Tuesday, March 16, 2010

COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010



Proof Committee Hansard



This is an uncorrected proof of evidence taken before the committee. It is made available under the condition that it is recognised as such. BY AUTHORITY OF THE SENATE [PROOF COPY] TO EXPEDITE DELIVERY, THIS TRANSCRIPT HAS NOT BEEN SUBEDITED


Friday, 5 February 2010 Senate RRA&T 1


Committee met at 9.01 am

CHAIR (Senator Nash)—I declare open this public hearing of the Rural and Regional Affairs and Transport References Committee. The committee is hearing evidence on the committee’s inquiry into the impact and consequences of the government’s decision to relax import restrictions on beef. Before the committee starts taking evidence I remind all witnesses that, in giving evidence to the committee, they are protected by parliamentary privilege. It is unlawful for anyone to threaten or disadvantage a witness on account of evidence given to a committee and such action may be treated by the Senate as a contempt. It is also a contempt to give false or misleading evidence to a committee. The committee prefers all evidence to be given in public but, under the Senate’s resolutions, witnesses have the right to request to be heard in private session. It is important that witnesses give the committee notice if they intend to ask to give evidence in camera. If a witness objects to answering a question, the witness should state the ground upon which the objection is taken and the committee will determine whether it will insist on an answer, having regard to the ground which is claimed. If the committee determines to insist on an answer, a witness may request that the answer be given in camera. Such a request may, of course, also been made at any other time. On behalf of the committee, I thank all those who have made submissions and sent representatives here today for their cooperation in this inquiry.

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[9.03 am]

BELLINGER, Mr Brad, Chairman, Australian Beef Association

CARTER, Mr John Edward, Director, Australian Beef Association

CHAIR—Welcome. Would you like to make an opening statement?

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:

You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heinemann variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:

The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.

Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:

The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE...tss)

I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—

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Senator HEFFERNAN—Which of course is total BS.

Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.

Mr Carter—We have an additional concern about human health. We are not scientists, but on 18 December, four days after the last hearing here, the BBC reported a new wave of deaths due to variant CJD linked to eating BSE infected beef could be underway. This is based on the work of Professor John Collinge of the National Prion Clinic, who reported that a 2009 death in Scotland was from a different genetic pool to that of the 166 deaths already reported in the UK. Those are all thought to share one gene, but Professor Collinge and his colleagues estimate that up to 350 people in this new group, represented by the person who died in Scotland, could get CJD. He thinks that CJD has moved into a new phase, and the incubation period is a long one. We tender the Australian Red Cross donor policy sheet, which bears out what Senator Back brought up last time, questioning the Chief Medical Officer, and we say that blood from people who were in the UK between 1980 and 1996 is not acceptable. That is the current ruling. We believe this now should be extended to anyone who has visited the UK, and this new evidence should ensure that Australia revisits the science of CJD.

CHAIR—Thank you, Mr Carter. Before we kick off, can I just remind colleagues that we are short of time today, so I ask that we do not traverse ground the we have previously covered and make sure that we stick to new information that is required. Mr Bellinger, when you started you referred to your view that this decision to allow the importation was politically based. I know you are going to go into this in the course of the next 20 minutes or so, but could you just give us a quick outline of what your definition of politically based is and why you think the decision was politically based?

Mr Bellinger—On the lowering of BSE standards: if you go back to 2006, for example, there were five categories for describing countries that had BSE and Australia was in the category for BSE free. Suddenly, by the time the United States got their third instance of BSE, through the influence of Robert Zoellick—who was the trade minister that signed the BSE corresponding side letter in 2004 and was George Bush’s appointment to the WTO—they suddenly changed the five categories to three categories and, instead of being BSE free, Australia became BSE negligible risk. At the time I put out a press release alerting the media to the dangers of this happening, and we are coming to the stage here when suddenly our government is saying, ‘Now let’s allow the importation of beef from BSE affected countries.’ I believe that the WTO has been influenced by large multinational meat processors and retailers to change and allow the trading of BSE beef throughout the world.

CHAIR—Thanks, Mr Bellinger.

Mr Carter—Of course, the side letter that Minister Vaile signed was at the request of Mr Zoellick, who is now in the position that Mr Bellinger has explained.

Senator HEFFERNAN—I just want to put the committee on notice that, if we do not get through what we have got to get through today, I suggest we have another hearing, because this

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is the greatest ambush of Australia’s farmers of all time by a government. The evidence given at the last meeting was deadset lies. The proposition that this whole change of government policy was led by the industry is a deadset lie. While Simon Crean might want to change his mind because of the WTO and his lack of knowledge, the Australian beef industry, as you know, is under great challenge, not only from the currency but also from the undermining of our markets. This is a disgrace.

I will go to the meat-off-the-shelves proposition. By the way, there is no obligation to take meat off the shelves; it was something dreamt up by someone buried in the bureaucracy, who is probably taking notes down in the department now. There is absolutely no obligation but, if they wanted to stick to it, all they really had to do was do mandatory SRM removal. Now the renderers did not like that idea. It was going to cost money. Can you explain to us where you think the meat-off-the-shelves proposition came from?

Mr Bellinger—I think it was an ill-informed, misguided statement delivered from RMAC to the minister. They may have thought, by some weird dream, that by having this beef-off-theshelves policy it would somehow illustrate to the WTO that we cannot import beef from BSE affected countries—totally erroneous and totally stupid. Of course, if you look at the legislation on food recalls, it is handled by the states. I did an interview on 2NZ, a local radio station, 10 days ago in reply to Tony Burke’s statement on this beef-off-the-shelves policy, where he said that if a beast was found to have BSE in the Northern Territory then beef would have to be taken off the shelves in Tasmania—totally erroneous. It does not exist. It is the states who handle this. I am amazed that a minister could make this sort of statement.

Senator HEFFERNAN—You were talking about the next wave of possible human infection in the UK. It is a fact, actually—I have done some work on it. There are three genes that have been identified. One is very accepting: if you have that gene and you eat the meat, you get the consequences—mad cow disease. There are two genes that they have not worked out yet. One is more resistant than the other. Are you aware that there is a lot of science around that says, through this new understanding of the gene mutation, there could well be a new wave of mad cow disease in humans?

Mr Bellinger—I will hand you over to John Carter. He has done more research on this than me.

Mr Carter—It is Professor Collinge and the National Prion Clinic in the UK who have done this work. It is not as though it is some backyard person. I am certainly not a geneticist, but it appears to me, particularly from the work that Bob Steel has done, that these things are crossing barriers. To me, the science is not proven at all.

Senator HEFFERNAN—No. There seems to have been a change of government position in assessing the science, to risk analysis from a lesser proposition. Are you aware of when the government changed from the precautionary principle to risk analysis in terms of assessing these sorts of risk?

Mr Carter—To me, those are just words. In 1997 the UK government Lord Phillips inquiry stated that up to 136,000 people could lose their lives to CJD, and later the Blair government raised this to 250,000. Then, of course, when America gets BSE suddenly it is really no problem.

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Senator HEFFERNAN—Look, this is just a trade issue. The government came in here.

Senator Sterle, I believe, will make some reflection upon your earlier remarks to say that this—

Senator STERLE—Absolutely, if you give me a chance. The clock is ticking.

Senator HEFFERNAN—Would you like to do it now?

Senator STERLE—Finish your question. No, because you will interrupt. So you have your run and then I will have my say.

Senator HEFFERNAN—The proposition was put to us last time that this was driven by the industry. I followed Simon Crean on 5AA the other day. He talked about ‘using the best principles’. He had idea what he was talking about, but they did say that this was driven by the industry—and the department accepted it, and I hope they are all listening down there, because they are a bunch of liars. They accepted the proposition—

Senator STERLE—Chair—

Senator O’BRIEN—Using this hearing to slander people in that way is completely unseemly.

Senator HEFFERNAN—Righto, I withdraw that. They overlooked the facts. We will correct the facts today, but this was driven by the industry, by demands from the industry, when in fact we now know from in an in-confidence answer to this committee there were 37 communications between the Canadian and US governments and the Australian government since November 2007 demanding that we allow their meat in here. Of course, the department of trade here— Simon Crean’s mob—said, ‘We’d better find a way,’ and this is the way they have done it. They have completely misled the Australian beef industry and I think it is a total disgrace. I might add also that, back when we knocked this on my head—

CHAIR—Do you have any questions, Senator Heffernan?

Senator HEFFERNAN—in 2005, I think it was, the then shadow health minister, Julia Gillard, was keen on maintaining the precautionary principle. We now seem to have gone from the precautionary principle, without any mention—by the way, this is all going to happen without coming to parliament—of risk analysis. I am going to deal with the risk analysis proposition when we get the guy that gave the so-called independent advice along. I will leave it at that.

Senator STERLE—I just have to clarify a few things, Mr Bellinger. You said that the OIE is an arm of the WTO. Do you want to clarify that? I am led to believe that they are not.

Mr Bellinger—I will explain it further. You have the World Trade Organisation, and then under that you have the World Health Organisation. The OIE, the organisation of international epizootics, then handles phytosanitary and animal health issues under that umbrella.

Senator STERLE—So they are not an arm of the WTO? I want to clarify it for the record.

