, triglycerides, glycerol, sorbitan esters and
intended for food, animal food, fertilisers, or as unprocessed material for
the preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics

Certification by the Veterinary Administration that the products and
by-products:

* have not been prepared using the following SRM or any protein products
derived from them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all animals aged 30 months or older;
o the small intestine and tonsils from animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive;
* have been subjected to a rigorous process of extraction or purification
approved by CFIA.

6.2.10. Commercially prepared pet food and finished pet chews, such as dried
processed ears, pizzles, hooves or tendons

Certification by the Veterinary Administration that the commercially
prepared pet food, ingredients for pet food or pet chews:

* do not contain or have not been prepared using the following SRM or any
protein products derived from them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all animals aged 30 months or older;
o the small intestine and tonsils from animals of all ages;
o the determination of the age of animals meets the standards prescribed in
the Government of Canada's Meat Hygiene Directive.

An exemption from these requirements for commercially prepared pet food and
finished pet chews will be considered on a case-by-case basis considering
the nature of the product, the source of materials of bovine origin, the
manufacturing methods employed, and the intended use.

6.2.11. Cell lines of bovine origin

Certification by the Veterinary Administration that the cell lines were:

* not prepared from bovine animals subjected to a stunning process, prior to
slaughter, with a device injecting compressed air or gas into the cranial
cavity or to a pithing process (laceration, after stunning, of central
nervous tissue by means of an elongated rod-shaped instrument introduced
into the cranial cavity), or;
* not prepared from the following SRM or any protein products derived from
them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all bovine animals aged 30 months or older;
o the small intestine and tonsils from bovine animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive.

An exemption from this requirement will be considered on a case-by-case
basis considering the nature of the cell lines, their intended use and
method of disposal.

6.2.12. Veterinary biologics (vaccines, antibody products and diagnostic
kits) containing material of bovine origin intended for use in animals

Certification by the Veterinary Administration that the veterinary biologics
were:

* not prepared from bovine animals subjected to a stunning process, prior to
slaughter, with a device injecting compressed air or gas into the cranial
cavity or to a pithing process (laceration, after stunning, of central
nervous tissue by means of an elongated rod-shaped instrument introduced
into the cranial cavity), or;
* not prepared from the following SRM or any protein products derived from
them:
o the skull including the brain, trigeminal ganglia and eyes, the spinal
cord and the vertebral column excluding the vertebrae of the tail, the
transverse processes of the thoracic and lumbar vertebrae, and the wings of
the sacrum from all bovine animals aged 30 months or older;
o the small intestine and tonsils from bovine animals of all ages;
o the determination of the age of animals, stunning, dressing and removal,
handling and disposition of SRM as inedible material meets the standards
prescribed in the Government of Canada's Meat Hygiene Directive.

An exemption from this requirement for veterinary biologics will be
considered on a case-by-case basis considering the nature of the product,
the source of materials of bovine origin, the manufacturing methods
employed, and the intended use.
6.3. Category 3 Countries (undetermined BSE-risk)

6.3.1. Definition

Category 3 countries are those countries where

either:

* a risk assessment has not been undertaken, completed4 or subjected to a
regular review,

or where:

* it is likely that imported commodities were contaminated or infected with
a TSE-agent, and/or;
* it is likely that a TSE exists in the country's domestic or wild ruminant
population, and;
* either indigenous BSE-cases have been reported or it is likely that
indigenous bovine animals have been exposed to a TSE-agent, and;
* the measures in place are unlikely to effectively control or eradicate
BSE.

6.3.2. Live bovine animals

This commodity is prohibited from Category 3 countries (undetermined
BSE-risk).

An exemption from this prohibition for live bovine animals will be
considered on a case-by-case basis considering the intended use of the
animals, for example, animals imported for a temporary stay; animals for
immediate slaughter; animals imported for medical use, scientific research
or zoological collections; bulls destined for semen production centers.

6.3.3. Meat and meat products from bovine animals other than deboned
skeletal muscle meat as defined in section 3 (g)

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.4.

6.3.4. Gelatin and collagen prepared from the bones of bovine animals

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.5.

6.3.5. Tallow (other than protein-free tallow as defined in section 3) and
dicalcium phosphate (other than protein or fat free dicalcium phosphate as
defined in section 3) derived from bovine animals

This commodity is prohibited from Category 3 countries (undetermined
BSE-risk).

6.3.6. For tallow derivatives (other than those made from protein-free
tallow as defined in section 3) derived from bovine animals and intended for
food, animal food, fertilisers, or as unprocessed material for the
preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.7.

6.3.7. Products derived from bovine animals by subjecting bones to rigorous
processes of extraction and purification such as ossein, bone ash, bone
charcoal and bone oil and intended for food, animal food, fertilisers, or as
unprocessed material for the preparation of cosmetics, drugs (including
pharmaceuticals and natural health products), medical devices or veterinary
biologics

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.8.

6.3.8. Products and by-products derived from bovine animals that have been
subjected to rigorous processes of extraction and purification such as
animal glue, oleosterin, triglycerides, glycerol, sorbitan esters and
intended for food, animal food, fertilisers, or as unprocessed material for
the preparation of cosmetics, drugs (including pharmaceuticals and natural
health products), medical devices or veterinary biologics

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.9.

6.3.9. Commercially prepared pet food and finished pet chews, such as dried
processed ears, pizzles, hooves or tendons

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.10.

6.3.10. Cell lines of bovine origin

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.11.

6.3.11. Veterinary biologics (vaccines, antibody products and diagnostic
kits) containing material of bovine origin intended for use in animals

The conditions set down for this commodity are the same as those specified
for a Category 2 country (controlled BSE-risk) in section 6.2.12.
Appendix 1
A. Determining the BSE-risk category of a country:

A risk assessment, to determine the BSE-risk status of the bovine animal
population and allocate an exporting country to a particular BSE-risk
category consists of four parts:

* Release assessment
* Exposure assessment
* Consequence assessment
* Risk estimation

A complete risk assessment should be undertaken for those countries that
have either not reported BSE-cases or have only reported BSE-cases in
imported animals. For countries that have reported BSE cases in indigenous
animals it may not be necessary to undertake a detailed release and exposure
assessment. Rather, a consequence assessment may be all that is required to
determine if BSE is being effectively controlled.

The risk assessment must be reviewed regularly to ensure that adequate
account is taken of changes in risk factors that could affect the BSE-risk
status of a country, including:

* the detection of BSE in a previously unaffected country that may have
exported commodities of concern to the country being evaluated;
* changes in the country's import policies and/or practices;
* data and/or information that was previously unavailable is provided;
* changes to the OIE Code;
* new scientific findings such as the confirmation of natural cases of BSE
in sheep;
* new diagnostic techniques, for example a live animal test;
* changes in assumptions;
* changes in the human epidemiology of BSE.

A.1. Release assessment

The release assessment determines the likelihood that a transmissible
spongiform encephalopathy (TSE) agent has been introduced into the exporting
country via importation of the following commodities potentially
contaminated with a TSE agent:

* meat-and-bone meal or greaves;
* live animals;
* animal feed and feed ingredients;
* products of animal origin for human consumption (with the exception of
those commodities that can be imported into or transit Canada without
BSE-related restrictions as listed in section 3);
* products of animal origin for in vivo use in bovine animals.

The range of commodities included here is based on a consideration that all
the evidence to date indicates that the vast majority of BSE cases have
arisen through the ingestion of animal food contaminated with the BSE-agent,
with vertical transmission from dam to offspring potentially accounting for
only a very small number of cases. Although there have been no reports of
BSE cases having arisen through the use of in vivo products contaminated
with a TSE-agent, considering the potential for widespread exposure, such
products also need to be taken into account.

Naturally occurring TSEs have been reported in several species from which
these commodities are derived. They are all members of the Order
Artiodactyla (even toed ungulates)5 and belong to the suborder Ruminantia
(the ruminants). The species involved are domestic cattle from the subfamily
Bovinae, which are affected by bovine spongiform encephalopathy (BSE);
domestic sheep and goats from the subfamily Caprinae, which are affected by
scrapie; and both wild and farmed deer and elk from the family Cervidae,
which are affected by chronic wasting disease (CWD). It is worth noting that
a naturally occurring TSE has not been reported in Camelids (llamas,
alpacas, vicunas and camels). While they are not classified as ruminants per
se they are closely related, belonging to the suborder Tylopda.

Apart from BSE none of these TSEs have been reported to affect species other
than their natural hosts under field conditions. BSE has been reported in
both domestic cats and a number of other species from the family Felidae
held in zoological gardens in the United Kingdom (UK). In addition BSE was
found in several ruminant species, also in zoological gardens in the UK.
These animals all belong to the family Bovidae6, the same family in which
cattle, sheep and goats are found. Recently, BSE was confirmed in a dairy
goat in France7. This was the first recorded naturally occurring case of BSE
affecting a commercially reared ruminant animal other than cattle.

Cross species transmission studies have demonstrated all of these TSEs are
capable of infecting species other than their natural host. For instance,
cattle are susceptible to experimental challenge with scrapie and CWD.
Similarly sheep and goats are susceptible to BSE8, 9 and recently BSE has
been confirmed in non-human primates (macaque monkeys) following oral
challenge10. However, significant uncertainty remains regarding the
likelihood of natural challenge and infection with these TSEs in non-host
species. Experimental challenge studies involving deer, elk and camelids
have not been reported in the literature to date. Although cattle have been
successfully challenged with CWD intracerebrally there appears to be a
significant species barrier. These findings are supported by field
observations over a number of years where cattle, which were co-pastured
with CWD-affected deer, did not develop the disease11. Whether or not this
is indicative of a species barrier in deer or elk for BSE is uncertain.

While the ultimate origin of BSE remains elusive there has been considerable
speculation concerning the role of a TSE agent from another mammalian
species such as scrapie in sheep12. In addition, readily commercially
diagnostic techniques that could easily discriminate between a TSE-agent
such as scrapie and BSE have not been validated until recently (2005) 13,
14.

Considering that:

* the origin of BSE remains uncertain;
* naturally occurring TSEs have been reported in a number of closely related
ruminant species;
* cross-species transmission studies have confirmed that at least several of
these species are susceptible to a TSE from another host species;
* significant uncertainty remains regarding the likelihood of natural
challenge and infection with any of these TSEs;
* tests that could discriminate readily between the various TSE agents have
not been commercially available until recently (2005).

the range of species to consider in the release assessment from which the
commodities listed at the beginning of this section are likely to be
derived, consist of the following animals, hereafter collectively referred
to as ruminants:

* bovine animals15
* sheep and goats
* deer and elk

Since BSE has a prolonged incubation period and by the time it is detected
in the bovine animal population it is likely to have been present for the
equivalent of two to three incubation periods16 or more, the release
assessment should extend back over at least the last 15 years and preferably
since the early 1980s.

Factors to consider in the release assessment include:

* the nature, extent and duration of past and current import legislation and
policies relative to the TSEs;
* whether any or all of the commodities being considered have been imported
from countries that have either reported a TSE in imported or indigenous
animals or from countries with an undetermined BSE-risk, and if so:
o the period during which these commodities were imported and their
respective quantities.

A.2. Exposure assessment

For the purposes of determining the BSE status of the bovine animal
population of an exporting country an exposure assessment:

* identifies and describes the biological pathways necessary for the
exposure of bovine animals to a TSE-agent through imported commodities
and/or from a TSE that already exists in the country's domestic or wild
ruminant population;
* determines the likelihood that bovine animals have been exposed to a
TSE-agent via these pathways;
* estimates the likely extent, timing and duration of exposure to a
TSE-agent in the bovine animal population.

The rationale for including all TSEs in the exposure assessment is based on
a consideration that significant uncertainties remain concerning:

* the origin of BSE;
* the potential for the BSE-agent to naturally infect species other than
bovine animals such as sheep and goats, which may then be indistinguishable
from scrapie;
* the potential for other TSEs, such as scrapie and chronic wasting disease,
to infect bovine animals naturally and be indistinguishable from BSE.

Factors to consider that would lead to the exposure of bovine animals in the
exporting country to a TSE-agent include:

* the intended use of imported ruminants or products derived from such
animals;
* the identification and tracking of imported ruminants including their
ultimate fate, whether they were tested for a TSE and if their carcass or
parts of their carcass potentially entered the animal feed chain;
* animal demographics which describes the extent of knowledge of the
population structure of ruminant animals including culling and slaughter
practices and disposal of dead or condemned animals;
* the epidemiological situation concerning all TSE-agents in the animal
population of the country;
* the nature, scope, duration and evidence of enforcement and/or compliance
with any legislation relative to TSEs including:
o control and/or eradication programs;
o controls over material potentially containing a TSE-agent such as a
specified risk materials (SRM) ban;
o controls over rendering methods and parameters;
o controls on the production, distribution and consumption of animal feed.
* the nature, extent and compliance with any bans, whether voluntary or
compulsory, on the feeding of material potentially containing a TSE-agent,
including meat-and-bone meal or greaves, to ruminant animals;
* measures to prevent cross-contamination of animal feed with material
potentially containing a TSE-agent , whether voluntary or compulsory and
evidence of enforcement and/or compliance;
* disposal practices:
o waste generated in slaughterhouses, meat processing facilities, domestic
households, restaurants or any other facility involved in the processing and
preparation of fresh meat and meat products that potentially contain a
TSE-agent;
o ruminant animals that die on farm, are dead on arrival in a
slaughterhouses and that are condemned at ante or post-mortem inspection.
* rendering practices including dedication of lines, facilities and the
parameters of the rendering process;
* methods of animal feed manufacture including ingredients and dedication of
lines or facilities;
* farming and husbandry practices that could lead to bovine animals
consuming feed potentially contaminated with a TSE-agent;
* measures to prevent the contamination of domestically manufactured
products destined for in vivo use with material potentially containing a
TSE-agent.