Mr Bellinger—They are an arm—


Senator STERLE—Let us get back to the law. Quite clearly, 152 WTO members have the policy that if there is an outbreak, regardless of where that outbreak is, all meat must be taken off the shelves. Whether that has happened in America or not, this is the previous government’s policy.

Senator HEFFERNAN—No, it is not. That is garbage.


Dr Clegg—Nothing. Until the assessments are complete, nothing does change.

Senator HEFFERNAN—With Brazil, the policy there was developed in 1999. We brought in those cartons of beef from Brazil. As Mr McCutcheon said it had this whoopee tick from OIE and that was the policy in 1999 and there was no trace-back mechanism. You mob are saying, ‘We don’t care if the country has no traceability because we are not interested in herd status or national status only beef status.’ So it could come from Mexico, across the border, into some abattoir in Texas.

With Brazil there was no trace-back mechanism at all. DAFF did not inspect any of the facilities and did not bother to go over there, let alone send out teams. You were going to after the event, until the cartons arrived. What is going to change? Aren’t we entitled, for God’s sake, to know what the bloody protocols are so we can test them? That is a bloody good example of an OIE certification that went badly wrong. How do we know it is not going to go wrong again, for God’s sake?

Dr Carroll—We are not using OIE certifications.

Senator HEFFERNAN—Mr McCutcheon just said that you were.

Dr Carroll—No, he said we are using an OIE process.

Senator HEFFERNAN—Do not give me that mumbo jumbo bureaucratic crap.

Dr Carroll—Sorry, Senator, but an OIE process is different to an OIE certification. Senator HEFFERNAN—You still have not reported back on Brazil and what went wrong there.

Dr Carroll—The OIE categorises countries.


Dr Steel—Absolutely. If you look at the American system, there is some interplay. The Canadians and the Mexicans are taking the Americans on in the WHO because of country-oforigin limitations, so they cannot import their beef. The United States Department of Agriculture was against the COOL decisions. Now they have totally changed around. Why have they changed? You do not have to be Einstein to realise it is because of the risk of BSE. Just getting back to the point about huge undeclared amounts: the analogy on that graph is from Professor Mathews. They are not required to state how many cases they have got; they are only required to say that they have got BSE.

Senator BACK—On another point that I will ask you to comment on as it seems ironic to me: you and I would recall that in the 1970s it was the US government that demanded that Australia be free of brucellosis, knowing very well that brucellosis never had any involvement with meat. Yet this country spent millions and millions of dollars becoming free of brucellosis, and that was what led initially to the herd identification schemes et cetera. Those were all demanded by the US government, not because of health issues but because of trade issues. They then demanded that we increase the quality of our export abattoirs to a level infinitely higher than existed elsewhere in the world, not because of any health issues but because of trade issues. Does it seem unusual to you, with the boot now being on the other foot because Australia and New Zealand are the only region that is free of this, that the demands are being made by those very same countries in reverse? Does that seem ironic to you?

Dr Steel—I do not know about that Senator, but I do know that I am extremely proud of what the departments of agriculture have done and their incredible schemes. Senator BACK—So am I. Some of us built our practices on them.

Dr Steel—It may be ironical, but I still think that we have every reason to laud the departments who look after us. Now, unfortunately, I feel that our departments are not looking after us. I feel, particularly because of the OIE science, and I have referred you to that, there are grey areas. There is one individual, who I will not mention, who I feel has not been appropriate for Australian agriculture.

Senator BACK—Thank you. I will stop it at that because others may have questions.

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Senator McGAURAN—Is that the minister you are talking about?

Senator STERLE—It might be you, Julian! Dr Steel, just very quickly, you referred to New Zealand in your opening statement, but New Zealand has the policy that the Australian government is trying to put in here. It is the same policy, and they have had it for eight years without any problems.

Dr Steel—They made the decision after the scrapie was there, I believe. They are in the soup, so what have they got to lose? They have lost that uniqueness that we both had of being free of any TSEs, officially anyway. What have they got to lose? And it improves their trade. Now, because of the new technological advances in detection of TSEs, BSE and scrapie, and because muscle tissue has been found to contain prions—misfolded prions—our government can no longer say, ‘We’re importing beef and it has got nothing in its muscles to suggest infection.’ If you have got BSE in undeclared or unknown numbers, in unidentified cattle, how could we possibly not have a risk? Does that answer your question?

Senator STERLE—Thanks, Dr Steel. I know time is of the essence here so I will hand back to the chair.

CHAIR—As there are no further questions, thank you very much for appearing here today Dr Steel. We do appreciate your giving us your time.

Proceedings suspended from 10.11 am to 10.33 am


Dr Lavender—I would have to say no. I know that in Japan they do test every carcass. Having been to Japan a few times, I think they probably would do that. I would not have absolute confidence here. In America, as I understand it, testing was at a higher level and has gradually been decreased because in their own meat they do not want to find it because it would impact on their markets in countries such as Japan.

CHAIR—That is a very interesting point.


Senator HEFFERNAN—All right, let us go to the risk. Do you accept that any increase in
the risk of contracting CJD is unacceptable?

Prof. Mathews—Hypothetical it is unacceptable. But we all accept risks every day. The one
substantial piece of feedback I got from the NHMRC committee, when they looked at my draft
report, was where I had written in my conclusions that I believed the risk to the Australian
population was negligible. They asked me to quantify the risk. Hence I revised the report to put
in the quantification comparing the risk of variant CJD in the Australian population with the risk
from motorcar accidents. As you see in the report, I conclude that it is orders of magnitude more
likely that anyone in Australia—

Senator HEFFERNAN—But what you are saying to me now is that it is acceptable to have
an increased risk because once we do this there is an increased risk. You are saying that is

Prof. Mathews—Of course.

Senator HEFFERNAN—That is all I want you to answer. You are happy to accept the risk.

Prof. Mathews—But you are not arguing that we ban motorcars, Senator, are you?

CHAIR—We have got enough to deal with with beef. I think we will leave cars to another

Senator HEFFERNAN—Do you support the proposition that importing beef products into
Australia from countries with a history of BSE overseas—given there is all sorts of work going
on and no live tests et cetera and there are a lot of likeable rogues in the beef industry—poses no,
and I mean absolutely no, increased risk to the Australian population?

Prof. Mathews—I am not really to comment on the political end of it.

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Senator HEFFERNAN—No, but as a scientist are you saying—and I will repeat it—that
importing beef products into Australia from countries with a history of BSE overseas poses no
increased risk to the Australian population?

Prof. Mathews—No. I am not saying that. I am saying that any increased risk would be
negligible and I tried to quantify how negligible in my report.


Senator HEFFERNAN—Yes, and obviously we will come to that, and Senator Back is anxious to get some questions in. But against the background, we know this is all just colour and movement for the trade position and the other countries wanting to undermine our clean, green and free status and get equal standing in the market. There is no question about that. I draw your attention to the development of new testing for BSE and CJD. Wouldn’t it be prudent for the Australian government to wait until these testing processes, or more comprehensive ones, were proven and available generally so we can provide certainty before lessening any of the protective controls, which is the ultimate control—that is, you cannot bring it in. Shouldn’t we wait?

Prof. Mathews—You are asking me to comment on economic and political issues.


Senator HEFFERNAN—All right, Dr Carroll. You are the genius on this. Why wouldn’t we have and demand full traceability if we are going to import meat from a country so that we know where it is coming from? I am talking about whole-of-life traceability. Not where it was killed but where it came from. Why wouldn’t we demand that?

Dr Carroll—Part of the FSANZ process will be around what measures are in place to ensure the beef comes from countries—

Senator HEFFERNAN—But aren’t we entitled to know that, God’s sake? This is many times bigger than the IRA that was remanding pork and you are saying, ‘Beef? Bugger off. We are not interested. We do not need an IRA.’ What an insult to Australia’s cattle farmers. What an insult. You are comfortable; I can see that. We are angry about this. You say we do not need an IRA. It is completely changed. We do not even know the science of the crossover of the wasting disease from deer.

Dr Carroll—There is no science on the crossover of the wasting disease from deer. Senator HEFFERNAN—We do not know, you see. We do not know. There is no need for an IRA you say?

Dr Carroll—Correct.

Senator HEFFERNAN—How do we know if someone says they are going to bring in meat from Canada that it does not come from somewhere else if there is no traceability? Dr Carroll—That will be part of the process that FSANZ will be—

Senator HEFFERNAN—Aren’t we entitled—

CHAIR—Hang on. Just let the witness answer.

Dr Carroll—That will be part of the process FSANZ will carry out in assessing the country to see if it is eligible for a category A or a category B status.

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Senator HEFFERNAN—But why, for God’s sake, can’t you at least set some standards that we can work on, or are you bureaucrats too scared to be human failure tested?

CHAIR—Senator Heffernan—

Senator HEFFERNAN—It is a fair thing to say. If they are not going to tell us until after the event and are saying, ‘We do not want you to test it. You are a farmer; you would not know,’ why wouldn’t we be entitled to say to other countries, ‘We demand full traceability as we have here.’ What is wrong with that?

Dr Carroll—We have full traceability here for a range of reasons that go far beyond BSE and far beyond various other—

CHAIR—If I am correct in distilling down through all of this to exactly what you mean, the only thing that has changed is that now more countries can use the same process that has already existed because of a policy change.