The risk assessment may be concluded at this point if the likelihoods of
both the release and exposure assessments are considered to be negligible.

A.3. Consequence assessment

A.3.1. For countries that have either not reported BSE-cases or have only
reported BSE-cases in imported animals

In this situation it is assumed that, if the outcome from the exposure
assessment is that the likelihood of bovine animals having been exposed to a
TSE-agent cannot be considered to be negligible, BSE infected animals are
likely to exist in the population.

A consequence assessment determines:

* the likelihood that BSE-cases would be detected if present in the bovine
animal population;
* the likelihood that any measures introduced for BSE, whether pre-emptive
or in response to the detection of BSE-cases in imported animals, would
effectively control BSE or lead to its eradication.

A.3.2. For countries that have reported BSE-cases in indigenous animals

A consequence assessment determines:

* the likelihood that current and past measures are either effectively
controlling BSE or will lead to its eventual eradication.

Factors to consider in addition to those listed under the exposure
assessment include:

* an evaluation of the capacity of a country's Veterinary Service and
legislative support for BSE surveillance, eradication and control;
* details and results of BSE control and/or eradication programs including
the measures taken in response to the detection of a BSE case ;
* opportunities for recycling and amplification of the BSE-agent through the
consumption by bovine animals of meat-and-bone meal or greaves, or other
feed or feed ingredients potentially contaminated with ruminant derived
meat-and-bone meal or greaves;
* the existence, duration and extent of on-going awareness program for
veterinarians, farmers, and workers involved in transportation, marketing
and slaughter of bovine animals to encourage reporting of all cases of
neurological disease in adult bovine animals and fallen stock;
* the existence and implementation date of compulsory notification and
investigation of all bovine animals showing clinical signs consistent with
BSE;
* the existence, duration and extent of BSE surveillance and monitoring
systems taking into account the guidelines in Appendix 3.8.4 of the Code;
* details of the diagnostic procedures for BSE, including:
o case definitions for BSE-suspects and surveillance candidates including
their age;
o whether an examination in an approved laboratory of brain or other tissues
is undertaken;
o the laboratory procedures for screening and confirmation of BSE.

A.4. Risk estimation

The criteria for determining the BSE-risk category of a country, based on
the outcomes from the release, exposure and consequence assessments are
outlined in the following sections:

A.4.1. Category 1. Negligible BSE-risk

*

a) For countries that have never reported a BSE-case
Either:
o If the conclusions of both the release and exposure assessment are
negligible the overall risk is estimated to be negligible and the country is
classified as negligible BSE-risk (Category 1).

Or:
*
o If the overall conclusion of the release and exposure assessment is
greater than negligible, but the likelihood of exposure during at least the
last 7 years is negligible, and the level of surveillance maintained during
throughout this period should have detected BSE cases if they were present,
the country is classified as negligible BSE-risk (Category 1).
*

b) For countries that have reported BSE-cases in imported and/or indigenous
animals

Before the country can be considered as presenting a negligible BSE-risk it
should satisfy each of the following conditions for a period of at least
seven years:

* the likelihood of imported commodities referred to in section A.1 being
contaminated or infected with a TSE-agent must remain negligible;
* the likelihood of bovine animals having been exposed to a TSE that exists
in the country's domestic or wild ruminant population must remain
negligible;
* the measures to eradicate BSE must be maintained to ensure that the
likelihood of bovine animals being exposed to a TSE-agent remains
negligible;
* a level of surveillance capable of demonstrating the effectiveness of
eradication measures has been maintained without the detection of any
BSE-cases.

A.4.2. Category 2. controlled BSE-risk:

If the conclusion of the risk assessment is that:

* it is likely that those commodities referred to in section A.1 were
contaminated or infected with a TSE-agent when imported, and/or;
* it is likely that a TSE exists in the country's domestic or wild ruminant
population, and;
* either indigenous BSE-cases have been reported, or it is likely that
indigenous bovine animals are likely to have been exposed to a TSE-agent,
and;
* the measures in place are effectively controlling BSE and are likely to
lead to its eradication;
* a level of surveillance capable of demonstrating the effectiveness of the
measures to control BSE has been maintained.

the country is classified as controlled BSE-risk (Category 2).

A.4.3. Category 3. Undetermined BSE-risk

If either:

* a risk assessment for a particular country has not been undertaken,
completed17 or subjected to a regular review

Or:

* the conclusion of the risk assessment is that:
o it is likely that those commodities referred to in section A.1 were
contaminated or infected with a TSE-agent when imported, and/or;
o it is likely that a TSE exists in the country's domestic or wild ruminant
population, and;
o either indigenous BSE-cases have been reported or it is likely that
indigenous bovine animals have been exposed to a TSE-agent, and;
o the measures in place are unlikely to effectively control or eradicate
BSE.

the country is classified as undetermined BSE-risk.

In those situations in which a risk assessment is no longer up to date,
provided that the assessment is reviewed with a favourable outcome, the
country may revert to its former status. For a country previously classified
as undetermined BSE-risk, provided that the measures are modified to ensure
that they would effectively control or eradicate BSE, the country could be
considered as presenting a controlled BSE-risk.

Original signed by
Dr. Jim Clark
A/Director
Animal Health and Production Division
Appendix 2
Glossary of legal definitions

Animal

* Health of Animals Act - includes an embryo and a fertilized egg or ovum.

Animal food

* Health of Animals Act - any thing that is capable of being a nutriment for
animals and includes any of the constituent elements of an animal ration
* Health of Animal Regulations - food containing an animal product or animal
by-product for chickens, turkeys, ducks, geese, ratites, game birds,
ruminants, swine or horses but does not include such things as fish meal or
vitamin or mineral supplements which do not contain animal products or
by-products.

Animal by-product

* Health of Animals Act - includes blood or any of its components, bones,
bristles, feathers, flesh, hair, hides, hoofs, horns, offal, skins and wool,
and any thing containing any of those things;
* Health of Animals Regulations - means an animal by-product that originated
from a bird or from any mammal except a member of the orders Rodentia,
Cetacea, Pinnipedia and Sirenia.

Animal product

* Health of Animals Act - includes cream, eggs, milk, non-fertilized ova and
semen;
* Health of Animals Regulations - means an animal product that originated
from a bird or from any mammal except a member of the orders Rodentia,
Cetacea, Pinnipedia and Sirenia.

Animal pathogen

* Health of Animals Regulations - includes any animal pathogen derived
through biotechnology.

Bovine

* Health of Animals Regulations - means cattle or bison domestically raised
or kept, but for the purposes of the import reference document does not
include a bison that has ever been in contact with or part of a wild herd.

Cosmetic

* Food and Drug Act - includes any substance or mixture of substances
manufactured, sold or represented for use in cleansing, improving or
altering the complexion, skin, hair or teeth, and includes deodorants and
perfumes.

Drug

* Food and Drug Act - includes any substance or mixture of substances
manufactured, sold or represented for use in (a) the diagnosis, treatment,
mitigation or prevention of a disease, disorder or abnormal physical state,
or its symptoms, in human beings or animals, (b) restoring, correcting or
modifying organic functions in human beings or animals, or (c) disinfection
in premises in which food is manufactured, prepared or kept.

Device

* Food and Drug Act - means any article, instrument, apparatus or
contrivance, including any component, part or accessory thereof,
manufactured, sold or represented for use in (a) the diagnosis, treatment,
mitigation or prevention of a disease, disorder or abnormal physical state,
or its symptoms, in human beings or animals, (b) restoring, correcting or
modifying a body function or the body structure of human beings or animals,
(c) the diagnosis of pregnancy in human beings or animals, or (d) the care
of human beings or animals during pregnancy and at and after birth of the
offspring, including care of the offspring, and includes a contraceptive
device but does not include a drug.

Food

* Food and Drug Act - includes any article manufactured, sold or represented
for use as food or drink for human beings, chewing gum, and any ingredient
that may be mixed with food for any purpose whatever.

Germplasm

* Health of Animals Regulations - means semen, male or female germ cells or
genetic material taken from a male or female germ cell for the purpose of
producing a zygote and includes embryos but does not include a hatching egg.

Meat

* Meat Inspection Regulations - means the edible part of a carcass tha
 
Meat

* Meat Inspection Regulations - means the edible part of a carcass that is
the muscle associated with the skeleton, tongue, diaphragm, heart, gizzard
or mammalian oesophagus, with or without accompanying and overlying fat,
together with those parts of the bones, skin, sinews, nerves, blood vessels
and other tissues that normally accompany the muscle and are not ordinarily
removed in dressing a carcass, but does not include the muscle associated
with the lips, snout, scalp or ears, mechanically separated meat or meat to
which an ingredient other than meat has been added.

Meat product

* Meat Inspection Act - means (a) a carcass, (b) the blood of an animal or a
product or by-product of a carcass, or (c) a product containing anything
described in (b);
* Meat Inspection Regulations - means edible blood, an edible organ or
edible tissue that was derived from the carcass of a food animal, but does
not include meat or mechanically separated meat.

Ruminant

* Health of Animals Regulations - means an animal of the suborder Ruminatiae
and includes an animal of the family Camelidae.

Specified risk material

* Food and Drug Regulations and Health of Animals Regulations - means (a)
the skull, brain, trigeminal ganglia, eyes, tonsils, spinal cord and dorsal
root ganglia of cattle aged 30 months or older; and (b) the distal ileum of
cattle of all ages.
o Through the application of the Meat Hygiene Directive (2003-18 of July 24,
2003), issued under the Meat Inspection Regulations, the tissues that are to
be removed to ensure that SRM are excluded consist of:
+ the skull including the brain, trigeminal ganglia and eyes, the tonsils,
the spinal cord and the vertebral column excluding the vertebrae of the
tail, the transverse processes of the thoracic and lumbar vertebrae, and the
wings of the sacrum from all cattle 18 aged 30 months or older;
+ the small intestine from cattle of all ages.
o For the purpose of this BSE import policy this same list of tissues, not
only from cattle but also from bison, is defined as SRM, that is:
+ the skull including the brain, trigeminal ganglia and eyes, the tonsils,
the spinal cord and the vertebral column excluding the vertebrae of the
tail, the transverse processes of the thoracic and lumbar vertebrae, and the
wings of the sacrum from all bovine animals aged 30 months or older;
+ the small intestine from bovine animals of all ages.

Veterinary biologic

* Health of Animals Act means (a) a helminth, protozoa or micro-organism,
(b) a substance or mixture of substances derived from animals, helminths,
protozoa or micro-organisms, or (c) a substance of synthetic origin that is
manufactured, sold or represented for use in restoring, correcting or
modifying organic functions in animals or for use in the diagnosis,
treatment, mitigation or prevention of a disease, disorder or abnormal
physical state, or the symptoms thereof, in animals;
* Health of Animal Regulations - includes any veterinary biologic derived
through biotechnology.

1 Integrated Taxonomic Information System.
http://www.itis.usda.gov/servlet/SingleRpt/SingleRpt

2 Products intended for human consumption from a Category 2 country
(controlled BSE-risk) or a Category 3 country (undetermined BSE-risk) must
not be prepared from material containing SRM or be derived from bovine
animals subjected to a stunning process, prior to slaughter, with a device
injecting compressed air or gas into the cranial cavity or to a pithing
process.

3 Details of the process deemed to be equivalent and supporting data and
references should be provided to CFIA for approval prior to the importation
of this commodity.

4 In some situations it may not be possible to complete the risk assessment
as a result of insufficient and or poor quality data.

5 The Ultimate Ungulate Page. http://www.ultimateungulate.com/index.html

6 OIE, Technical Disease Cards, BSE, 2004.
http://www.oie.int/eng/maladies/fiches/a_B115.htm Bovidae (domestic cattle,
nyala [Tragelaphus angasi], greater kudu [Tragelaphus strepsiceros] and
presumed similar origin for cases in gemsbok [Oryx gazella], Arabian oryx
[Oryx leucoryx], eland [Taurotragus oryx], scimitar-horned oryx [Oryx
dammah] and bison [Bison bison]). Felidae (domestic cat and presumed bovine
origin in cheetah [Acinonyx jubatus], puma [Felis concolor], ocelot [Felis
pardalis] and tiger [Panthera tigris]). Experimentally transmissible to
cattle, pigs, sheep, goats, mice, mink, marmosets and macaque monkeys.

7 EUROPA - Food and Feed Safety. BSE/Scrapie - TSE in goats. February 2005.
http://www.europa.eu.int/comm/food/food/biosafety/bse/goats_index_en.htm

8 Lasmezas CI. The transmissible spongiform encephalophathies. Rev. sci.
tech. Off. Int. Epiz., 2003, 22 (1), 23-36

9 Schreuder BEC, Somerville RA. Bovine spongiform encephalopathy in sheep?
Rev. sci. tech. Off. Int. Epiz., 2003, 22 (1), 103-120

10 Lasmézas CI, Comoy E, Hawkins S, Herzog C, Mouthon F, Konold T, Auvré F,
Correia E, Lescoutra-Etchegaray N, Salès N, Wells G, Brown P, Deslys J-P.
Risk of oral infection with bovine spongiform encephalopathy agent in
primates. The Lancet, Volume 365, Issue 9461, 26 February 2005-4 March 2005,
Pages 781-783

11 Salman MD. Chronic Wasting Disease in Deer and Elk: Scientific Facts and
Findings. J. Vet. Med. Sci. 65 (7): 761-768, 2003

12 Prince MJ, Bailey JA, Barrowman PR, Bishop KJ, Campbell GR, Wood JM.
Bovine Spongiform Encephalopathy. Rev. sci. tech. Off. Int. Epiz, 2003, 22
(1) 37-60

13 Heim D. Kihm U. Risk management of transmissible spongiform
encephalopathies in Europe. Rev. sci. tech. Off. Int. Epiz, 2003, 22 (1),
179-199

14 VLA lunches new discriminatort diagnostic test. April, 2005.
http://www.defra.gov.uk/news/2005/050404h.htm

15 In this policy the term bovine refers to animals belonging to the Genus
Bos, which includes cattle (Bos taurus and Bos indicus) and bison (Bos
bison).

16 The average incubation period is approximately 5 - 6 years.

17 In some situations it may not be possible to complete the risk assessment
as a result of insufficient and or poor quality data.

18 The Meat Hygiene Directive defines cattle as animals of the species Bos
taurus or Bos indicus; but not including other ruminants such as bison,
muskox, yak or water buffalo.

http://www.inspection.gc.ca/english/anima/heasan/policy/ie-2005-9e.shtml


http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retriev
econtent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/3/_th/J_2_9D/_s.7_0_A/7_0_1OB?
PC_7_2_5JM_contentid=2005%2F12%2F0543.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_p
arentnav=TRANSCRIPTS_SPEECHES&PC_7_2_5JM_navid=TRANSCRIPT#7_2_5JM

>>>The other thing I would tell you about Japan, and this is really unique
to Japan -- as you know we've agreed in this first phase with Japan to start
at meat from animals 20 months and under. And you're just not going to find
BSE there. It's just not there. So from a number of standpoints, I can
safely assure the Japanese consumer that beef is safe. <<<


r i g h t! kinda like the WMD issue and gitmo, no lies here either.


the myth that cattle under 30 months of age are free from BSE/TSE is just
that, a myth, and it's a false myth !


the youngest age of BSE case to date is 20 months old; As at: 31 May
2003 Year of onset Age youngest case (mnths) Age 2nd youngest case
(mnths) Age 2nd oldest case (yrs.mnths) Age oldest case (yrs.mnths) 1986
30 33 5.03 5.07 1987 30 31 9.09 10.00 1988 24 27 10.02 11.01(2) 1989 21
24(4) 12.00(2) 15.04 1990 24(2) 26 13.03 14.00 1991 24 26(3) 14.02 17.05
1992 20 26 15.02 16.02 1993 29 30(3) 14.10 18.10 1994 30(2) 31(2) 14.05
16.07 1995 24 32 14.09 15.05 1996 29 30 15.07 17.02 1997 37(7) 38(3)
14.09 15.01 1998 34 36 14.07 15.05 1999 39(2) 41 13.07 13.10 2000 40 42
17.08 19.09 2001 48(2) 56 14.10 14.11 2002 51 52 15.08 15.09(2) 2003 50
62 11.11 14.11

http://www.defra.gov.uk/animalh/bse/bse-statistics/bse/yng-old.html

http://www.defra.gov.uk/animalh/bse/index.html

The implications of the Swiss result for Britain, which has had the most
BSE, are complex. Only cattle aged 30 months or younger are eaten in
Britain, on the assumption, based on feeding trials, that cattle of that
age, even if they were infected as calves, have not yet accumulated
enough prions to be infectious. But the youngest cow to develop BSE on
record in Britain was 20 months old, showing some are fast incubators.
Models predict that 200-300 cattle under 30 months per year are infected
with BSE and enter the food chain currently in Britain. Of these 3-5
could be fast incubators and carrying detectable quantities of prion.

http://www.sare.org/htdocs/hypermail/html-home/28-html/0359.html

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


SO, with GWs BSE MRR policy, like i said, it is nothing more than a legal
tool to trade ALL STRAINS of this mad cow agent around the globe. WE know of
atypical TSE in USA via Marsh et al, and we know when USA scrapie is
transmitted to USA cow, it does not look like UK BSE. BUT what about Japans
beef brought into USA? seems they have atypical TSE in Japan cattle that is
in very young cattle and evidently, there TSE agent has even been detected
in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve), so why
would USA want to import that into USA$ With our much superior BSE/TSE
surveillance system in USA cattle and the fact we have had this fabulous
ruminant to ruminant mad cow feed ban in effect since 8/4/97, where no
cattle have been fed ruminant protein since then;-), why should we risk this
new phenotype of TSE to the USA, since we have all the other TSEs here in
the USA under control:-(not)$


Muscle tissue has recently been detected with PrPSc
in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve) of the
11th BSE
cow in Japan (Yoshifumi Iwamaru et al). also recently, Aguzzi et al Letter
to the Editor
Vet Pathol 42:107-108 (2005), Prusiner et al CDI test is another example of
detection
of the TSE agent in muscle in sCJD, Herbert Budka et al CJD and inclusion
body myositis:
Abundant Disease-Associated Prion Protein in Muscle, and older studies from
Watson
Meldrum et al Scrapie agent in muscle - Pattison I A (1990), references as
follow ;


PrPSc distribution of a natural case of bovine
spongiform encephalopathy

Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori-
kazu Imamura, Takashi Yokoyama and Morikazu Shinagawa

Priori Disease Research Center, National Institute of Animal Health, 3-1-5
Kannondai, Tsukuba 305-0856 Japan [email protected]

Abstract

Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes
progressive neurodegeneration of the central nervous system. Infectivity
of BSE agent is accompanied with an abnormal isoform of prion protein
(PrPSc).

The specified risk materials (SRM) are tissues potentially carrying BSE
infectivity. The following tissues are designated as SRM in Japan: the
skull including the brain and eyes but excluding the glossa and the masse-
ter muscle, the vertebral column excluding the vertebrae of the tail, spinal
cord, distal illeum. For a risk management step, the use of SRM in both
animal feed or human food has been prohibited. However, detailed
PrPSc distribution remains obscure in BSE cattle and it has caused con-
troversies about definitions of SRM. Therefore we have examined PrPSc
distribution in a BSE cattle by Western blotting to reassess definitions of
SRM.

The 11th BSE case in Japan was detected in fallen stock surveillance.
The carcass was stocked in the refrigerator. For the detection of PrPSc,
200 mg of tissue samples were homogenized. Following collagenase
treatment, samples were digested with proteinase K. After digestion,
PrPSc was precipitated by sodium phosphotungstate (PTA). The pellets
were subjected to Western blotting using the standard procedure.
Anti-prion protein monoclonal antibody (mAb) T2 conjugated horseradish
peroxidase was used for the detection of PrPSc.

PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal
ganglia, sublingual ganglion, retina. In addition, PrPSc was also detected
in the peripheral nerves (sciatic nerve, tibial nerve, vagus nerve).

Our results suggest that the currently accepted definitions of SRM in
BSE cattle may need to be reexamined. ...

179

T. Kitamoto (Ed.)
PRIONS
Food and Drug Safety
================


ALSO from the International Symposium of Prion Diseases held in Sendai,
October 31, to
November 2, 2004;


Bovine spongiform encephalopathy (BSE) in Japan


snip...


"Furthermore, current studies into transmission of cases of BSE that are
atypical or that develop in young cattle are expected to amplify the BSE
prion"


NO. Date conf. Farm Birth place and Date Age at diagnosis


8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23


9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21


Test results


# 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology
negative


b = atypical BSE case


c = case of BSE in a young animal


b,c, No PrPSc on IHC, and no spongiform change on histology


International Symposium of Prion Diseases held in Sendai, October 31, to
November 2, 2004.

The hardback book title is 'PRIONS' Food and Drug Safety
T. Kitamoto (Ed.)


Tetsuyuki Kitamoto
Professor and Chairman
Department of Prion Research
Tohoku University School of Medicine
2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN
TEL +81-22-717-8147 FAX +81-22-717-8148
e-mail; [email protected]
Symposium Secretariat
Kyomi Sasaki
TEL +81-22-717-8233 FAX +81-22-717-7656
e-mail: [email protected]


snip...end


THIS brings up about another 9,200 points of concern. IF you look above at
these two atypical TSE cows from Japan, (of which we could very well export
more just like it), please notice the testing protocol;


>>># 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology
negative <<<


9,200 points of mad cow concern is the fact the USDA et al DID NOT use rapid
TSE test OR WB test to test for BSE/TSE on 9,200 cattle, they used the least
likely to find the agent only, the IHC, of which, DID NOT show up on two of
those very young atypical positive Japanese cows, PLUS, like the one TEXAS
cow they did finally confirm after 7+ months of trying to cover up. besides
this, we have some 500,000 bse/tse test, the infamous June 2004 enhanced
BSE/TSE surveillance (cover-up) program, where here the testing protocol was
terribly flawwed on all these cows, where only IHC and rapid testing was
used, no WB. Dr. Detwiler warned of this problem way back;


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


National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC)
Testing Summary

The BSE enhanced surveillance program involves the use of a rapid screening
test, followed by confirmatory testing for any samples that come back
"inconclusive." The weekly summary below captures all rapid tests conducted
as part of the enhanced surveillance effort. It should be noted that since
the enhanced surveillance program began, USDA has also conducted
approximately 9,200 routine IHC tests on samples that did not first undergo
rapid testing. This was done to ensure that samples inappropriate for the
rapid screen test were still tested, and also to monitor and improve upon
IHC testing protocols. Of those 9,200 routine tests, one test returned a
non-definitive result on July 27, 2005. That sample underwent additional
testing at NVSL, as well as at the Veterinary Laboratories Agency in
Weybridge, England, and results were negative. ...


http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html


APHIS et al forgets to add here that on that one additional non-definitive
test of July 27, 2005, here again they could not use WB due to samples being
preserved. Here in 2005 we have still not gotten the proper BSE/TSE testing
protocol done correctly, after being told that we did since 1997.


hey, but its not about 'sound science' or 'human health'. GWs enhanced SRM
program was nothing more than commodities and futures in action;


Our analysis suggests that if all slaughter animals are tested, but

there is no increase in access to either the Japanese or

South Korean markets, the result would be a net loss of

$17.50 (the estimated cost of testing) per head. Alternatively,

if full access to the Japanese and South Korean

markets is regained without implementing a broad

based BSE testing program, the potential revenue gain

ranges from about $45 to $66 per head (Figure 1).


http://www.oznet.ksu.edu/library/agec2/MF2679.pdf


GW seems to get his cake and eat it too $

nothing like 'sound science' in this administration, to hell with human
health.


>>>Then you do a comparison of the countries. We have a herd size of about
90 million. We process about 30 million animals a year, thereabouts,
probably a little bit more than that. We've been able to identify since the
enhanced surveillance started one case that was actually so difficult to
find we had to test and test and test to find it even. <<<


IN TEXAS we feed our cattle 5.5 grams of potentially BSE/TSE tainted
protein, and that's o.k. per the FDA;


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


WE know what happens to most stumbling and staggering suspect mad cows in
TEXAS too. THERE tissue samples either sit up on a shelf for 7+ months
waiting for everyone to forget about, OR ;


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


WE know now, and we knew decades ago, that 5.5 grams of suspect feed in
TEXAS was enough to kill 100 cows.


look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;


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.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (icip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log.
icip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula


Published online January 27, 2005

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

It is clear that the designing scientists must

also have shared Mr Bradley's surprise at the results because all the dose

levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf


2

6. It also appears to me that Mr Bradley's answer (that it would take less
than say 100

grams) was probably given with the benefit of hindsight; particularly if one

considers that later in the same answer Mr Bradley expresses his surprise
that it

could take as little of 1 gram of brain to cause BSE by the oral route
within the

same species. This information did not become available until the "attack
rate"

experiment had been completed in 1995/96. This was a titration experiment

designed to ascertain the infective dose. A range of dosages was used to
ensure

that the actual result was within both a lower and an upper limit within the
study

and the designing scientists would not have expected all the dose levels to
trigger

infection. The dose ranges chosen by the most informed scientists at that
time

ranged from 1 gram to three times one hundred grams. It is clear that the
designing

scientists must have also shared Mr Bradley's surprise at the results
because all the

dose levels right down to 1 gram triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s147f.pdf


Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts

[BBC radio 4 FARM news]

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

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


2) Infectious dose:

To cattle: 1 gram of infected brain material (by oral ingestion)

http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml


SADLY, DEC 2005 SHOWS THAT WE STILL HAVE A SERIOUS PROBLEM WITH BSE/TSE MAD
COW DISEASE FEED

GAO


GAO-06-157R FDA Feed Testing Program

October 11, 2005


SNIP...FULL TEXT 29 PAGES ;


http://www.gao.gov/new.items/d06157r.pdf


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


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


http://www.fda.gov/cvm/5580.htm


[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. [[email protected]]

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

To: [email protected].

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=090007d48099
3808


http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d48
0993808


http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007
d48096b40d


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

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

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/eff9eff1f7c5cf2b87256ecf000df08
d?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?O
penDocument&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. [[email protected]] 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


still disgusted in cold cold Bacliff, Texas, dreaming of the warm Caribbean
Isands. take us away...


TSS

#################### https://lists.aegee.org/bse-l.html ####################


TSS


----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Saturday, December 10, 2005 9:04 PM
Subject: Gov't confirms dead cow in Hokkaido as 21st case of BSE


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

From: TSS ()
Subject: Gov't confirms dead cow in Hokkaido as 21st case of BSE
Date: December 10, 2005 at 6:45 pm PST

Gov't confirms dead cow in Hokkaido as 21st case of BSE


Sunday, December 11, 2005 at 06:40 JST
SAPPORO — Japan's agriculture ministry said Saturday a cow that died on a
farm in Chitose, Hokkaido Prefecture, earlier this week had bovine
spongiform encephalopathy, the 21st mad cow disease case reported in Japan.

The body of the cow was incinerated and meat from the carcass will not enter
the market, the Agriculture, Forestry and Fisheries Ministry said. The
Holstein cow, 5 years and 9 months old, was born before the government
banned the use of meat-and-bone-meal feed.