Dr Carroll—The previous policy position—

CHAIR—Can you just give me a yes or a no.

Dr Clegg—No.


Dr Clegg—There is a policy already on the website today that describes the assessment for countries—the Australian BSE assessment committee. That is on the FSANZ website now. You can have a look at that. The one that comes into place from 1 March 2010 differs slightly. There are differences in country categorisations. In the current policy, countries are categorised as A, B, C or D. In the new policy they are categories 1 and 2, with category 3 not assessed or not permitted.

CHAIR—So the policy is just broadening out—sorry if I am being really simplistic here— those countries that are now eligible to send their beef to Australia.

Dr Clegg—No. It is to be considered by the assessment panel. It has to be considered. It is just the terms of reference under which they are considered that has altered slightly. That is all. CHAIR—I will put it differently. At the moment there are countries that are precluded on the basis that they have had BSE.

Dr Clegg—Yes.

CHAIR—The change is that it is now opened up and those countries have an opportunity to apply.

Dr Clegg—Correct.

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CHAIR—All right. That then goes back to—and I want to get to the process for assessment shortly—how important the protocols are if those countries that previously have had BSE are now going to have an opportunity that they previously did not.

Dr Clegg—Sure.

CHAIR—That is how important the protocols and there is no way to have any kind of accountability to determine what those protocols should be because it is all in the hands of FSANZ.

Dr Clegg—They are the risk assessors.

CHAIR—I understand they are the risk assessors, but there are an awful lot of people in this country who would be very pleased to be able to have input if they feel that those protocols are not correct. Who is actually drawing them up, Mr McCutcheon?

Mr McCutcheon—They are being drawn up by officers of FSANZ.

CHAIR—Which ones?

Mr McCutcheon—The team consists of Andrew Bartholomaeus—he is leading that team— Amanda Hill and Dr Scott Crerar, at this stage. We are also employing another three officers to be part of that team. The recruitment process is pretty much nearing its conclusion.

CHAIR—So there are three people and three assistants. Does that go to the board?

Mr McCutcheon—No, those sorts of things do not go to the board. As I indicated at the last hearing, this was an additional function provided to FSANZ and we were provided with additional money to do that. Essentially, we are tailoring our resources with that additional budgetary funding.

CHAIR—So there are essentially those three key people who are writing the protocols? Mr McCutcheon—That is right, but they are not starting from scratch, if I can just reassure you, Senator.

CHAIR—No, I understand all that, but, at the end of the day, somebody has to sit down with a bit of paper or in front of a keyboard and write down what they are going to be. What is the process once they have finished writing?

Mr McCutcheon—Once they have finished it, there will certainly be consultation within the Australian government as we finalise those. Then, as I mentioned earlier in the hearing today, we will be getting an independent look at that by an OIE appointed expert. That will be done. Once it passes that test, we can finalise that protocol and that will be the protocol upon which countries will be able to make their applications.

CHAIR—Which, as you have said before, you can change at any time—FSANZ.

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Mr McCutcheon—That is correct in theory, but it is not something that—

CHAIR—No, but I just want to know what is possible and what is not possible down the track. At the moment, what is the process for assessing a country’s risk status?

Dr Clegg—Risk status for BSE or for any beef—


Mr McCutcheon—At the moment, if a country has had a BSE case, then it is not eligible to have an assessment done.

CHAIR—So it is as simple as that.

Mr McCutcheon—That is right.

CHAIR—What happens from 1 March?

Mr McCutcheon—For those countries that have a history of BSE, they are eligible to lodge an application to have their categorisation re-examined.

CHAIR—Who is going to do that?

Mr McCutcheon—That would be the Australian BSE safety assessment committee, which is essentially a FSANZ committee with one outsider from Biosecurity Australia.

Senator HEFFERNAN—Where will they get their advice from?

Mr McCutcheon—Much of the information we hope will be contained in the applications that come in from countries that lodge applications. Again, we have access to a whole range of experts within and outside Australia, so if we need additional information we will consult with those experts.

CHAIR—Could you just clarify for me exactly the change in policy? There is nothing in regulation, there is nothing in legislation, so this is just something that happens within the department or departments—I am not quite sure where. Perhaps you could outline for me very clearly how the policy change decision manifests itself in a departmental arrangement. What actually happens to trigger this whole change of arrangement? There is a policy decision here by the minister, who has opened this up and says, ‘It’s okay now—we’ve got countries that had BSE, but that’s okay, they can have the opportunity to apply.’

Senator HEFFERNAN—Against the background, while you are thinking about that, that Minister Crean said this was driven by the beef industry. It is here in a press release. He has quoted Lucy Knight. You blokes have said today that it was driven by the industry. Do you agree with that? Who drove it? Come on, who drove it?

Mr Yeend—I have said that, over a number of years, there have been concerns expressed by industry and—

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Senator HEFFERNAN—No—we will go back to the Hansard. You said it was triggered by the industry—words to that effect.

Mr Yeend—I did not say that. I said that the industry, over a number of years, has been expressing concerns. There have also been other factors; there have been the changes in the science—that has moved on—

Senator HEFFERNAN—Then I will ask you—

CHAIR—No, let him finish.

Mr Yeend—and also there have been concerns raised by some of our trading partners. All of these factors were considerations. But the driving factor in why the government commenced this review process was that, through the regular industry consultation that takes place, these issues had been raised, and raised, and then, in August—

Senator HEFFERNAN—In other words, it would be fair to interpret what you are saying as, ‘It was driven by the industry.’ Is that what you are telling me? I take that to be what you are saying.

Mr Yeend—I am saying that industry, through the consultation process, has raised concerns, and industry was wanting us to review the policy to see whether the current arrangements were appropriate or not.

Senator HEFFERNAN—Could you provide the advice from the industry that triggered this? Mr Yeend—I think we can detail the contact we have had with the industry. Senator HEFFERNAN—No, no—it would have had to be a written request to make such a catastrophic change of direction of the beef industry. You say it was driven by continuous pleadings from the industry and that that eventually triggered the government to do it; could you show us the continuous pleadings?

Mr Yeend—I think we could outline to you what I have been talking about.

Senator HEFFERNAN—But is there correspondence that supports what you are saying as more than hearsay?

Mr Yeend—There has been contact between the government and the industry.

Senator HEFFERNAN—No, I am saying: is there written evidence that what you are saying is not just hearsay?

CHAIR—Could the committee have any record of that contact is what we are asking.

Mr Yeend—Yes, I think we can provide you with detail of the contact there has been between government and industry through the consultation process.

Friday, 5 February 2010 Senate RRA&T 89


CHAIR—All right. It is not just today and not just your evidence, Mr Yeend; it has been coming through quite clearly that there has been a very strong indication that this has been driven by industry. Would you say, then, that if industry had not driven it we would not be in this position today? Or would the departments have seen this as the best course forward and given that advice to the minister anyway?

Mr Yeend—What I am saying is that the concerns expressed by industry were a key factor in the decision to change the policy, but there were a combination of factors. You are asking me a hypothetical question but, from the perspective of the issues for which I have responsibility, this issue has been raised with us by our trading partners; concerns have been expressed both by trading partners and domestically that the science has moved on and it was something that needed to be looked at again. There were questions of consistency with our international trade obligations.

Senator HEFFERNAN—You are too well-trained as a bureaucrat. That will do.

Mr Yeend—So all of—

CHAIR—That is fine, Mr Yeend. Thank you. Senator Heffernan has the call.

Senator HEFFERNAN—Stop there, mate. Stop there. You are talking gobbledygook.

According to your minister, Minister Crean: IT was the Australian beef industry’s lobbying that triggered this week’s decision to change food policy laws … So could you show us written evidence of the lobbying that Mr Crean refers to?

Mr Yeend—I think I have already said to Senator Nash that we will be happy to provide you with more information, but I would refer you to paragraph 6 of our submission that I think does say that the timing of the specific request from AHMAC was related to a discussion on 28 July 2009 within an AHMAC meeting. So I think we have addressed these issues on a number of occasions and we have put it in writing. I am happy to elaborate on it if you would like me to.

Senator HEFFERNAN—Did you say, Mr Morris, that the change of policy was announced on 20 October?

Mr Yeend—Yes, that is correct.

Senator HEFFERNAN—And yet, in earlier evidence, Professor Mathews said he did not send in his draft report until the 20th—so you made the decision before you got the draft report?

Mr Yeend—That is not correct.

CHAIR—Well, which one is not correct?

Senator HEFFERNAN—Which one is telling a lie?

CHAIR—Professor Mathews said it was 20 October—or September?

RRA&T 90 Senate Friday, 5 February 2010


Senator HEFFERNAN—Who is lying?


McCutcheon—If we are not satisfied with the country’s traceability requirements—

CHAIR—No, I am not even talking about countries. I am talking about individual exporters.

Mr McCutcheon—We do not look at individuals; we look at countries.

CHAIR—Who does? Who looks at the individuals?

Mr McCutcheon—That is the responsibility of the individual country making an assessment.