© 2005 Kyodo News. All rights reserved. No reproduction or republication
without written permission.

http://japantoday.com/e/?content=news&cat=1&id=358092


TSS

#################### https://lists.aegee.org/bse-l.html ####################

#################### https://lists.aegee.org/bse-l.html ####################
 
From: TSS
Subject: Beef-safety report being misused: panelist
Date: December 12, 2005 at 8:39 am PST

Beef-safety report being misused: panelist

By MAYUMI NEGISHI
Staff writer

The key messages in Thursday's report by the Food Safety Commission's prion committee have been misinterpreted by the media and the government, and the panel itself was used to serve political ends, the panel's deputy chairman declared Thursday.

Kiyotoshi Kaneko

In an interview with The Japan Times, Kiyotoshi Kaneko described his time on the panel assessing the risk of mad cow disease in North American beef as being "filled with a sense of helplessness."

Kaneko, professor and chairman of Tokyo Medical University's second department of physiology, helped draft the report that was finalized Thursday. The report states that the difference in mad cow disease risks posed by North American and Japanese beef is minimal, given certain conditions.

The report has thus been widely interpreted as a green light for lifting Japan's two-year ban on U.S. beef.

But Kaneko insisted: "The report does not recommend the resumption of U.S. beef imports. To say so is incorrect.

"The fact is that the renewal of beef imports was a diplomatic decision, made for us months in advance."

Kaneko said he fought tooth and nail for a clause in the Food Safety Commission's report stating that it is unclear whether the U.S. and Canada will be able to take adequate measures to minimize the risk of mad cow disease.

The clause is in the report, but Kaneko said it has been largely ignored in the coverage of the report's release.

"Regardless of the contents, Japan was ready to import beef," Kaneko said.

The report says the mad cow disease panel had to base its findings on the assumption that the U.S. would take measures to ascertain the precise age of slaughtered cattle and ensure that no high-risk parts would be included among imports.

The prion committee's job was problematic, Kaneko said, because it was given specific questions from the health and agriculture ministries. Namely, it was asked what the risk of mad cow disease would be if the U.S. were to only export beef from cows aged under 21 months, with high-risk parts removed.

"Answering only the questions the government gave us would mislead the public," Kaneko said. "That's not science."

He added that he does not intend to serve on any similar government committees again.

Debate over the past two years has left the public with the distinct impression that trade concerns override worries about food safety, he said.

That would be fine if the government had been up front about prioritizing trade concerns, explained why it thought trade was more important than food safety, and made it mandatory to label all beef with its country of origin, he stressed.

"When you lose people's trust, you've already failed at communicating risks. It's then your responsibility to regain that trust," Kaneko said, noting it will take years.

"The report is only a starting point. It's up to the Japanese government and ultimately the consumers to judge whether these conditions are being met."

The Japan Times: Dec. 9, 2005
(C) All rights reserved


http://www.japantimes.co.jp/cgi-bin/getarticle.pl5?nb20051209a1.htm


TSS
 
Here is a quote taken from:
"HALF LIVES, WARBLE FLIES AND GOVERNMENT LIES -THE DIRTY THREE PREREQUISITES THAT CAUSED BSE?" by Mark Purdey.

You can read the whole article at the link; http://www.markpurdey.com/news_the_cause_of_bse.htm

Note: the reference to Hokkaido, Japan - the location of Japan's newest case of BSE.

I have subsequently identified this same correlation between exposure to these munition metals and the vast majority of the outbreaks of TSE around the world. For instance, the largest cluster of new variant CJD in humans is located at Queniborough village in Leicestershire in the UK. This tiny village is sited one mile away from what was the largest munitions factory for the manufacture of detonators, triggers and chemical warfare agents in the UK – at East Goscote. Aerial photos indicate that during the 1950s, the munitions were actually stored along the edge of the lanes around Queniborough itself.

In Italy, I came across a cluster of CJD in humans who were all employed or connected to a munitions factory in the Po valley in Italy during the 1970s; as well as another cluster of 20 cases of CJD in a remote Calabrian village which had resulted from the contamination of the local water source by illegally dumped radioactive metals.

I unearthed another mysterious cluster of scrapie TSE that had emerged in sheep that were kept upon a block of common land at Ashoro in Hokkaido in Northern Japan – land which was formerly occupied by the Japanese military during world war two; where, according to the local farmers, many covert tests were carried out with "munitions". Sheep can no longer be pastured in this region, because they invariably contract scrapie. The correlations between TSEs and exposure to munitions are just too close for comfort.
 
EUROPEAN COMMISSION
HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL
Scientific Steering Committee
OPINION ON
ORGANOPHOSPHATE (OP) POISONING AND
HYPOTHETICAL INVOLVEMENT IN THE ORIGIN OF BSE
Background
In its opinion on possible links between BSE and Organophosphates adopted on 25-26 June
1998 and in its opinion on Hypotheses on the origin and transmission of BSE adopted on 29-
30 November 2001 the SSC concluded that there is no scientific evidence in support of the
hypothesis of an OP origin of BSE.
The issue of organophosphate poisoning has not been dealt with by the SSC so far. The
concerns expressed in the enquiries cover mainly intoxication by occupational exposure of
shepherds and farmers to OPs upon use against ecto-parasites, especially in sheep dipping and
treatment of cattle against Warble Fly infestation. Risks from residues are addressed to a
lesser extend.
In early 2003, a large number of additional enquiries on the issue have been addressed to
European Commission's Health and Consumer Directorate General. Four of these with
substantial enclosures were by one person. Most of them are addressing both issues: chronic
organophosphate (OP) poisoning and the origin of BSE.
Information provided with the enquiries
In addition to numerous newspaper and magazine articles the enclosures to the enquiries
provide the Material Safety Data Sheet on diazinon, the OHSA Occupational Safety and
Health Guideline for Tetraethylpyrophosphate (TEPP), an US agency Hazardous Substances
Fact Sheet on crufomate, company safety information sheets, some correspondence with UK
authorities including their activities to improve safe use of these chemicals. The information
regarding claimed OP chronic poisoning of cases presented does not provide evidence, neither
for OPs being the cause for diseases nor for their exclusion (i.e., "very low" bloodcholinesterase
levels, provided without data or comparison with the normal distribution of
values; successful treatment of a patient for OP clearance without giving any OP data). It
C:\WINNT\Temporary Internet Files\SSC_Last_OP_Final.doc 2
seems however, that due to insufficient, non-prudent use of the safety requirements undue
exposures of shepherds and farmers have occurred.
There is no additional information on the claimed involvement of OPs in the origin of BSE.
This applies for both, the hypotheses on the direct effect of OPs as well as on their
hypothetical role for Cu-deficiency to be involved in the origin of BSE (Cu binding of prion
protein is known). New publications are mentioned in one enquiry but they have not yet been
provided. In an Internet search no recent scientifically valid publications were traceable. The
SSC had been informed that research would be launched on this hypothesis, but no
information has been provided so far on its status or on results.
Conclusions
a) As regards the involvement of organophosphates in the origin of BSE, no new scientific
information providing evidence or supporting the hypothesis by valid data became
available after the adoption of the last opinion of the SSC on this issue. Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for registration of
plant protection products and veterinary medicines – addressed in the enquiries – provide
the basis for safe use of registered compounds and their formulations. Regarding the
alleged intoxication cases reported and OP exposure it must be concluded that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R., Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar, H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and transmission of BSE. Adopted
on 29-30 November 2001.


http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf




Volume 11: Scientists after Southwood
5. Challenges to the Government's approach
Mr Mark Purdey
Introduction
Discussion

Subject: O.P.'s Mark Purdey -- Vol.11 - 5. Challenges to the Government's approach





Volume 11: Scientists after Southwood
5. Challenges to the Government's approach
Mr Mark Purdey
Introduction
Discussion




Introduction

5.290 Mr Mark Purdey is an organic farmer who for many years was concerned about the use of organophosphorus compounds (OPs) for the treatment of cattle for warble fly infestation. In the early 1980s, prior to the emergence of BSE, Mr Purdey had entered into correspondence with the Animal Health Division of MAFF, highlighting his concerns about the use of OPs and seeking permission to use alternative warblecide compounds (see vol. 12: Livestock Farming, for details of the use of OPs in warble fly eradication programmes). He did not accept the assurances given to him by MAFF and, in 1985, sought a judicial review of the Warble Fly (England and Wales) Order 1982. Following an out-of-court settlement, he was exempted from treating his cattle with OP compounds. 1

5.291 To the present day Mr Purdey continues to argue the case for an OP-linked aetiology for BSE.


Mr Purdey's letter to Farmers Weekly proposing a link between OPs and BSE
5.292 Following the identification of BSE, Mr Purdey developed a theory that OPs had a possible role in the BSE epidemic. He set out his theory in a letter to the Farmers Weekly in January 1988. He highlighted the similarities between the pathological observations of BSE infected brain tissue and those of the nerve tissue of laboratory animals exposed to known OP neurotoxic agents. He wrote:

My own independent survey on some of the farms inflicted with this crippling neurotoxicity have revealed that warble fly liquids containing 'phosmet' and a brand of feeding stuff (compounded from insecticide-treated raw materials) are the common denominators upon these farms. Either, or both, of these inputs could serve as the delayed neurotoxic culprits to those genetically susceptible Holstein cattle bewitched by BSE. 2
5.293 Mr Purdey told the Inquiry that his independent survey consisted of telephoning five farmers who had cases of BSE on their farms in Devon. 3 He questioned the farmers about their feeding stuff policies and their use of warble fly treatment through the life of the cattle, including the time spent in utero. On the basis of his observations, he suggested a link between BSE and OP compounds.

5.294 The concluding paragraph of Mr Purdey's Farmers Weekly letter read:

Is Farmers Weekly for free thought and development of the farmer or for shielding the embarrassing hiccups boomeranging directly from the compulsory clinical regimes resurrected from the multi-national ministerial alliance?
5.295 Mr Purdey gave us an explanation of this passage:

I suppose I was - even then had a rather cynical view over this. It is the way that I perceived those ministerial bodies. I felt - I suppose I had a bit of a chip on my shoulder, but I think there was some sense to what I was saying that there did seem to be this cohesion between the interests of the multi-nationals selling chemicals and the Ministry of Agriculture, particularly at that time. A lot of the research that the Ministry was doing was always tailored on the side of looking at effects of agrochemicals, rather than looking at the alternative biological means of control. Being an organic farmer, this was obviously causing me a sort of problem. 4
5.296 Mr Purdey wrote a further letter to Farmers Weekly that was published on 3 August 1990 under the heading, 'Look for missing BSE link'. He said:

I find it interesting that the 250 or so cattle that have grown up through my dairy unit were consistently fed the brands of cake alleged to contain the BSE agent, yet not one of them has developed BSE symptoms. Perhaps the unique feature of my herd is that I have consistently refused and banned the use of anti-cholinesterase-based insecticides and wormers in my management. 5

Suspect BSE case on Mr Purdey's farm
5.297 On 14 July 1991, Mr Purdey wrote to Mr Keith Meldrum (CVO) outlining a suspected case of BSE in one of his cattle. He sought a guarantee that MAFF, once the afflicted cow was handed over for slaughter, would grant him access to the animal so that he could carry out an independent examination of its central nervous tissue. 6 He recognised that such work would have to be carried out at a MAFF or other specialist laboratory. He also outlined 'various correlations which suggests why BSE could be a sequel to an acute or chronic neurotoxic exposure some years previous to the surfacing of the outward symptoms.' He reiterated his claim that there were no other cases of BSE on his farm although the cattle had been fed with alleged contaminated feed.

5.298 Mr Meldrum replied to the letter on 25 July 1991 saying that under the terms of the Form A (under the slaughter and compensation scheme) Mr Purdey must surrender the carcass of the animal to MAFF and that they could not grant independent access for examination of central nervous tissue. 7

5.299 Towards the end of 1991, Mr Purdey wrote to his local DVO, Mr G W C Wilson, at MAFF's Taunton office. His letter included a suggestion that there was a connection between BSE and warble fly treatment. The letter was received on 22 November 1991. In his reply dated 25 November, Mr Wilson commented:

You also suggest that there is a correlation between BSE and warble fly eradication areas. I enclose extracts from the Chief Veterinary Officer's Annual Reports for 1984-1986, the years in which warble fly infected areas were declared. As you will see these areas are clearly defined and circumscribed. The incidence of BSE, both in location and in the number of cases per 1,000 of the cattle population, show no correlation with the warble fly infected areas.
Circumstantial evidence continues to indicate a food-borne origin ie scrapie-contaminated meat and bonemeal in cattle rations. This would also account for the considerable number of BSE cases born after the final warble fly infected areas in 1986. 8
5.300 In March 1992, an article by Mr Purdey entitled, 'Mad cows and warble flies: A link between BSE and organophosphates?' was published in The Ecologist. 9 The article stated that scientific establishments were ignoring the importance of genetic and environmental factors that could influence the chances of an animal succumbing to infection by the BSE agent. He presented data that he said demonstrated that, in some cases, there was a correlation between warble-fly eradication zones and incidences of BSE cases.

5.301 In addition, Mr Purdey suggested that TSEs were linked to other degenerative disorders such as Parkinson's and Alzheimer's diseases in the way that they developed. 10 He referred to a review article published in 1985 by Professor Gajdusek of the National Institute of Neurological Disorders, USA, which discussed the similarities between these diseases. Mr Purdey concluded his article by stating that 'a link between BSE and organophosphate treatments is more than plausible, yet MAFF refuses to carry out the necessary research to prove or disprove the OP theory'.

5.302 Mr Purdey entered into correspondence with Mr Tom King, his constituency MP, informing him of his concerns and theories in order that these matters could be brought to the attention of the Ministry. 11 Mr King subsequently wrote to Mr Gummer on 18 May 1992. In his reply of 8 June, Mr Gummer stated in relation to the suggestion that BSE was attributable to organophosphate compounds that 'on the information currently available to us, it is not possible to draw any conclusions in support of Mr Purdey's argument.' 12


Treatment of a BSE suspect with compounds used as antidotes for nerve gas
5.303 On 8 July 1992, Mr Purdey wrote to Mr Meldrum notifying him about a second suspect case of BSE in his herd. He demanded the right to treat the cow with compounds used as antidotes to nerve gas, to test it for OP toxicity, and, in the event of death, to examine the CNS tissue in a certified laboratory. 13

5.304 Mr Kevin Taylor briefed Mr Soames on this request in a minute on 13 July 1992. 14 He said of Mr Purdey that:

Although he claims that MAFF refuses to investigate the 'link' between BSE and OPs the original epidemiological study did in fact consider whether any chemical or medical treatment was the cause of BSE, and found no evidence to support the theory.
The CVO will reply to Mr Purdey. We have no objection to samples being taken from the live cow for analysis, or to delaying slaughter provided that the welfare of the animal is not prejudiced. A veterinary officer will make regular visits to assess clinical progress, as is done for any suspect where slaughter is delayed. If welfare considerations require, the cow will be slaughtered whether Mr Purdey agrees or not. The question of access to tissues post mortem is less easily resolved: Mr Purdey will be asked to provide more detail of what he proposes and where work will be done. The prevention of any risk to human or animal health will be paramount in any decision which is taken.
On past evidence Mr Purdey is likely to seek publicity about this case to further his arguments, and we believe that he has already contacted the Times. The July issue of Dairy Farmer also carried an interview in which he expounded his opinions, although this was written before his second suspect case occurred. Press Office are aware of the situation. 15
5.305 In a letter to Mr Purdey on 14 July, Mr Meldrum agreed to the tests being carried out and treatment given, on condition that the animal's welfare was not compromised:

. . . I do appreciate that your prime concern is that you are given the opportunity to carry out further investigations on the suspect to confirm your theories on organophosphorous toxicity. I have no hesitation in agreeing to your carrying out further tests on your animal while it is under restriction, with the proviso that it will be subject to regular clinical inspection by a veterinary officer. Our overriding concern is for the welfare of the animal, and if at any time it is deemed to be suffering unnecessarily, it will be slaughtered . . .
With respect to carrying out examinations on CNS tissue after slaughter however, I must ask for further information before agreeing to vary our procedures. Our primary concern at this stage is to investigate whether or not there are lesions in the brain which confirm the clinical diagnosis of BSE, and to conduct those investigations under conditions that do not prejudice animal or public health. We do this in our own laboratories by following strict protocols in controlled conditions, by exposing only those tissues needed for diagnosis, and by incinerating the headless carcass without further dismemberment . . .
I can assure you that we have not closed our eyes to the needs to individual farmers, or to the fact that symptoms characteristic of BSE may be caused by other syndromes. It is in our interest, as well as that of the owner, to permit differential diagnosis or treatment of the suspect while under restriction, subject to welfare considerations . . . None of our investigations, however, link either clinical signs or the development of lesions of BSE with prior treatment with organophosphorous drugs. 16
5.306 Mr Purdey's treatment of this second BSE suspect was the subject of much press coverage during mid-July 1992. On 13 July, Mr Kevin Taylor minuted those SVS staff likely to come into contact with Mr Purdey, and others in MAFF, stating that:

All involved in this case will be well aware that the situation is being milked for publicity by Mr Purdey, with enthusiastic support from Professor Lacey. As a result all we do is subject to constant scrutiny by those who will not hesitate to use any unwise action or careless comment for their own ends.
It is therefore essential that all staff who visit the farm, or who may be asked to comment, act with the utmost circumspection. No interviews should be given to TV, radio or the press, and requests should be immediately referred to the Press Office in Whitehall. Action on the farm and contacts with Mr Purdey should be restricted to those necessary to observe the development of clinical symptoms in a suspect animal (as on any other farm with a suspect), and to protect the welfare of the cow. This implies more frequent veterinary inspection than is usual, but this is made necessary by Mr Purdey's own demand that the animal be kept alive for treatment. The details and effectiveness of that treatment are a matter for Mr Purdey and his veterinary surgeon, not MAFF. Our concerns are BSE and welfare. 17
5.307 Mr Purdey told the Inquiry that the DVO at Taunton had agreed to his request to carry out a course of treatment on the suspect BSE cow. Further:

The DVO also said that he had no objection to delaying the service of the Notice of Intended Slaughter to allow treatment to take place, provided that the cow's welfare was not prejudiced. On 16 July I injected 'Damson' with oxime and atropine sulphate, pharmaceuticals carried by troops in the Gulf War as an antidote to nerve gas. Within 90 minutes the cow appeared to have remitted. On Friday 18 July Mr Budge, my vet and Mr Cohen, the MAFF vet, examined 'Damson'. Over the following weekend 'Damson''s condition deteriorated. I asked my vet to continue with the injections. On Monday 19 July Mr Cohen visited my farm and told me that 'Damson' should be put down. Mr Budge later arrived and said that he had to take further advice before reinjecting 'Damson'. On 20 July 'Damson' was down on the ground. I wanted to go to the High Court to force the Ministry to let me continue the treatment. Mr Cohen then paid me a further visit and I had no choice but to consent to 'Damson' being put down on welfare grounds. 18
5.308 BSE was confirmed in this cow by MAFF on 20 August. 19 Mr Purdey wrote to the Mr Wilson on 29 September about various aspects of 'Damson's' case. Mr Bradley replied to this letter on 5 November with the aim of following up and clarifying some of the statements Mr Purdey had made:

That your Jersey cow, Damson (RBSE 92/23076) had BSE confirmed is beyond dispute. You say you had assumed the cow had chronic OP-induced spongiform encephalopathy (SE) and this was supported by blood tests and response to 2 PAM and atropine. If you are satisfied and agree the final diagnosis of BSE so be it. However if you are suggesting that the cow had concurrent, chronic OP-induced SE we would like to see the supporting evidence for this conclusion with the agreement of your veterinary surgeon. This would include a clear description of the clinical signs (with dates of examination) the nature, result and interpretation of the blood tests, and when the blood samples were collected in relation to the clinical signs and treatments. 20
5.309 In his evidence to the Inquiry, Mr Purdey said that he supplied Mr Bradley with the appropriate details. 21

5.310 In his letter of 5 November 1992, Mr Bradley also referred to Mr Purdey's suggestions that MAFF should initiate some research into BSE. However, he said that Mr Purdey had presented no new evidence that suggested this would be necessary, but should he do so, his proposals could be reconsidered. He added:

However it would be helpful to us in considering any proposals for further research to have a clear statement of the objective or the hypothesis to test. 22
5.311 When asked about his reaction to this, Mr Purdey said:

I felt sort of that it was putting the onus on me to do the research, which - obviously I am a very small farmer and I have not got much money, so to do the sort of extent of tests that would be necessary to provide some sound scientific evidence that would in my mind spearhead MAFF to take it up was obviously out of my pocket. All I was able to do was to do what I had been trying to do, to test BSE cows on my farm in relation to the healthy cows on my farm. I felt I was in a no-win situation. I was limited in what I could actually do to achieve that requirement that Ray Bradley was putting on me. 23

Suggestions of maternal transmission
5.312 In April 1993, MAFF were notified by Taunton Animal Health Office that the offspring of a confirmed BSE-affected animal in Mr Purdey's herd, was showing symptoms of the disease. 24 A veterinary officer at MAFF, Mrs Helen Crea, and Animal Health Officer, Mr Keith Slater, examined the animal. They found that whilst it was in poor condition, the symptoms were only suggestive of BSE. A Form A notice was issued for the animal on 22 April, and its movement restricted accordingly. Mr Purdey claimed that this was the first example of maternal transmission and made this point to the Independent. 25 Subsequent inspections of this animal by MAFF officials on 10 May resulted in the lifting of the restriction since symptoms appeared to have subsided. 26 Mr Purdey wrote to Mr Prettejohn, his local Divisional Veterinary Officer, stating that he was unhappy with this decision and he maintained his conclusion that the cow had been affected in-utero. 27 The cow however recovered and continued milking on the farm. 28


Tom King writes to MAFF Ministers about Mr Purdey's views
5.313 On 5 April 1993, Mr Tom King sent to Mr Gummer a letter that he had received from Mr Purdey. Mr Purdey's letter contained details of his theory that OPs caused BSE, and suggestions of a link between CJD and the use of serotonin agonist drugs for the treatment of hypertension. He had also enclosed a letter from Professor Satoshi Ishikawa of Kitasato University, who considered that Mr Purdey's description 'about Mad cows to organophosphates compounds and warble fly is exactly true' and expressed interest in the similarity between the histopathology of BSE and chronic OP poisoning. 29

5.314 Mr Gummer replied to Mr King on 16 April, saying that detailed studies of cattle with BSE had 'not shown any connection between the use of such chemicals, either in a primary or contributory role'. He also remarked, in relation to CJD, that 'the Department of Health are not aware of any links between drugs used in the treatment of hypertension and the subsequent development of CJD-like illnesses'. 30

5.315 In relation to Professor Ishikawa's remarks, Mr Gummer commented:

Whilst it is true that there are superficial similarities in the histopathology, as observed under light microscopy, of the lesions in brain tissue of animals affected by organophosphate toxicity and spongiform encephalopathy disease, there are clear and important differences in the ways in which the nerve cells are affected. These differences are agreed and have been extensively studied and documented by neuropathologists. 31
5.316 Mr Gummer concluded his letter by commenting that much research was underway to investigate the many aspects of this group of diseases. He enclosed an interim report describing research that was underway which he thought Mr Purdey might find interesting.

5.317 In evidence to the Inquiry, Mr Purdey described his reaction to the letter:

Well, when I read the list of research that was being carried out, I could not see anything at all that was relevant to my hypothesis, nothing at all. It seemed to be all tailored to investigate the official scrapie leap theory as the cause, and some work on the prion protein, but that obviously involved - you know, they were saying that the abnormal prion from sheep had jumped into cows and mutated, or whatever it was. 32
5.318 On 17 May, Mr King sent a further letter that he had received from Mr Purdey, to Mr Gummer. Mr Purdey said that he did not think that the studies initiated by MAFF at the outset of investigating BSE were sufficient to determine whether chronic or delayed OP toxicity played a role in either triggering or exacerbating the disease. He also said that Mr Wilesmith's report that no correlation between BSE and acute exposures to OPs could be identified, did not rule out what he considered to be the most likely cause, namely chronic OP poisoning. Further he said:

From international research into chronic OP toxicity in humanity (Professor Ishikawa is a renowned expert in this field), there are more than (as the Department terms it) just "superficial similarities" in the lesions and pathogenesis of BSE. 33
5.319 On 16 June Mrs Gillian Shephard, the new Minister of Agriculture, replied to Mr King. She commented that:

Although OPs can react with a variety of biological substances, I am advised that OP poisoning differs so greatly from BSE that the link is most unlikely. Clinically, OP poisoning is so dissimilar to BSE that the two are unlikely to be confused, and there is no evidence to link any immunotoxic or mutagenic effects of OPs with BSE. 34
5.320 Mr Purdey said in evidence that he did not agree with Mrs Shephard's comments. He continued:

. . . she had not differentiated between acute OP poisoning and chronic OP poisoning, which show markedly different symptoms and pathology. It was a mainstay of my theory that this was a chronic problem, if you like, a high dose chronic problem. And this had been sort of ignored. This vague generalisation was in a sense a misrepresentation of what I was actually saying. Also, I can never recall having linked the immunotoxic effects of acute high doses of organophosphates to BSE because work has shown that in mice the immune system is actually required for the disease process to ensue, because when they have engineered mice with an immune knock-out, they cannot develop the disease. 35

Article in the Sunday Telegraph about OPs
5.321 On 22 August 1993 an article by Mr Greg Neale, the Environment Correspondent, was published in the Sunday Telegraph. 36 The article stated that:

The Government is reviewing the safety of chemical veterinary products, including some used in the home, amid fears that they could be linked to illness in farmers using sheep dip, or even bovine spongiform encephalopathy - BSE or 'mad cow' disease.
Gillian Shephard, the Agriculture Minister, has ordered the review of all veterinary products containing chemical organophosphates (OPs) including flea collars used on cats and dogs as well as on cattle and sheep.
5.322 The article continued:

An Agriculture Ministry spokesman said yesterday that the review did not mean there were grounds for linking 'mad cow' disease with OPs, as has been suggested by some researchers.
5.323 Mr Purdey commented in his evidence that:

I did not know anything about it at all. Certainly in relation to BSE, I was not aware that there was any proposed review into looking at the chemicals as a possible link to BSE or CJD. 37

Further correspondence with Mrs Shephard
5.324 On 1 Sept 1993 Mr King sent a letter to Mrs Shephard, enclosing a letter from Mr Purdey requesting a meeting with her to discuss his theories. 38 Mrs Shephard replied to Mr King on 17 Sept 1993 saying that:

In view of the highly technical nature of the issues involved, I suggest that Mr Purdey should meet my scientific advisors so that he can fully explain his views and they, in turn, can raise any points which they may have for Mr Purdey to consider. 39
5.325 Mrs Shephard also proposed that Mr Purdey:

. . . supply a pre-publication copy of his paper for distribution to the appropriate experts on a strictly 'In Confidence' basis (as is usual with such papers), then this would also facilitate the understanding of his hypothesis.
She suggested that he write to Mr Adrian Dixon of the Animal Health (Disease Control) Division to make arrangements for the meeting.