Senator HEFFERNAN—But if the evidence—

Senator BACK—Can I just stay with this for a second? I thought the responsibility rested with Australian authorities, not that it was the responsibility of other countries. I hope we are not divesting this to other countries to assure us that everything is in place. Are we not going to actually satisfy the Australian consumer by being able to say that Australian people under your direction are going to be satisfied? We are not going to be satisfied by some statement of an overseas country’s inspectorate, are we?

Mr McCutcheon—The first step will be for us to assess what traceability mechanisms a country has and how effectively they are claimed to be used.

Senator BACK—And if they do not have—

Mr McCutcheon—Second, if we are not satisfied then we do have the scope to go and visit countries for an inspection. I will ask AQIS to jump in here, but basically if a country is put into category 1 or 2 and they are deemed to be eligible to export to Australia, subject to all the other sanitary requirements being met, then it is another country’s responsibility to make sure that they satisfy our requirements. But, again, that is getting into AQIS territory.

Senator HEFFERNAN—Rather than mince your words, the US and Canada do not have full traceability at all. They have no traceability, as Senator Back points out, from the day an animal was born to when it was killed.

Senator BACK—Where would that place them?

Senator HEFFERNAN—So are they knocked out automatically?

Mr McCutcheon—If Canada or the US lodge an application then we will be examining traceability as part of that.

Senator HEFFERNAN—For God’s sake, we have been here for two hours talking bureaucratic nonspeak. Wouldn’t it be reasonable for Australia’s cattle producers to expect you fellows, who are in charge of this without reference to the parliament or the industry, to at least demand full traceability? Isn’t that a reasonable request?

RRA&T 94 Senate Friday, 5 February 2010


Senator BACK—Can I ask the question—

Senator HEFFERNAN—No, just let him answer that.

Mr McCutcheon—I think I have already answered that question. I said we will need to be satisfied that the traceability arrangements that a country have manage the risks associated with BSE.

Senator HEFFERNAN—That is bureaucratic crap. They do not have any.


snip...see full text 110 pages ;


Backflip over mad cow beef ban

Nicola Berkovic

From: The Australian March 09, 2010 12:00AM

THE importation of beef from countries that have had outbreaks of mad cow disease will be delayed by at least two years following a backdown by the Rudd government. Agriculture Minister Tony Burke yesterday bowed to community pressure and ordered a full risk analysis of beef imports from countries where bovine spongiform encephalopathy, or mad cow disease, had been reported.

The review comes eight days after the lifting of a ban on beef imports from countries that have had the disease.

That decision followed a threat by meat exporters, including Canada, to go to the World Trade Organisation over unfair trade barriers.

A spokeswoman for Mr Burke said the review would cover fresh or frozen beef, but not processed or cooked beef products, such as oxtail soup, and drinks such as the beef tea product Bovril.

The review, to be conducted by Biosecurity Australia, will examine beef imports from all countries other than New Zealand.

Start of sidebar. Skip to end of sidebar. Related CoverageRisky red meat imports shelved Daily Telegraph, 3 hours ago Turnaround sees risk study on beef imports Adelaide Now, 10 hours ago Oxtail soup first beef import The Australian, 5 days ago Labor to axe drought relief The Australian, 6 days ago N American push on mad cow ban The Australian, 24 Feb 2010 .End of sidebar. Return to start of sidebar. Mr Burke said he had taken the decision following "significant community concern" about import standards.

Admitting it was unusual for a minister to intervene in such a decision, Mr Burke said the level of concern had warranted the formal review process.

"Conducting an import risk analysis is the best way of reassuring the Australian community that effective protocols will be put in place to provide for the safety of imports."

He said he believed the two-year review process would not put Australia in breach of its international trade obligations, because it was a science-based procedure.

Independent senator Nick Xenophon, who campaigned against the lifting of the ban, welcomed the review as a "victory for commonsense".

"The importation of meat from mad cow disease-affected areas could have potentially put Australian consumers at risk, and could have destroyed Australia's claims that we are a clean, green, BSE-free market," Senator Xenophon said.

Nationals senators Fiona Nash and John Williams also hailed the decision as a sensible move to protect consumers and beef producers.

However, the Cattle Council of Australia, which argued that the analysis would only burden international trade, said it was disappointed a protectionist "scare campaign" influenced the decision.

President Greg Brown said he was worried about the delay the process would create. "If the Americans put a 24-month process on us, we would be out of the market . . . considering they take a hell of a lot more beef from us than we do from them," he said.

The confusion over beef imports had also damaged the reputation of Australian beef in the domestic market, Mr Brown said.

Australia banned British beef in 1996.



The WTO and the World Organization for Animal Health (OIE)

Collaboration between WTO and OIE concerns the use of international standards in the context of the SPS Agreement.


Mandate The OIE STDF

See also: OIE website

Note: The World Organization for Animal Health was originally called the Office International des Epizooties, and is referred to as such in the SPS Agreement

Mandate back to top

The WTO's SPS Agreement states that “to harmonize sanitary and phytosanitary measures on as wide a basis as possible, Members shall base their sanitary or phytosanitary measures on international standards, guidelines or recommendations”. The Agreement names the OIE as the relevant organization for animal health.

A formal cooperation between OIE and WTO was agreed in July 1998 WT/L/272

See SPS Agreement Introduction, Article 12.3 and Annex A paragraph 3(a)


The OIE and the WTO strengthen their cooperation

Paris, 14 March 2009 – During a visit by Mr Pascal Lamy, Director-General of the World Trade Organization (WTO), to the OIE Headquarters in Paris, the leaders of the two organisations further emphasised the benefits to the international community of the animal health standards published by the OIE, which are considered as the reference within the framework of the WTO SPS Agreement.

Dr Bernard Vallat, Director General of the OIE, stated that “a large majority of the standards adopted by OIE Member Countries and Territories are designed to prevent sanitary risks linked with the world trade in animals and animal products. This trade is indispensable, especially to supply the poorest countries with animal protein, including in times of crisis. Yet compliance with OIE standards also results in the improvement of veterinary health governance in each Member country and territory, and in so doing improves animal health and welfare throughout the world, while at the same time improving public health by preventing and controlling animal diseases transmissible to humans.”

The two organisations also raised the need for joint discussions on how to avoid the potential disadvantages arising from the use of “private” standards relating to sanitary risks, since such standards have not been adopted within the framework of the SPS Agreement and may contradict existing public standards democratically adopted by the OIE and the Codex Alimentarius Commission in a fully transparent procedure and based on scientific evidence.

The OIE also referred to its standard-setting work in the field of animal welfare and the rise in stricter consumer demands in this respect in all countries of the world.

In the field of improving the competencies of stakeholders in all countries of the world on international sanitary rules applicable to trade, the WTO and the OIE reaffirmed their commitment to the Doha Declaration issued by the WTO, OIE, WHO, the World Bank and FAO, and to the Standards and Trade Development Facility (STDF) to help developing countries fulfil the requirements of the SPS Agreement.

“The value of the WTO organising information and training seminars in all regions with the OIE for the benefit of Veterinary Service officials, and especially those in charge of sanitary certification of animals and animal products for export, is now a well established fact. These seminars should be continued, along with the allocation of STDF grants aimed at facilitating the preparation of national or regional projects to strengthen the sanitary safety of international trade and market access opportunities for all those that so wish”, declared Pascal Lamy.

Lastly, the two organisations reiterated their shared interest in strengthening collaboration in order to facilitate the settlement of sanitary disputes, notably by making more frequent use of the OIE mediation procedure.

March 2009


THE O.I.E. IS nothing more than an industry group set up to abolish all protocols for the safety of humans from all strains of Transmissible Spongiform Encephalopathy. The O.I.E., the U.S.D.A., and evidently the W.T.O. have all come to the conclusion, that the trading of all strains of mad cow disease and or any animal Transmissible Spongiform Encephalopathy should now legal. TSEs are now nothing more than a commodity, a legally traded commodity, and any body bags there from are simply a casualty of trade and the almighty dollar. humans have now become expendable. AFTER what happened with Global trade and typical BSE, the governing bodies of global trade have pressed forward with the fact (without any scientific proof whatsoever), that any atypical TSE is nothing more than an spontaneous old animal disease, and that it has become an acceptable trading commodity, even though we know that atypical BSE is transmissible to humans (Kong et al 2009). these trading partners have manipulated science to be able to trade these TSE globally, and any ramifications there from is simply an acceptable death either from direct consumption, or the 'friendly fire' i.e. 'pass it forward' mode of transmission. i kinda compare the O.I.E., W.T.O., U.S.D.A. et al with the Mafia. no i am not kidding. have you ever ead the 'mad sheep of mad river valley' ?

Saturday, February 27, 2010



see history here ;


odd how when c-BSE was linked with nvCJD of humans with pathology that is very similar to each other, they confirmed a link between humans. HOWEVER, with the atypical Nor-98 scrapie being very similar to some sub-types of sporadic CJD, and GSS, it's just the opposite, its all spontaneous $$$ will the corruption ever end ?



(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............