5.326 On 30 September 1993, Mr Purdey wrote to Mr Dixon as proposed noting that he had asked Mr King to forward his pre-publication paper. He also set out a suggested format for the proposed meeting. 40

5.327 In October 1993, Mr Purdey sent his pre-publication paper to Mr King, who in turn forwarded the paper to Mrs Shephard. 41 In her letter to Mr King of 14 October, Mrs Shephard confirmed that the paper had been sent to the Veterinary Medicines Directorate and that 'his [Purdey's] points will be noted and borne in mind during the consideration of the OP sheep dip issue by the Veterinary Products Committee'. 42

5.328 At around this time, MAFF complained to the Press Complaints Commission about a Sunday Telegraph article which, amongst other things, had advocated 'a theory that the symptoms of BSE result from organo-phosphorus poisoning rather than from a transmissible disease agent'. 43 Mr Purdey told us:

The Ministry had complained to the Press Complaints Commission about articles by Christopher Booker in the Sunday Telegraph which had supported my theories on BSE and which had criticised MAFF staff. The Ministry included an evaluation of my theories and they included an extract of the paper, which I had sent to the Minister. Mrs Shephard wrote to Mr King MP about this on 13 December 1993 and in the circumstances said that they did not regard what they had done as a breach of confidence. I did not accept this understanding of the situation. 44
5.329 On 13 December, Mrs Shephard wrote to Mr King apologising for any misunderstanding about the handling of Mr Purdey's paper. She said, however, that she did not construe the use of the material as a breach of confidence. She said that a meeting would take place on 17 January 1994 to enable Mr Purdey to discuss his paper. She noted that '[we] have gone to a great deal of trouble to assemble a team of experts in the wide range of fields covered by Mr Purdey's paper, including the flying in of an expert from the NPU in Scotland'. 45


Meeting between Mr Purdey and MAFF
5.330 The meeting arranged by Mrs Shephard took place at the CVL on 17 January 1994. 46 It was chaired by Mr Eddy and attended by Mr Purdey, his brother Mr Nigel Purdey, Mr Wilesmith, Mr Bradley, Mr Jackman, Mr Livesey, Mr Austin, Dr Hope from the NPU, Mr Salahud Din, Dr Marrs from DH and Dr Woodward. Mr Purdey explained his theory that OPs had caused BSE by mutating the PrP gene or by action at the level of transcription or translation, and that the disease had become an epidemic because of recycling animal waste into cattle feed. Mr Wilesmith said that he had considered the use of OPs as a possible cause of BSE in his early epidemiological investigation, but had ultimately rejected it since no correlation between OP usage and BSE incidence was found. A lengthy discussion followed where Mr Purdey's theories were considered individually in terms of existing scientific evidence. Mr Purdey said that his objective had been to stimulate MAFF interest in his theory and consider the possibility of research into it. He did not suggest avenues of further research. It was agreed to look further into Mr Purdey's theories, especially in relation to pesticide-contaminated citrus pulp and cereal by-products, though specific research was ruled out.

5.331 A minute from Mr Eddy to Ms Mannix in the Press Office on 17 January 1994, described the meeting as amicable and as one which had resulted in agreement between MAFF and Mr Purdey on three matters, namely:

that the risk to humans is remote; that the present regulations are adequate to control the disease in cattle and that the number of cases is declining; on the importance of recycled animal protein in the spread of disease.' 47
5.332 In evidence to the Inquiry, Mr Purdey said in relation to the third point: 'I did agree I felt it had a role, but I would not say I felt it was quite as important as the Ministry considered it.' 48

5.333 In June 1994 Mr Purdey published in the British Journal of Nutritional Medicine his paper entitled, 'Are Organophosphate Pesticides involved in the Causation of Bovine Spongiform Encephalopathy (BSE)? Hypothesis Based upon a Literature Review and Limited Trials on BSE Cattle'. 49 The paper described the various elements of the theory of OP-induced disruption of prion protein synthesis as a cause of BSE, the different sources of OPs and the role of magnesium and calcium. Serotonergic deficits, genetic susceptibility, and possible auto-immune responses were also described. Mr Purdey concluded that the best way of preventing neurodegenerative disease would be by rigorous screening of chemicals before they are approved.

5.334 On 2 June 1994, Mr Eddy wrote to Mr Purdey, following up various issues raised at the January meeting along with further points raised by Mr Purdey in subsequent letters to MAFF. 50 Mr Eddy said:

The idea that you mentioned in your letters of in vitro experiments is certainly an interesting one, but as you will no doubt recall at the meeting, there is no obvious model system which could be used at the present time to do these experiments, nor as I understand it, do you have any unique or particular chemical from the OP family which you hypothesise as the responsible agent which could be tested. Screening all OP agents, and all possible contaminants, and synergistic effects of combinations of chemicals would of course lead to an impossibly complicated set of experiments.
5.335 Mr Eddy went on to address specific points which he had promised to look at during the January meeting. Mr Purdey had been concerned about OP build up in citrus pulp, a major component of animal feed. Mr Eddy said that if the OP content of citrus pulp was responsible for the initiation of BSE, it was unlikely that BSE occurred only in the UK, since citrus pulp is an imported feedstuff. Mr Purdey had also expressed concern about pesticides binding to grain. Mr Eddy said that some residues bound to grain and some of these were toxicologically active if digested and absorbed. He went on to say:

'Legislation is based on concentrations of free (unbound) residues. Research carried out by the Central Science Laboratory of MAFF has shown OP residues in grain could cause underestimation of total OP concentration by up to 1.5ppm. That is an acceptable error because the UK maximum residue levels (MRLs) for the OP commonly used in grain are 10 ppm except for malathion, for which the MRL is 8ppm.'
5.336 Mr Eddy concluded that:

I have to say that we remain of the view that the probability of OPs having caused BSE is very low, because the toxicology of OPs has been very extensively studied and their usage is worldwide. The epidemiological and pathological findings simply do not support this hypothesis.
5.337 Following this letter, Mr Purdey wrote to Mr William Waldegrave, the new Minister of Agriculture, on 8 July expressing his disappointment at the response from MAFF and his suspicion that his requests for further research were being deliberately misunderstood. 51 He then went on to outline his theories.

5.338 Replying for the Minister, Mr Adrian Dixon assured Mr Purdey that his work was not being dismissed outright and that significant consideration had been given to it. 52 The main scientific points of Mr Purdey's letter were considered and answered. Mr Purdey was reminded that the epidemiological evidence still supported the food-borne hypothesis for the origin of infection and was not discredited by the incidence of diseased animals born after the feed ban. Mr Purdey's theory with respect to OP use could not, however, explain the epidemiological observations.

5.339 Additionally, Mr Dixon expressed confusion as to an apparent change in Mr Purdey's hypothesis, which suggested that disease was induced by a chemical-only mechanism as opposed to earlier assertions that it was caused by the interaction of OPs with the scrapie-like agent. On the matter of similarities between chronic OP poisoning and BSE, Mr Dixon relayed his advice that major differences existed between the clinical and histopathological aspects of the two conditions. In reply to Mr Purdey's request for PrPc, he was told PrPBSE was available for research purposes and was advised that, should he wish to use this reagent, he should submit a written research proposal to the Ministry.

5.340 Mr Purdey wrote to MAFF again on 15 and 27 October 1994. Mr Dixon replied on 10 November 1994 explaining again that Mr Purdey's theories could not adequately explain the occurrence of BSE. Mr Purdey was advised to apply for funding by contacting Dr MacOwan. He was also told that his research proposals stood a better chance of being viewed favourably if he would collaborate with a scientific body of reputable standing. 53


Correspondence with Dr Stephen Whatley
5.341 During 1995, Mr Purdey contacted Dr Stephen Whatley, a researcher at the Department of Neuroscience, Institute of Psychiatry in London. 54 Dr Whatley told us in oral evidence that Mr Purdey had written to him asking him if he was interested in testing Mr Purdey's theories. This appeared to be as a result of MAFF suggesting that he ought to ally himself with somebody who was more experienced in the field of research. Dr Whatley looked at Mr Purdey's paper and found it very difficult to understand, but felt that there was perhaps 'perhaps a core there that required some explanation'. The paper was later published in 1996. 55

5.342 Dr Whatley recalled that in the course of correspondence with Mr Purdey, he suggested various avenues for him as to how the theory could be tested. Mr Purdey eventually decided that it might be possible to do some research in the laboratory. When Mr Whatley explained how things worked in a scientific laboratory, he thought that Mr Purdey had probably been dissuaded, and because of his inexperience, decided to try to raise some money to fund research instead. 56


MRC experiments into the link between OPs and BSE
5.343 On 28 April 1995, an article appeared in Farmers Weekly stating that the MRC would be involved in preliminary trials to test the link between OPs and BSE. 57 The article stated that:

The trial will determine whether OPs can bind to normal prion protein and then convert it into the 'mutant version'. If this is the case then it will also test whether the deformed protein is itself the BSE agent and if it is infectious.
5.344 Initially, it was proposed that the work be funded by Channel 4, with the intention that the results could be used in a programme about Mr Purdey as a lone voice against the scientific establishment. However, in contrast to the claims made by Farmers Weekly, the experiments would only test whether OPs bound directly to the prion protein. 58

5.345 On 12 May 1995 Dr Ray of the MRC Toxicology Unit wrote to Mr Nigel Gregory of Lauderdale Productions, confirming that the experiment was still valid as planned. 59 He added that the statement made in Farmer's Weekly that Mr Purdey had 'strong support from the establishment' was 'rather overstated'. He also said that he had:

. . . been in touch with MAFF to clarify that I am only involved in testing those first steps of his hypothesis which relate to the organophosphate-protein interaction, and not with the question of infectivity.
5.346 The report of the experiment was published on 28 July 1995. 60 It concluded that the experiment:

. . . provides no evidence that any part of the protein would represent a particular target for organophosphorous compounds in general.
5.347 Mr Purdey disputed these results. In a letter to Mr Tom King, he voiced his concerns and requested that MAFF should appraise the MRC results and continue with further research. 61 Mr Purdey also suggested that MAFF was changing its own theories on BSE, by suggesting that very small oral doses of BSE were rendering cattle susceptible to infection. He proposed that this undermined the position of MAFF with respect to foreign cattle, which during the 1980s had been fed UK derived feed and had not shown signs of BSE. On 12 September 1995 Mr King wrote to Mr Douglas Hogg, who had succeeded Mr Waldegrave as Minister of Agriculture, Fisheries and Food, relaying Mr Purdey's concerns. 62

5.348 On 17 October Mr Hogg replied to Mr King expressing surprise that Mr Purdey should need MAFF to interpret the results of the experiment that he had designed to test his theories. 63 He also suggested that since MAFF did not subscribe to the OP theory, there was no reason to carry out further experiments to substantiate the MRC findings. Mr Hogg also rejected claims that MAFF had altered its theory on the cause of BSE.


Channel Four programme on BSE and Mr Purdey's theories
5.349 On 26 July 1995, Mr Hayward sent a minute to Mrs Browning making her aware of the forthcoming Channel Four programme which would discuss Mr Purdey's theories on the cause of BSE. 64 It was noted that the programme would like to interview Mr Wilesmith. It was agreed that this would be agreeable as long as certain conditions were met, such as provision of a set of pre-interview questions.

5.350 On 25 September 1995, a further minute from Dr Render was sent to all interested parties, including the Minister and the Minister of State. 65 It described the background to the story and noted that:

It is unlikely that the programme will raise concerns about a link between BSE and risks to human health. Mr Purdey has previously confirmed to officials in MAFF that he does not feel that our measures to protect human health need strengthening.
5.351 The Channel 4 programme ('Frontline') was shown on 27 September 1995. In the programme, Mr Purdey asserted that the MRC results did in fact show the modification of PrP by OPs. Reviews of the programme appeared in The Times and the Daily Mail. 66 Following the broadcast, Dr Ray from the MRC was interviewed on 'Farming Today'. 67 He expressed the opinion that the programme gave a distorted view of OPs, incorrectly linking the toxicity of OPs with long-term disease shown in only a few people. Dr Ray explained the experiment to us in the following terms:

We looked at the prion protein in two different forms, one more soluble than the other, and we made a comparison between that and acetylcholinesterase. Now acetylcholinesterase is the known target for acute toxicity. What we wanted to do was to make a relative comparison between the susceptibility of the prion protein and the acetylcholinesterase. Because it is possible to wind up concentration of the toxic agent so high that it becomes irrelevant to any kind of human or animal toxicology, it is best to have an internal reference. We used, therefore, acetylcholinesterase as an internal reference. If you look at the numbers, you can see that with acetylcholinesterase, there was a concentration of the protein-related increase in radio-labelling which went up to about 4,000 or 5,000 in one case, or about 8,000 counts in the other case.
MR WALKER: That other case is marked 'A' and 'B'?
DR RAY: Acetylcholinesterase A and acetylcholinesterase B. When you look at the case of the prion protein, you will see there is not this large increase. There appears to be a very small, possibly suggestive, possibly significant, possibly not increase at the very highest concentration, but at most this is about 1,000 times smaller than the increase in counts with the acetylcholinesterase. Therefore I concluded that there was no significant interaction with the prion protein. 68

Further correspondence with MAFF
5.352 On 1 January 1996, Mr Purdey wrote to Mrs Angela Browning, the Parliamentary Secretary at MAFF. 69 He made an accusation that MAFF deliberately misrepresented his theories to others. In addition to restating his central theories, he criticised the MRC experiments, first for not using Phosmet and second on the basis that the experiments that were carried out would not address the mechanism by which disruption of the tertiary structure could affect PrP.

5.353 Mrs Browning replied on 1 February 1996. 70 The letter reaffirmed the previous position of MAFF and reasserted the advice received from SEAC. The letter also discussed the research carried out by the MRC in collaboration with Mr Purdey, stating that 'it is not the case, contrary to what you allege, that the Government "hijacked" this research'.


Discussion

5.354 Mr Purdey believed that OPs could cause delayed neuro-toxic effects, and based his evidence of a link between OPs and BSE on the correlation between warble-fly eradication zones and the incidence of BSE. Later, he proposed that the OP-induced toxic effect led to the conversion of PrPc to the disease-producing PrPSc. We are not in this volume concerned to explore the technical aspects of Mr Purdey's theories about the connection between OPs and BSE. These have evolved over time, and are considered in vol. 2: Science. Here we are concerned with suggestions made by Mr Purdey and many of his considerable following to the effect that MAFF were blinkered in that they were not prepared to consider any possible cause of BSE other than their own theory that it resulted from contaminated feed.

5.355 Mr Purdey wrote to various MAFF officials and to his MP, Mr Tom King, in April 1993 about his theory that OPs caused BSE. He was concerned that MAFF were not responding to his ideas by initiating appropriate research, and wrote to Mr William Waldegrave in July 1994 indicating his disappointment.

5.356 In April 1995, the MRC Toxicology Unit agreed to undertake an experiment to determine if OPs could bind to prion protein and convert it to the disease-producing isoform, PrPSc. By July 1995, the result of this experiment was known and this indicated that OPs did not convert normal prion protein into PrPSc.

5.357 No further experiments were made to test the OP hypothesis until after March 1996 when Dr Stephen Whatley tested the effect of OPs on a neuroblastoma cell line. The only observed effect was an increase in the expression of normal PrP. If such occurred in vivo in the brain it was theoretically possible that OPs could be a factor in susceptibility to the BSE agent. This type of effect could be tested by experiments in mice to determine if treatment with OPs reduced the incubation period following intracerebral inoculation with BSE.

5.358 Mr Purdey is an unusual farmer. Although not a scientist, he has mastered much of the complex science relating to TSEs. His general concern about the use of OPs as a systemic treatment of cattle is not irrational. Nor are his theories of the link between this treatment and BSE.

5.359 MAFF did not reject these theories out of hand, but considered that the epidemiology was not consistent with the observed cases of BSE being induced by treatment with OPs. Mr Purdey came to accept that feed was the significant factor in the recycling of BSE, but persisted in his view that OPs could have been responsible for the original outbreak. More recently, he has suggested that the effect of OPs could increase the susceptibility of cattle to contracting BSE. Dr Whatley's limited experiment lends a modicum of support to this possibility.

5.360 We would commend Mr Purdey for the tenacity with which he has pursued his theories in the public interest. We understand that this has involved him and his family in financial sacrifice. We have considered the manner in which he, and his theories, were treated by Government scientists and have concluded that they received fair consideration. At times his persistence irritated MAFF officials who believed that he was barking up a number of wrong trees. To an extent they were correct, but the door is not yet closed on the possibility that OPs played a role in rendering cattle susceptible to BSE infectivity.



http://www.bseinquiry.gov.uk/report/volume11/chaptec5.htm#482213





transmission studies do not lie, amplification and transmission!!!




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





amplification and transmission is what we must stop now, and we know how to do it. we just have to do it.

the origin of the agent, would be nice to know, but this is not what is as important to _me_ , amplification and transmission (routes and sources) must take priority.

transmission studies prove this. ...TSS
 
I would say the most important factor in Mark Purdey's hypothesis, is he does not make stark statements which rule-out any factors without the evidence to do so. Unlike the UK government, who refuses to do the science behind Mark's hypothesis, whether on living cattle, cultured cells , or Genetically Modified mice. Just because no science existed to prove a link at a "specific time period", does not mean that the science was there to disprove it.

How can anyone call his observations unfounded? He has travelled to dozens of TSE hotspots (which is high-lighted by the article link which I posted above:
"I unearthed another mysterious cluster of scrapie TSE that had emerged in sheep that were kept upon a block of common land at Ashoro in Hokkaido in Northern Japan – land which was formerly occupied by the Japanese military during world war two; where, according to the local farmers, many covert tests were carried out with "munitions". Sheep can no longer be pastured in this region, because they invariably contract scrapie. The correlations between TSEs and exposure to munitions are just too close for comfort."

Mark pegged this place as a scrapie/military area (Hokkaido) over one year ago (Aug. 2004 is when he published this article).

In Mark's case, there is ever-more science coming forward connecting the importance of a proper Cu homeostasis in the brain. As well as the effects of sonication on PrP, the tertiary structure, et. al changes caused by manganese replacement of Cu (copper).

There is a great cloud of suspicion hanging over any government that refuses to do some simple testing to prove him wrong.

If this disease was caused and progressed, by the same set of criteria every single time, we would have the answer by now. But since it is highly more likely that a multitude of factors relate to the cause/initiation of, and progression of these misfolding protein diseases - we need to be a heck of a lot more open-minded than flounder, and all the others out there who have made up their minds (closed their minds) to any other possiblities other than the "infectious protein".

There is no debating with a closed mind.

Mark Purdey has no one to answer to, but himself. He is lucky in that sense, as most of the scientists out there are beholding to some company for funding their research.

Ask anyone working in the research field, whether their results are being nudged in a specific direction? How many scientists get more work/funding when they come out with research which conflicts with the expected results?

How many times have you been told you shouldn't do this or that, because someone else said it was a stupid idea? The power of suggestion, has been a menacing force in stopping all kinds of research and good ideas.
 
kathy writes;


> The power of suggestion, has been a menacing force in stopping all kinds

> of research and good ideas.


this is not about good ideas and bad ideas. it's about science.
'sound science'. no sound science with ops being the cause of
all human/animal TSEs. it's just not there no.

nothing suggestive about TSE aka mad cow transmission studies.
transmission studies do not lie. no OPs in transmission studies either.
so, nothing suggestive here as far as 'sound science'. ''amplification and transmission'' are key to stopping this agent. ...


TSS
 
What is the true agent of this disease? A protein, a metal, a metalliod?

There can be no true control of the agent, without an absolute understanding of what is causing the toxicity.

If man-made contamination is resulting in the source of the agent, we can control our actions.

If the agent is naturally occurring, then we need to make people aware of the situation.

But, what if the situation was amplified in the UK, by their excessive use of OPs? The tests on the (modified Phosmet) caused 3 of the 4 changes necessary for prion formation, that is not to be ignored. Something else pushed it over the edge, why?

Don't think for a minute, I have forgotten the suffering of anybody from diseases, such as sCJD. This stuff eats away at my consciousness everyday, and I want to help stop the suffering too.

I find the work presently being done on glycolation patterns exciting.
 
##################### Bovine Spongiform Encephalopathy #####################


Science 16 December 2005:
Vol. 310. no. 5755, pp. 1756 - 1758
DOI: 10.1126/science.310.5755.1756




News Focus
SPONGIFORM DISEASES:
After the Crisis: More Questions About Prions
Martin Enserink

With "mad cow disease" declining sharply, public anxiety about prion diseases has diminished. But cutting funds would be a big mistake, prion researchers say
DÜSSELDORF, GERMANY--Peering over an audience of more than 700 researchers on19 October, Nobel laureate Stanley Prusiner seemed pleased. "This is probably the largest gathering of prion scientists ever," boasted the field's controversial godfather, who gave the keynote speech at a recent meeting.* As the crowd attested, prion science had come along way since Prusiner proposed a heretical idea 23 years ago that it is not viruses or bacteria, but weird proteins, that cause a family of lethal brain diseases.
But now, leaner times may be ahead. Public health efforts to combat prion infections in cattle have worked so well that reports about "mad cow disease" have all but vanished from the newspapers; the clamor for action is fading, and governments are looking for ways to scale back costly safety measures. And many worry that research may suffer; trimming has begun in Germany and France. Prusiner captured the atmosphere best in a private quip after his keynote speech, according to conference organizer Detlev Riesner of Heinrich Heine University, when he said the largest prion meeting to date could end up being the largest in history.

Prion researchers admit there's reason to breathe a little easier. Outbreaks of mad cow disease, or bovine spongiform encephalopathy (BSE), have declined ever since reaching a peak in the United Kingdom, by far the hardest-hit nation, in1992. Fears of a massive wave of an associated human brain disease called variant Creutzfeldt-Jakob disease (vCJD) have not materialized.

But a slowdown in research would be the wrong response, prion scientists say. The British vCJD outbreak could still be in its infancy, and medical procedures could trigger a second wave. (Tests to screen blood, organs, and tissue are still some time away.) There are other reasons to stay alert as well. Europeans have reported the appearance of a new form of scrapie, an age-old prion disease in sheep. And a prion disease in North American deer and elk is spreading rapidly. "The fire is out, but there are still glowing red spots everywhere," says Jean-Philippe Deslys, head of the prion research group at the French Atomic Energy Commission.


Twin peaks. Both mad cow disease (BSE) and human variant CJD cases have declined sharply in Britain. But some experts warn that vCJD could bounce back.
CREDIT: SOURCES: OIE (BSE); NATIONAL CJD SURVEILLANCE UNIT (VCJD)


And leaving aside public and animal health, researchers say their field has barely begun to crack its mysteries.
Debatable
Even after decades of research, the most fundamental question about the prion family of diseases remains open: What is the infectious agent? Many researchers today say recent experiments have convinced them that Prusiner's dogma-defying theory is correct: A rogue protein imposes its own misfolded shape on other, healthy proteins--but some still have doubts (see sidebar on p.1758).

And other riddles remain. For example: After oral infection, how do prions travel from the gut to the brain? They are known to pass through lymphoid tissue and peripheral nerves, but do individual misfolded proteins make that journey, or do they infect their neighbors, causing them to fall like dominoes? Once present in the brain, misfolded proteins form aggregates that appear to be involved in killing neurons. But exactly how is unclear.

Fortunately, answers to these questions weren't needed to start bringing the BSE and vCJD epidemics under control. Primarily as a result of a 1988 ban on feeding so-called rendered protein, including brain tissue, from ruminants to ruminants, the number of BSE cases in the United Kingdom began to fall in 1993; there were only 343 last year and just 151 so far in 2005 (see graphic). Other countries in Europe, after discovering about the year2000 that they had their own BSE problems, now report rapid declines, too.

In reaction, the European Union (E.U.) is beginning to loosen measures to stop BSE and limit human exposure. A "road map" for prion diseases, published by the European Commission in July, listed restrictions that might eventually be lifted, arguing that resources should be concentrated on new health threats such as avian influenza. (Testing of apparently healthy animals at the slaughterhouse cost about €1.6 billion between 2001 and 2004--€1.6 million per BSE case detected.)

And in October, the commission delighted lovers of T-bone steak and other meat on the bone by raising the age from 12 to 24 months at which the vertebral column--one place where prions concentrate--is removed. (Generally produced from cattle aged 22 to 30 months, such cuts had virtually disappeared.) That decision was premature, says Martin Groschup of the Friedrich Löeffler Institute, Germany's federal animal health center. His lab is still carrying out a long-term BSE pathology study to discover at what age and where in the cow's body infectious particles collect; the decision should have been stayed pending the outcome, he says.

Thanks in part to the decline of BSE, more scientists are now turning their attention to sheep. Scrapie has been known to infect flocks for at least 250 years and is harmless to humans. But in the lab, sheep can also be infected with BSE. Researchers have long worried that the resulting disease--simply called "BSE in sheep"--could get into Europe's flocks, for instance, through feed. If it were transmissible among sheep, like scrapie, it would pose a special problem because a feed ban would not get rid of it, says Lucien van Keulen of the Central Institute for Animal Disease Control in Lelystad, the Netherlands. But so far, there's no evidence of this.

The increased surveillance has turned up a new problem, however. In the last 3 years, researchers in Germany, Portugal, and France have discovered a new variety of scrapie whose prion proteins accumulate in different parts of the brain, have different biochemical properties, and produce a slightly different set of symptoms. Most likely, says Groschup, it's a variant of scrapie that flew under the radar until now. What's disconcerting is that it also appears to affect sheep with a genotype called ARR/ARR, thought to confer resistance to scrapie. Now, some worry that an ambitious E.U. breeding program aimed at spreading that genotype could just replace classical scrapie with a new form. "It's another thing we need to get to the bottom of," says Neil Cashman of the University of British Columbia in Vancouver, Canada.

Meanwhile, in the United States and Canada, chronic wasting disease (CWD), first discovered in deer and elk in Colorado and Wyoming in the 1980s, keeps turning up in new places. In 2005, New York became the 13th state affected, and moose the fourth species. So far, there is no evidence that CWD can cross the species barrier to humans--nor, for that matter, nonmembers of the deer family. CWD hasn't appeared in Europe, but the E.U. is planning a survey in 2006 to make sure.

Deceptive calm?
In BSE's wake, vCJD is declining too; there were just nine deaths last year in the United Kingdom, down from 28 in 2000 (see graph), and the total death toll stands at 153 (plus fewer than 20 in other countries), far below worst-case predictions in the late 1990s.


Old news. Concern about vCJD cases made headlines in the 1990s. Now that the crisis seems to be over, some public health and research measures are being scaled back.
CREDIT: TOUHIG SION/CORBIS


But some believe the curve may be deceptive. John Collinge of the National Hospital for Neurology and Neurosurgery in London notes that vCJD's peak came barely 10 years after the highest BSE exposure in Britain. The delay is just too short, he says. Kuru, a disease among the Fore people in the highlands of New Guinea that resulted from cannibalistic rituals in the 1950s, has a mean incubation period of about 12 years. BSE ought to take longer, Collinge says, because in all known instances, crossing a species barrier lengthens a prion disease's incubation period.
Collinge suggests another possibility: Only the most genetically susceptible people have developed symptoms so far. Researchers know that having the "wrong" amino acid at codon 129 of both copies of the prion gene makes a person more susceptible to vCJD. All patients so far except one, who likely contracted vCJD through a blood transfusion, had this genotype, called MM. But other genes may be involved as well, says Collinge; the victims so far may just be an especially susceptible vanguard of the MM population at large, which comprises 40% of U.K. residents.