IN OTHER WORDS, THE O.I.E. TAKES WHATEVER JUNK SCIENCE THAT A COUNTRY SUBMITS TO THEM, AND THEY CLASSIFY THAT COUNTRY BY THAT JUNK SCIENCE. it's like the wolf guarding the henhouse. it would be like the big bad wolf coming to the door and saying nobody is home. and you believing them, and then basing the BSE risk assessment on that. WE ALL know what kind of junk science the USDA and the FDA et al have used over the years. ...TSS

Posted: Wed Dec 19, 2007 3:47 pm Post subject: OIE


Question wrote:

Quote: Maybe familirise yourself with the OIE. The primary concern is animal health of the world they are the animal version of the WHO. It is a long way down from that ivory tower but here we go, until pressured by the USA repesentatives a country could not export animals for 6 years after finding a BSE/BASE positive animal so under the old rules the US would not be able to export anywhere in the world for another 4 1/2 years. Who got the risk levels system put in to allow some trade - your US representatives. You guys want to change rules - OK , but you do not get special rules that only apply to the US. As i have told you before Sand h I market all my own slaughter animals and you know that, so don't do the whole holier than thow act.

With all due respect, it is obvious that you know little about the OIE and how it actually works. Having been to their offices in Paris and talked personally with the Head of the Animal Test Section, you would choke if you knew how many lobby groups attend that office daily. There is a steady stream of paid lobby groups that have one goal in life and that is to sway the Section Heads of each department within the OIE to suit the needs of different juristictions around the world, which curiously enough, also includes the USA and Canada. Anyone can go there and chat with them - providing they can privide valid cause to be let in. To say that the only goal of the OIE is animal health is actually only part of their function. They are more than that and my discussions with Dr. Diaz there has showed me that. But to blindly make a statement regarding what they do when you have no idea what they actually do is like eating the skin of the orange and not knowing what is actually under.

Interstingly you state that the US Government applied pressure (to the OIE) I assume and that is a great example of the lobby groups doing their job. So, at the end of the day, one can safely assume that it is the pressure applied by certain influential lobby groups that will determine a likely aoutcome to an apparent OIE directive. Man alive, isn't it great to live in a democracy wherein the people get to make the choices and not just some "other" interested party or group - say like........Cargyll or Tyson for example?

So, one last question, question?

Who wags the tail of that dog?? And for what reason other than one that is purely associated with trade and international agreements and greed?

And you think it is so simply explainable.


SCRAPIE The United States is unable to support the proposed new draft Code Chapter on Scrapie. The draft chapter, as written, departs significantly from the existing chapter, is confusing and is difficult to understand. This version of the scrapie chapter uses much of the same wording as the BSE chapter and is written as if the predominance of evidence revealed that scrapie was a food-borne disease similar to BSE in cattle which is inappropriate. Moreover, several of the new changes are not supported by current scientific evidence. As a result, detailed comments on individual articles would not meaningful at this time. The United States is not supportive of the proposed draft chapter for the following reasons: 1. Inclusion of “atypical” scrapie: The scientific evidence indicates that “atypical” scrapie, also referred to as Nor-98, Nor-98-like, or non-classical scrapie, is not the same disease as classical scrapie. Further, “atypical” scrapie does not meet the criteria for listing diseases of trade concern by the OIE, as described in Chapter 2.1.1 of the Code. The United States recommends that the scope of this chapter be limited to classical scrapie in sheep and goats. Further, the United States recommends that OIE clearly adopt the position that “atypical” scrapie represents a distinct disease entity from classical scrapie and that it not be a listed disease. • There is no evidence that “atypical” scrapie is a contagious disease. If it is contagious, available evidence suggests that it has a much lower transmission efficiency. (Hopp, et al, 2006; Green, et al, 2007; Benestad, et al 2008; McIntyre, et al, 2008) • The disease appears to be ubiquitous in that it has been found wherever sufficient surveillance has been conducted. (Buschmann et al, 2004; De Bosschere et al, 2004; Orge, et al, 2004; Everest et al, 2006; Arsac, 2007; Benestad, et al 2008; Fediaevsky, et al, 2008) • The disease does not appear to be economically significant in that the prevalence of clinical disease is low and it typically occurs in older animals. (Luhken, et al., 2007; Benestad, et al 2008). • The disease is as likely as not to be the result of a spontaneous conversion of normal prion protein. (Benestad, et al 2008, De Bosschere et al 2007) • Removal of exposed sheep is unlikely to reduce the prevalence of “atypical” scrapie infection and removing only those exposed sheep that are phenylalanine (F) at codon 141 is scientifically unsound since the disease is known to affect sheep of most other genotypes. Further, sheep with AHQ alleles have a similar risk of infection with “atypical” strains as sheep with F at codon 141. (Luhken, et al., 2007). • If “atypical” scrapie is included as a listed disease, the surveillance and diagnostic requirements which are needed to identify these cases should be described in detail in both this Chapter and the Manual of Diagnostic Tests and Vaccines for Terrestrial 2 Animals. Data from Europe illustrates that using the proper test(s) is essential for the identification of atypical scrapie (Fediaevsky et al., 2008).


6. Overemphasis on importation and use of bovine meat and bone meal as a route of scrapie transmission: Given that the draft Chapter is not intended to address risk mitigation for BSE in small ruminants, we believe there is an over-emphasis on this potential route of transmission in the current draft. The United States recommends that the requirements in this chapter be limited to the inclusion of products from sheep and goats (instead of from all ruminants) in feed or feed ingredients intended for consumption by animals • The use of products from sheep and goats as feed or feed ingredients for ruminant or non-ruminant animals represent one possible route of transmission (Philippe, et al, 2005) and a source of environmental contamination with the classical scrapie agent. However, this is not the primary route of transmission for the scrapie agent. • The need for the exclusion of cattle-derived protein or other animal protein to mitigate BSE risk should be based on a country’s BSE risk status and should be addressed in Chapter 2.3.13 of the Code.


14. Failure to provide scientific justification for the list of permitted commodities in Item 1 of Article . We recommend that the list be re-evaluated and those items that have not been substantiated as presenting no risk be excluded or those with some risk but where the intended use mitigates the risk the use be specified. • There is no known human health risk associated with scrapie. As such, if meat and meat products for human consumption are included in this list, sheep and/or goat milk intended for human consumption should also be added to the list of permitted commodities in Item 1 of Article • In the vast majority of sheep infected with classical scrapie, actual infectivity or PrPres has been identified in most tissues including the lymphoreticular system (tonsils, spleen, lymph nodes), the gastrointestinal tract, brain, and spinal cord (Hadlow et. al. 1979; Hadlow et al., 1980; van Kuelen et al., 1996; van Kuelen et al., 1999, Andreoletti et al., 2000; Heggebø et al., 2002; Caplazi et al., 2004). Infectivity and/or PrPres has also been identified in the placenta (see Hourrigan et al., 1979; Onodera et al., 1993; Pattison et al., 1972; Pattison et al., 1974; Race et al., 1998), blood (Hunter et al., 2002; Houston et al. 2008); peripheral nerves (Groschup et al., 1996), muscle (Pattison and Millson, 1962; Andreoletti et al., 2004; Casalone et al., 2005), salivary gland (Hadlow et al., 1980; Vascellari et al., 2007), kidney (Siso et al., 2006), and skin ( Thomzig et al., 2007). In addition, recent work has shown milk and/or colostrum from scrapie infected ewes transmitted the disease to 17 of 18 lambs (Konold et al., 2008). • The data on the risk of low protein tallow made from scrapie infected tissues particularly for use in milk replacer is limited and some epidemiologic studies suggest an association of milk replacer use with scrapie risk. Taylor et al., 1997 examined the inactivation capacity of different rendering system in regards to scrapie. The presence of infectivity was determined by bioassay into mice. From the onset of this study, it was assumed that tallow was not the vehicle for the transmission of TSE. Hence only 2 tallow samples were examined.



The OIE Terrestrial Animal Health Standards Commission (the Code Commission) met at the OIE Headquarters in Paris from 10 to 14 March 2008.