The possibility that many more people harbor the disease without symptoms--and the fact that probable vCJD transmission through blood transfusions has now been shown twice--means that, rather than slacking off now, efforts to develop drugs and diagnostic techniques should be intensified, Riesner says. At the meeting, several groups reported encouraging data that could lead to a blood test within the next several years. Drug development has been slower, in part because the pharmaceutical industry has little interest in a disease that affects about one in a million people.

Researchers have tried at least half a dozen compounds on CJD patients, but most seem to prolong life by only a few weeks--if they do anything. An ongoing U.K. trial of a drug called quinacrine for vCJD and CJD, in which 53 patients have been enrolled, is primarily a way to discover how to run future tests, says Collinge, whose group is one of three massscreening small compounds in vitro in a search for promising new candidates.

Because of the countless remaining questions, many scientists say they worry about the unmistakable decline in public interest. Cashman, for instance, says he was amazed a "media firestorm" didn't break out after a paper in the October issue of Nature Medicine showed that prions can lurk in the inflamed mammary glands of scrapie-infected sheep--and presumably their milk as well. If the same is true in cows, he said, "it would be a hugely important finding for public health."

So far, funding doesn't appear under threat in the United States or the United Kingdom, and it is even expanding in Canada. Three weeks ago, the Canadian government announced a new U.S. $30 million network of centers of excellence; separately, the government of the province of Alberta has committed $33 million to launch a prion research institute. The reason: Canada recently learned how devastating prion diseases be. Four cases of BSE since 2003 have cost the economy an estimated $5.5 billion. (As Cashman puts it, "those cattle might as well have been space shuttles--they cost the same.")

But in Germany, prion projects worth about €10 million, funded by three federal ministries since 2001, will come to an end in 2006; they include the German Transmissible Spongiform Encephalopathy Research Platform, which coordinates studies and sample sharing through three depositories. Several German states' programs will end next year as well, says Kerstin Dressel, the platform's scientific secretary. In France, funding is set to decline as well, Deslys says.

Still, not everyone is worried. If it turns out that after BSE, prion diseases pose no major new health risks, well, "then it would only be natural that the money goes elsewhere," says Byron Caughey, a veteran prion researcher at the U.S. National Institute of Allergy and Infectious Diseases Rocky Mountain Laboratories in Hamilton, Montana. "Then we'll have to adapt, as scientists do."

* Prion 2005. Between Fundamentals and Society's Needs. Düsseldorf, 19-21 October.



http://www.sciencemag.org/TSS

#################### https://lists.aegee.org/bse-l.html ####################


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



Science 16 December 2005:
Vol. 310. no. 5755, p. 1758
DOI: 10.1126/science.310.5755.1758
Prev | Table of Contents | Next

News Focus
SPONGIFORM DISEASES:
Waiting for the Final Experiment
Martin Enserink
The Nobel Committee went out on a limb in 1997, some biologists thought, when it awarded science's highest honor to neurologist Stanley Prusiner of the University of California, San Francisco. Prusiner had championed the idea that a mysterious class of infectious particles called prions consisted of nothing but protein. Even some who thought he was on the right track wanted more evidence.

The theory has stronger support today. Some, like Detlev Riesner of Heinrich Heine University in Düsseldorf, Germany, say papers published in the past 18 months, including one by Prusiner, have nailed the case for infectious proteins. "It's beyond any doubt now," says Riesner. But not everyone agrees. A few researchers believe Prusiner is spectacularly wrong; many more say the evidence is getting stronger but isn't irrefutable yet.

The "protein-only hypothesis," as it's often called, holds that the infectious agent in prion diseases consists of an abnormally folded protein, PrPSc, with a bizarre power over its neighbors. It can impose its own three-dimensional shape on an abundant protein in mammalian cells (called PrPC) that has the same amino acid sequence but a different structure. The altered proteins then help recruit more PrPC, according to theory, and over the years the chain reaction causes large amounts of PrPSc to build up in the brain and cause death. No bacterium or virus is needed to accomplish this.

Yale researcher Laura Manuelidis is among the people who think this scenario is all wrong. For decades, she has advocated the notion that the true culprits in prion diseases are slow-acting, elusive viruses. That would explain far better why so-called strains of prion diseases with slightly different characteristics have been found, she says. Manuelidis published a paper in Science in October showing that infection with a slow-acting Creutzfeldt-Jakob strain protects mouse cells from infection with a faster one--a finding she says points to an immune defense reaction and thus a virus. But many researchers say her results can also be interpreted within the protein-only theory. Although Manuelidis's studies are good, says Riesner, "her conclusions are wrong."


Prion factory. By mixing scrapie-infected brain material with healthy brain in a process called PMCA, researchers say they made infectious proteins in a test tube.
CREDIT: K. BUCKHEIT/SCIENCE; SOURCE: C. SOTO


The experiment that could irrefutably prove Prusiner right, meanwhile, is easy on paper but difficult to perform, says Byron Caughey of the U.S. National Institute for Allergy and Infectious Diseases lab in Hamilton, Montana: Synthesize PrPSc in vitro and show that it can, by itself, produce an infectious disease in healthy animals. Several labs have tried to do this and failed, leading to renewed speculation that something other than proteins is involved after all, Caughey says.
Prusiner and his team reported last year in Science (30 July 2004, p. 673) that they had created such "synthetic prions. "The group engineered Escherichia coli bacteria to produce part of a mouse prion protein, polymerized it into misfolded fibrils akin to PrPSc, and injected these into the brains of mice, where they triggered a neurodegenerative disease that could be transmitted to other animals. The work won over Riesner, but other researchers saw problems. Prusiner's mice were engineered to express 16 times the normal amount of prion protein, which could lead them to develop prions spontaneously, Caughey says. The "very important control" to show that they don't is missing.

Meanwhile, a group led by Claudio Soto of the University of Texas Medical Branch in Galveston has tried a different tack. Building on earlier work by Caughey, Soto developed a technique called protein misfolding cyclic amplification (PMCA), which can multiply PrPSc in the test tube. In PMCA, the brain of a hamster infected with a prion disease called scrapie is ground up till it becomes a cell-free soup called a homogenate; when a similar brain homogenate from a healthy hamster is added, PrPSc from the sick brain will transform any PrPC to PrPSc. (The test tubes are blasted periodically with a short sound wave to break up growing PrPSc fibers.) The mixture is diluted into more healthy brain homogenate, and the process is repeated.

In a Cell paper published in April, the group showed that even after hundreds of cycles and a 1020-fold dilution--meaning not a single molecule of the original sick brain was left--the reaction produced PrPSc that sickened healthy hamsters. The study demonstrates that molecules made entirely in vitro and free of viruses--which can't live without cells--can generate infection, Soto says.

Although it's a "fantastic result," Caughey says, the study doesn't clinch the case for the protein-only theory. Because the reaction takes place in a complex, brain-derived chemical mix, one cannot rule out that, say, a small piece of nucleic acid that's essential to infectivity was replicated along with PrPSc in each cycle. Soto says that's unlikely. Nonetheless, he is now planning experiments in which the PMCA process is fed with purified PrPC rather than brain homogenate. He believes that should dispel the skepticism once and for all.




http://www.sciencemag.org/TSS

#################### https://lists.aegee.org/bse-l.html ####################


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


CJD WATCH MESSAGE BOARD
TSS
Strain-specified characteristics of mouse synthetic prions
Fri Dec 16, 2005 11:11
70.110.88.73


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



snip...



Discussion






In addition to establishing beyond a reasonable doubt that prions are infectious proteins, the production of synthetic prions opens many approaches to the investigation of prion structure and biology. Before the production of WT synthetic prions using the 142-residue protein recMoPrP(89-230) (5), we used a 55-mer synthetic peptide carrying the analogous Gerstmann-Sträussler-Scheinker mutation at mouse residue 101 to create synthetic prions (4, 19). The strains of mutant synthetic prions were protease-sensitive and required Tg196 mice expressing low levels of MoPrP(P101L) to demonstrate prion infectivity. Moreover, the mutant prions in Tg196 mice could not be passaged into WT mice. Development of a system using recMoPrP(89-230) to produce synthetic prions has facilitated investigations because these prions are protease-resistant and can be passaged in WT mice.

Evidence that MoSP1 Is a Distinct Strain. The data presented here and in an earlier study (5) argue that MoSP1 is a distinct strain. The neuropathologic changes produced by MoSP1 in Tg9949 mice differ from all other mouse prion strains that we have previously investigated. Most noticeable are focal aggregates of large vacuoles in the cerebellar gray matter and brainstem (Figs. 2 and 3). This finding contrasts with Tg9949 mice inoculated with RML prions, in which vacuolation is widespread, including in the neocortex, hippocampus, thalamus, brainstem, and cerebellar white matter.

In our studies of the conformational stability of more than a dozen prion strains, we have not found any strain that is as stable as MoSP1 (Table 1). MoSP1 is more resistant to denaturation by GdnHCl (Fig. 5) than bovine spongiform encephalopathy prions in cattle (20) as well as the mouse 301V strain that originated in cattle (Table 1). In heat denaturation studies, 301V was more stable than four other mouse prion strains, all of which were derived from sheep with scrapie (21).

The incubation times, neuropathologic lesion profiles, and resistance to GdnHCl denaturation contends that MoSP1 is unlike any that we have previously studied. This finding is fortuitous because it provides yet another line of evidence supporting our earlier assertion that MoSP1 was produced from recMoPrP(89-230) polymerized into amyloid fibrils and not a contaminant derived from a naturally occurring prion (5).

Correlating Incubation Times, Neuropathology, and Stability. The mean incubation time for MoSP1 was reduced from 516 days to 258 days on second passage, presumably reflecting the higher titer of prions in the inoculum on second passage (Fig. 1 A). On first passage, the titer might well be low because the inoculum was composed of amyloid fibrils assembled from recMoPrP(89-230). When MoSP1 was passaged into FVB mice, the incubation period on first passage was 154 days and decreased to 130 days on second passage (Fig. 1B). This difference presumably reflects a transmission barrier caused by the difference in PrP sequences between FVB and Tg9949 mice: FVB mice express full-length MoPrP, and Tg9949 mice express only the C-terminal 65% of the protein, MoPrP(22-88).

The neuropathology in Tg9949 mice induced by MoSP1 is distinct from that produced by RML prions. Most important, the neuropathology in Tg9949 mice produced by MoSP1 remained constant on second passage in the Tg9949 line. Passage of MoSP1 into FVB mice reduced the incubation time (Fig. 1), changed the distribution of neuropil vacuolation (Figs. 2 and 3), and dramatically reduced the conformational stability of the prions (Fig. 6). These changes in incubation times, neuropatho-logic lesions, and conformational stability are reminiscent of the alterations seen when Sc237 prions from Syrian hamsters were passaged in Tg mice expressing chimeric mouse-hamster (MH2M) PrP (22).

Whether MoSP1 passaged in FVB mice can regain its former properties by subsequent passage in Tg9949 mice remains to be determined. Although some investigators have reported that strain alterations are reversible (23), this idea is not well studied. Passage of MoSP1 through FVB mice changed the properties of this strain to resemble those of RML prions. It will be of considerable interest if passaging MoSP1 through FVB mice and back into Tg9949 mice results in the recovery of the original MoSP1 strain properties.

In contrast to the passage of MoSP1 into FVB mice, the converse passage of RML prions into Tg9949 mice was not accompanied by alterations in the incubation time and conformational stability even though there was a substantial change in the neuropathologic phenotype (compare Fig. 3 B and D). In Tg9949 mice inoculated with RML prions, vacuolation scores were diminished in all brain regions, and large vacuoles lined with PrPSc were seen. In this instance, it seems likely that the strain of prion did not change appreciably even though the PrP molecule is N-terminally truncated. Before the development of the conformational stability assay, the profound change in neuropathology might have been ascribed to a change in strain, but in fact, it seems to be dictated by the host. Teasing out strain and host PrP effects can at times be difficult (20).

Spectrum of Prion Strains. The discovery of MoSP1 dramatically widens the spectrum of prion strains. It will be important to determine the structure of MoSP1 passaged in Tg9949 mice and FVB mice; extreme differences in stability may be evident in how the protein is folded or assembled into oligomers. Unfortunately, such structural studies currently are limited by the insolubility of PrPSc. Whether electron crystallography can give sufficient detail to distinguish between two strains with such different conformational stabilities is unknown (24, 25).

As new synthetic prions are created, it will be important to build a catalog of strains. Identifying an array of strains with very different, readily measurable properties is critical to advancing our understanding of prion diversity. By correlating structural and biological characteristics of prion strains, it should be possible to begin to decipher how strain-specified properties are encrypted in the conformation of PrPSc. Clearly, learning the language of prion strains is an important avenue of investigation.



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


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:
[email protected] .

© 2005 by The National Academy of Sciences
of the USA



http://www.pnas.org/cgi/reprint/102/6/2168?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Strain-specified+characteristics+of+mouse+synthetic+prions+&searchid=1134752116283_4056&stored_search=&FIRSTINDEX=0&journalcode=pnas





Greetings list members,



PLEASE take note to the infamous spontaneous synthetic TSE, does not look like any other natural TSE.

SO again, where does the 85%+ of all CJD i.e. the sporadic CJDs come from, what is the source and route?


> 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.





TSS

#################### https://lists.aegee.org/bse-l.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




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


TSS
 

Latest posts

Top