13. Bovine spongiform encephalopathy (BSE) a) BSE (Chapter 2.3.13.) EN EN The Code Commission received comments from Argentina, Australia, Canada, the EU, Japan, New Zealand, the People’s Republic of China and the USA, and industry organisations. The Code Commission again expressed its concern that Members continued to resubmit comments on texts already discussed and adopted in previous meetings without providing any new justification. With regard to the request of Members to modify the text currently found in Article 1, the Code Commission noted that the European Food Safety Authority (EFSA) has conducted a study on the production of protein free tallow. The results of this study have already been considered by the Code Commission and found not to provide justification for modifying the current text. Some Members raised questions about the safety of deboned muscle meat and proposed that this be removed from Article 1, while other Members are questioning the limitation to 30 months of age. The Code Commission reminded Members that the measures relating to the safety of deboned muscle meat were formulated several years ago, when the magnitude of risk to human health was unknown. These precautionary measures were appropriate at that time. Since that time, scientific understanding regarding the BSE risk classification of countries and the risk to human health associated with BSE in bovine products has progressed. The Code Commission considered that it is timely to reconsider whether there is any need to maintain the current requirement in Chapter 2.3.13. for cattle to be 30 months of age or less for deboned muscle meat to be considered a safe commodity. The Code Commission agreed with Member comments regarding the need to provide annual updates to support the retention of countries/zones on the list of negligible or controlled risk countries and zones and modified Articles 3 and 4 accordingly. Members again raised comments on Article 7, proposing to modify this Article by adding the following text: ‘or after the date of birth of the last indigenous case if that indigenous case was born after the date of the feed ban’. The Code Commission disagreed with this proposed modification as this principle is already covered in Article 7, i.e. the birth of an indigenous case is an indication that the feed ban has not been effective and the relevant date would be adjusted accordingly. On the safety of gelatine, the Code Commission reiterated its position that the safety of the gelatine manufacturing process has been well established by peer-reviewed scientific studies and risk assessments on the production of gelatine from bones, regardless of their origin. Recognizing the fact that skulls are not used in the commercial manufacture of gelatine, the Code Commission proposed the exclusion of skulls, thus removing the point of contention raised by Members. Relevant references include the following: Grobben AH, Steele PJ, Somerville RA, Taylor DM (2004). Inactivation of the bovine spongiform encephalopathy (BSE) agent by the acid and alkaline processes used in the manufacture of bone gelatin. Biotechnology and Applied Biochemistry, 39; 329-338. EN EN Grobben AH, Steel PJ, Taylor DM, Somerville RA, Schreuder BEC (2005). Inactivation of the BSE agent by heat and pressure process for manufacturing gelatin. Veterinary Record, 157; 277-289. Grobben AH, Steele PH, Somerville RA, Taylor DM (2006). Inactivation of transmissible spongiform encephalopathy agents during the manufacture of dicalcium phosphate from bone. Veterinary Record, 158; 361- 366. NZFSA (2005). Officials’ Review of New Zealand’s BSE Country-Categorisation Measure. New Zealand Food Safety Authority, Wellington and published in “Prions in Humans and Animals”. Ed. Hornlimann, B., Riesner, D. Kretzschmar, H. De Gruyter Verlag, Berlin (ISBN 978-3-11-018275-0) The Code Commission noted that the approach taken to gelatine in Chapter 2.3.13. is fully consistent with approaches elsewhere in the Code whereby commodities originating from countries/zones that are not free of specified diseases are identified as safe for trade, based on the processing of the commodity as evaluated by scientific studies and risk assessment. b) Guidelines on surveillance for BSE (Appendix 3.8.4.) The Code Commission received comments from Argentina, Canada, the EU, New Zealand and the People’s Republic of China. The Code Commission accepted a comment on Article 4, a modification to correct a typographical error in Table 2 (Surveillance Point Values for Samples Collected from Animals in the Given Subpopulation and Age Category). c) Factors to consider in conducting the BSE risk analysis in Chapter 2.3.13. (Appendix 3.8.5.) The Code Commission received comments from Argentina. The Code Commission also considered recommendations of the ad hoc Group on Atypical Scrapie and Atypical Bovine Spongiform Encephalopathy, as endorsed by the Scientific Commission, and modified texts accordingly. The revised texts are presented at Annex XV of this report for adoption. Community position: The Community would like to stress in particular the comments related to the ruminant to ruminant feed ban provisions (Article, 4, 7, 8, 9 and 10), SRM definition (Article, 15, 16, 16bis), tallow (Article, the annual update (Article, gelatine (Article and the use of the risk assessment guidelines (Article of Appendix 3.8.5.). Thus the Community cannot support the proposed chapter, and wishes its comments to be taken into account.


30. Scrapie (Chapter 2.4.8) The Code Commission thanked the Scientific Department for convening relevant experts and providing advice on atypical scrapie and atypical bovine spongiform encephalopathy. The Code Commission noted the statement in the report of the ad hoc Group to the effect that there is insufficient information to support the establishment of rules or guidelines specific to atypical scrapie, other than in relation to the choice of diagnostic tests used for surveillance. The ad hoc Group also observed that scrapie does not represent a public health risk and should not therefore be treated in the same way as BSE. The Code Commission noted that the revised draft Chapter represents a helpful step towards updating the Code’s provisions on scrapie, bringing it into line with the structure of the BSE Chapter. To facilitate review, the texts are presented as clean texts. The revised text is presented at Annex XXXIII for Member comments. Community position: The Community will provide the OIE with comments before the 15th of August 2008.


OIE Scrapie Chapter Revision • Current draft recognizes Nor98-like scrapie as a separate disease from classical scrapie • USDA provided comments on the draft to OIE


Atypical scrapie/Nor 98 October 2009

Last year, after examining member country submissions and investigating rigorous scientific research, the World Organisation for Animal Health (OIE) decided that Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around Nor 98.



Sutton reported that USDA has urged the World Organization for Animal Health (OIE) to categorize Nor98-like scrapie as a separate disease from classical scrapie. Currently, the OIE has proposed a draft revision of their scrapie chapter that would exclude Nor98-like scrapie from the chapter. USDA will be submitting it's comments on this proposal soon.


Monday, November 30, 2009




This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........


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.


The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404




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

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

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

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

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

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




Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC.

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)


National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).



Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.




R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.



A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.


Monday, December 1, 2008

When Atypical Scrapie cross species barriers


Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.


Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.


“The U.S. has lower sanitary and phyto-sanitary standards (SPS) for imports than many other countries, especially those concerning bovine spongiform encephalopathy (BSE). These low standards have made the U.S. a dumping ground for beef from the countries that have experienced BSE problems. Food Safety and SPS issues continue to be problematic for our industry, as some countries comply with OIE standards, while others ignore them either for cultural reasons, or too often use them as trade barriers. The USITC October 7, 2008 release reported, ‘U.S. beef processors and beef cattle ranchers lose billions of dollars in export opportunities each year because of animal health and food safety measures in other countries that are inconsistent with international standards and vary by country.


Epidemiology of Scrapie in the United States 1977


Wednesday, March 3, 2010



Thursday, March 11, 2010



Tuesday, April 28, 2009

Nor98-like Scrapie in the United States of America


Scrapie USA


LIKE i said before, the OIE not only sold their soul to the devil over the BSE MRR, they sold yours too ;

Wednesday, February 10, 2010



The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.


Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of the USA Question number: EFSA-Q-2003-083

Adopted: 1 July 2004 Summary (0.1Mb)

Report (0.2Mb)


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

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

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

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


Monday, November 23, 2009



Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary


THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure. ...


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;



THE OIE has now shown they are nothing more than a National Trading Brokerage for all strains of animal TSE. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.


IT'S as obvious as day and night, either Larry, Curley, and Mo have been at the helm of the USDA/APHIS/FSIS/FDA/CDC/NIH et al for many many years, or the incompetence of these agencies are so inept, either through ignorance and or just too overweight with industry reps., they then should be all done away with and a single agency brought forth, and if not, how will you correct this ongoing problem ?

Thank you, I am sincerely disgusted,

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


full text ;

Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)





''they don't wanna know, the dont' care''

''nothing else matters''

watch and listen to Stanley Prusiner, turn it up ;


Prions: Protein Aggregation and Infectious Diseases ADRIANO AGUZZI AND ANNA MARIA CALELLA Institute of Neuropathology, University Hospital of Zurich, Zurich, Switzerland

3. Sporadic Creutzfeldt-Jakob disease Approximately 85% of all human prion diseases are sporadic forms of CJD. For sCJD, there is no association with a mutant PRNP allele, nor is there any epidemiological evidence for exposure to a TSE agent through contact with people or animals infected with TSEs. sCJD cases are currently subclassified according to the methionine/valine polymorphism at codon 129 of the PRNP gene and the size and glycoform ratio of proteaseresistant prion protein identified on western blot (type 1 or type 2) (174). Heterozygosity (Met/Val) at PrP codon 129 appears to be associated with a lower risk (378) and/or prolonged incubation time (119, 387). The lack of routine laboratory testing for preclinical diagnosis makes the search for agent sources and other risk factors extremely difficult. At present, the means of acquisition of a TSE agent in these patients remains a mystery. So far, there is no evidence for spontaneous PrPSc formation in any animal or human TSE. In humans, the peak age incidence of sporadic CJD is 55–60 years. However, if spontaneous misfolding were the primary event, one might expect a continuously increasing incidence with age because more time would allow more opportunity for rare misfolding events.

Physiol Rev • VOL 89 • OCTOBER 2009 • www.prv.org

Perspectives BIOMEDICINE: A Fresh Look at BSE Bruce Chesebro*

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

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

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

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


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

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

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

snip...full text ;


Release No. 0106.04

Contact: Office of Communications (202) 720-4623

Transcript of Remarks From Technical Briefing on BSE and Related Issues With Agriculture Secretary Ann M. Veneman and USDA Chief Veterinary Officer Dr. Ron DeHaven Washington D.C. - March 15, 2004


OPERATOR : “Yes. Our next one is coming from Elizabeth Weiss. Please state your company.”

ELIZABETH WEISS: “This is Elizabeth Weiss with USA Today.”

“I actually had two questions. First off, when you say you're looking for 1 in 10,000 cases, is USDA doing any work to find out the possibility of whether or not BSE exists in a spontaneous form in the way that it does in humans and elk populations?

“And secondly, how will any of this fit into some of the consternation that's been raised in California and with the Midwest packer that wanted to test all of its cattle?


DR. DEHAVEN: “All right. I think we've got three different questions in there, and I'll try to touch on each one of them.

“First of all, let me correct just a technical issue, and that is you mentioned 1 in 10,000. And actually our surveillance system currently is designed, the one that we have in place now is designed to detect 1 positive in 1 million cattle, and I gave some numbers between 200,000 and 268,000 that would allow us to detect 1 in 10 million as opposed to 1 in 10,000.

“So we would, if we were able to collect in the ballpark of those numbers of samples then we with increasing numbers of samples have an increasingly statistically valid sample from which to determine, one, whether or not the disease exists and, if so, at what prevalence level.

“So our real emphasis is to test as many of those animals as we can, ensure that we get an appropriate geographical distribution, but not setting a specific number as far as a target. Again, consistent with the recommendation from the International Review Team, their recommendation was to test all of them.

“So that's consistent with where we're going is to test as many as we possibly can.

“As far as spontaneous cases, that is a very difficult issue. There is no evidence to prove that spontaneous BSE occurs in cattle; but here again it's an issue of proving a negative. We do know that CJD, the human version of the disease, does occur spontaneously in humans at the rate of about 1 in 1 million. We don't have enough data to definitively say that spontaneous cases of BSE in cattle occur or do not occur.

“Again, it's a very difficult situation to prove a negative.

“So a lot of research is ongoing. Certainly if we do come up with any positive samples in the course of this surveillance we will be looking at that question in evaluating those samples but no scientifically hard evidence to confirm or refute whether or not spontaneous cases of BSE occur.




Matthews confirmed that the brain tissue samples from the US animal had arrived at Weybridge. Test results were likely to be ready by the end of next week, he said.

The suspect animal has already undergone a series of tests. A rapid screening test on Nov. 15 returned inconclusive results. Sophisticated immunohistochemistry (IHC) tests cleared the animal of any infection, but a third round of testing using a Western blot procedure showed a "weak positive".

Weybridge will do an IHC test plus three kinds of Western Blot tests on the samples. They will use "methods of slightly different analytical sensitivity that give us the greatest number of opportunities to interpret what we see," he said.

US beef industry leaders say scientists should not speculate about the unusual case.

"There's no evidence that it's atypical ... and there's absolutely no evidence that it's spontaneous," said Gary Weber, head of regulatory affairs at the National Cattlemen's Beef Association.

Matthews noted scientists are still grappling with what is typical and atypical BSE.

"Far too few people have looked at BSE in depth using all of the tests to be able to define 'this is normal and that one isn't'," he said.

Weber noted Japan used the term to describe two very young infected cattle because BSE is usually found in older animals. Italy labeled a case "atypical" because the misshaped prions were found in unexpected parts of the animal's brain. ...snip...end


Atypical BSE strain -- In July 2007, the UK Spongiform Encephalopathy Advisory Committee (SEAC) suggested that atypical BSE may be a distinct strain of prion disease. Unlike typical BSE, cases of atypical BSE, according to SEAC, may have risen spontaneously (although transmission through feed or the environment cannot be ruled out). Recently reported French surveillance data support this theory that unlike typical BSE, atypical BSE appears to represent sporadic disease



Spontaneous occurrence

14. Spontaneous cases of classical CJD in humans are found at a rate of about 1/million around the world (Will, 1993), without appreciable racial or geographical variation except in a few specific cases, notably Jews of Libyan origin that have a mutation in the open reading frame of the PRNP gene (Chapman and Korczyn, 1991). Thus it is theoretically possible that spontaneous cases of BSE could occur as a consequence of a germ line mutation, in which case relatives would also have a certain or increased incidence of the disease, or a somatic mutation, which would be unlikely to be detectable unless the appropriate tissue were identified, or after some transformation in the PrP protein in the animal concerned. BSE was unknown prior to its detection in Britain in the mid 1980s, and Index cases found around the world since then can all be explained in terms of export from the UK directly or indirectly of cattle or of feed components. No BSE affected animals have been reported in many developed countries with large cattle populations, including Australia, New Zealand, Norway and Sweden, which have mixed cattle populations; and the only infected animal detected in the US was of Canadian origin. The disease seems to have a highly homogeneous aetiology (e.g. Bruce, 2003). 15. Data from the USA, where the dairy population in particular is highly related to that in GB provide an upper limit to the spontaneous rate. A programme of testing is in place of a target population of adult cattle exhibiting some clinical sign that might be consistent with BSE (animals reported as having CNS or clinical signs of BSE or were non-ambulatory). In the intensive programme from June 2004 over 375000 animals were tested in the following 12 months. No positive results have yet been obtained in these or previous tests (USDA BSE Testing). This implies a putative upper limit of under 10 per million in this target group. Assuming, as analysis has shown, the relative risk in this group is about 30 times higher than in the population as a whole (European Commission, 2002c), then the incidence in the population as a whole is under 3 per 10 million. This figure could possibly be biased downwards if affected animals are diagnosed and disposed of without being tested. Taking account of testing done and the lack of clinical cases seen in many other countries also, it seems highly unlikely that the spontaneous rate can be as much as 3 per 10 million head. Nor can spontaneous occurrence explain incidences of ca. 30 cases of BARBs per year in 2002/4 in the UK adult cattle population of ca. 4 million. [NOTE ADDED 30 JUNE: The recent confirmation of a previously inconclusive case in the USA affects these calculations. If the animal did not have access to infected feed, the calculations have to be revised: they suggest a sporadic incidence in the population of 1/(375000 x 30) or almost 1 per 10 million, with the upper limit under 5 per 10 million.] 16. Calculation of a maximum rate of possible transformation from scrapie to BSE is less feasible. Nevertheless, BSE appears not to have arisen in the UK until around the early 1980s, despite the presence of scrapie in sheep here for at least 200 years. Although a change in the scrapie prion may have been the cause of the initial cases of BSE, the difference between their properties in mice and the uniformity of the BSE brain lesions suggest it is unlikely that more than one such mutation was the source of BSE. It is most unlikely that the same mutation could be occurring often enough to contribute significantly to BARBs cases. Furthermore BARBs cases do not match the geographical distribution of the sheep population. The evidence from the absence of BSE in many countries and the surveillance schemes abroad indicates that most BARBs cases cannot have arisen spontaneously, although the possibility cannot be excluded that a very


242 Atypical and classical BSE are different strains based upon Western blot profiles 243 (Hill, 2004; Normile, 2004; Baron et al., 2006), and this study indicates that disease Page 11 of 23 Journal of Animal Science Downloaded from jas.fass.org by on November 12, 2008. 12 progresses via different routes for these strains. The disparate 244 routes of pathogenesis in 245 atypical BSE can occur by 1 of 2 means. One possibility is that the source of infectivity 246 in atypical BSE is exposure to contaminated feedstuffs, as is the case for classical BSE, 247 but progression occurs in a disparate manner that bypasses the influence of the indel 248 polymorphisms. The other possibility is that atypical BSE is occurring spontaneously in 249 the host. Support for atypical BSE occurring spontaneously are the parallels to sporadic 250 TSE in humans, specifically, occurrence in older hosts and a comparable low incidence 251 rate (Baron and Biacabe, 2006). Furthermore, atypical BSE occurs as isolated, sporadic 252 cases in contrast to the clustering of cases observed for feed borne classical BSE 253 (Donnelly et al., 1997). Interestingly, the only native born cases of BSE in the United 254 States identified to date have been classified as atypical BSE.

255 No experiment can conclusively confirm a spontaneous nature for atypical BSE.



Monday, February 11, 2008 7:00 am Registration and Morning Coffee

Emerging Concerns: De novo Formation of Prions

9:05 De novo Generation of Prion Infectivity in a Cell-Free System Joaquin Castilla, Ph.D., Assistant Professor, Department of Infectology, Scripps Research Institute-Florida Transmissible spongiform encephalopathies (TSEs) are a group of neurodegenerative disorders affecting both humans and animals. There is no available treatment or therapy for these fatal diseases. The infectious agent associated with TSEs (termed prion) appears to be composed uniquely of a protein, which is a conformationally-modified version (PrPSc) of the cellular prion protein (PrPC). The disease is propagated by the conversion of host PrPC into PrPSc induced by small quantities of PrPSc. Interestingly, prions occur in the form of different strains that show distinct biological and physicochemical properties. TSEs can have diverse origins, including genetic, sporadic (putatively spontaneous) and infectious. The occurrence of sporadic cases of prion diseases in humans and maybe in other species, i.e. atypical bovine spongiform encephalopathy (BSE) in European and USA cattle and atypical scrapie cases in sheep suggest that spontaneous prion diseases may happen infrequently but ubiquitously. However, there are no reported cases of spontaneously-occurring prion disease in experimental wild-type rodent models. We have used a novel technique, Protein Misfolding Cyclic Amplification (PMCA) to rapidly propagate prions in the test tube, using normal brain homogenate as substrate. Prions propagated in vitro are infectious in vivo and maintain their prion strain specificity. PMCA has been used to efficiently amplify a variety of prion strains from mouse, hamster, bank vole, deer, cattle, sheep and human. Therefore, to mimic spontaneous generation of infectivity in vitro becomes one of the most important challenges in the prion field. We show here, for the first time, the de novo generation of infectious prions from bank voles (Clethrionomys glareolus) starting with non-infectious brain homogenates. Several biochemically different prion strains were generated using two different wild-type vole genotypes. The de novo in vitro generated PrPSc was highly infectious after its inoculation in bank voles. We show an extensive characterization of this "spontaneous" phenomenon.


Pathogenesis Chairperson: Suzette Priola, Ph.D.

11:10 Accumulation of Prion Protein in the Brain That is Not Associated with Transmissible Disease Pedro Piccardo, M.D., Senior Investigator, OBRR / DETTD / LBPUA, FDA (Invited)

11:35 High Levels of TSE Infectivity Can Be Associated with Little or No Detectable PrPSc in Vivo Rona Barron, Ph.D., Neuropathogenesis Unit, Roslin Institute and Royal (Dick) School of Veterinary Studies This work examines the relationship between TSE infectivity and the abnormal prion protein, PrPSc. In a mouse model of disease we have shown high titres of TSE infectivity in brain tissue which contains little or no PrP-res. We also found no evidence of other abnormal PrP isofoms such as PK-sen PrPSc. These data question the true relationship between PrPSc and TSE infectivity, and the current reliance on PrPSc as the sole diagnostic marker for TSE disease.

12:00 Conversion of the BASE Prion into the BSE Prion: The Origin of BSE? Fabrizio Tagliavini, Ph.D., Director, Division of Neurology 5 & Neuropathology, Neurological Institute "Carlo Besta" Twenty years after the identification of bovine spongiform encephalopathy (BSE), the origin of the causal agent is still unknown. This issue is of fundamental importance, since knowledge of the origin of the BSE agent is essential for prevention of future outbreak of the disease or variants thereof in cattle and other mammals. We carried out transmission studies with transgenic mice expressing bovine PrP and four lines of non-transgenic mice and found that an atypical form of spongiform encephalopathy of cattle, termed BASE or BSE-L, is caused by a prion strain distinct from that of classical BSE. Noteworthy, this newly characterized prion strain has the ability to convert into the classical BSE strain upon serial transmission to inbred mouse lines. According to these results, BASE--which is regarded as a sporadic form of prion disease in cattle--may be the origin of BSE, following conversion of the causal agent in an intermediate host.

12:45 Luncheon Technology Workshop (Sponsorship Available) or Lunch on Your Own

2:00 Sporadic CJD and Atypical BSE: Two Children of One Protein Maurizio Pocchiari, Ph.D., Director of Research, Virology, Istituto Superiore Di Sanita The identification of forms of TSE diseases in cattle caused by prion strains different from BSE has raised new concerns on the possibility that these novel agents might induce disease in humans with a phenotype resembling sporadic CJD. The analysis of the distribution of the different molecular subtypes of sporadic CJD might give some answers.


Originally published as JGV in Press, 10.1099/vir.0.010801-0 on July 22, 2009 Originally published as JGV in Press, 10.1099/vir.0.010801-0 on June 17, 2009 J Gen Virol 90 (2009), 2563-2568; DOI 10.1099/vir.0.010801-0

Short Communication

PrPTSE in muscle-associated lymphatic tissue during the preclinical stage of mice infected orally with bovine spongiform encephalopathy

Franco Cardone1,, Achim Thomzig2,, Walter Schulz-Schaeffer3, Angelina Valanzano1, Marco Sbriccoli1, Hanin Abdel-Haq1, Silvia Graziano1, Sandra Pritzkow2, Maria Puopolo1, Paul Brown4, Michael Beekes2 and Maurizio Pocchiari1

1 Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy 2 Robert Koch-Institut (P24 – Transmissible Spongiform Encephalopathies), Nordufer 20, 13353 Berlin, Germany 3 Prion and Dementia Research Unit, Department of Neuropathology, University Medical Center, Georg-August University Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany 4 7815 Exeter Road, Bethesda, MD 20814, USA

Correspondence Franco Cardone franco.cardone@iss.it

The involvement of muscles in the pathogenesis of transmissible spongiform encephalopathies (TSEs) is irregular and unpredictable. We show that the TSE-specific protein (PrPTSE) is present in muscles of mice fed with a mouse-adapted strain of bovine spongiform encephalopathy as early as 100 days post-infection, corresponding to about one-third of the incubation period. The proportion of mice with PrPTSE-positive muscles and the number of muscles involved increased as infection progressed, but never attained more than a limited distribution, even at the clinical stage of disease. The appearance of PrPTSE in muscles during the preclinical stage of disease was probably due to the haematogenous/lymphatic spread of infectivity from the gastrointestinal tract to lymphatic tissues associated with muscles, whereas in symptomatic animals, the presence of PrPTSE in the nervous system, in neuromuscular junctions and in muscle fibres suggests a centrifugal spread from the central nervous system, as already observed in other TSE models.

These authors contributed equally to this work.


14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America

update October 2009

T. Singeltary

Bacliff, TX, USA


An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


12 years independent research of available data


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.


International Society for Infectious Diseases Web: http://www.isid.org

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***


my comments to PLosone here ;


Friday, February 05, 2010

New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review


Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)


Wednesday, February 24, 2010

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th

ICID International Scientific Exchange Brochure -



Rangen Inc 2/11/10

Department of Health and Human Services Public Health Service Food and Drug Administration Seattle District Pacific Region 22201 23rd Drive SE Bothell, WA 98021-4421 Telephone: 425-486-8788 FAX: 425-483-4996

February 11, 2010



In reply refer to Warning Letter SEA 10-11

Christopher T. Rangen, President Rangen, Inc. 115-13th Avenue South PO Box 706 Buhl, Idaho 83316


Dear Mr. Rangen: On June 9-11, 2009, U.S. Food and Drug Administration (FDA) investigators inspected your animal feed manufacturing facilities located at 115-13th Avenue South, Buhl, Idaho. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Section 589.2000 (21 C.F.R. 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility that were adulterated within the meaning of section 402(a)(4) of the Federal Food, Drug, and Cosmetic Act (the Act), 21 U.S.C. § 342(a)(4), and misbranded within the meaning of section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). Our investigation determined that adulteration resulted from the failure of your firm to provide for measures to avoid commingling or cross-contamination. The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found:

1. Your firm failed to provide for and use cleanout procedures or other means adequate to prevent carry-over of products that contain or may contain proteins derived from mammalian tissues into animal feed that may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B). Since your feed is prepared, packed, or held under these conditions it is, therefore, adulterated under section 402(a)(4) of the Act, 21 U.S.C. § 342(a)(4).

. Mink feed that was not labeled "Do not feed to cattle or other ruminants," in accordance with 21 CFR 589.2000(e)(1)(i) and that, therefore, might be fed to ruminants, was produced using the same equipment as aquaculture feed that contains proteins derived from mammalian tissues, such as meat and bone meal. You conducted no clean-outs or flushes of equipment to remove proteins derived from mammalian tissues that may have been present before manufacturing the mink feed that might be fed to ruminants.

. The auger trucks you used to deliver bulk mink feed which contained or may have contained proteins derived from mammalian tissues were not subject to an effective clean-out prior to their use to deliver bulk animal feed, including ruminant feed, that did not contain such materials. There were no procedures to clean the trucks to remove proteins derived from mammalian tissues before shipment of animal feeds that did not contain such materials.

2. You failed to label all products which contained or may have contained proteins derived from mammalian tissues with the statement, "Do not feed to cattle or other ruminants," as required by 21 C.F.R. 589.2000(e)(1)(i). Such products are misbranded under Section 403(a)(1) of the Act, 21 U.S.C. § 343(a)(1). The misbranded product includes bulk mink feed.

. On June 9, 2009, the investigators observed approximately (b)(4) pallets of (b)(4) 50 pound bags of (b)(4) MINK FEED, lot 06/05/09. All bagged mink feed, as well as approximately (b)(4)% of bulk mink feed, manufactured at your facility, was produced using the aquaculture feed production equipment used to produce feed containing proteins derived from mammalian tissues. Because mink feed produced using this equipment may have contained mammalian tissues, it was not properly labeled, as required by 21 C.F.R. 589.2000(e)(1)(i).

This letter is not intended to serve as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct the above violations and you should establish a system whereby violations do not occur. Failure to promptly correct these violations may result in regulatory action, such seizure and/or injunction, without further notice.

We acknowledge your July 31, 2009 letter detailing procedures you had implemented or planned to implement to prevent future violations of FDA regulations relating to mammalian proteins in animal feed. In particular the letter stated that Rangen would no longer purchase meat and bone meal for use in any of its animal feeds and that existing inventories of mammalian protein ingredients would be exhausted by December 31, 2009. Division Manager, Joy Kinyon made similar assertions in the course of FDA's June 2009 inspection. The July 31, 2009 letter further set out procedures Rangen would use to remedy observed violations of FDA regulations while mammalian proteins were still being used at Rangen. Finally you explained steps taken to recover or relabel feed that may have been contaminated due to commingling resulting from your manufacturing and distribution procedures. Within fifteen (15) working days of receiving this letter you should, in writing, confirm the steps you took prior to receiving this letter and notify FDA of steps you have taken since receiving this letter to bring your firm into compliance with the law. Your response should include each step that has been taken or will be taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within fifteen (15) working days, state the reason for the delay and the time frame within which the corrections will be completed. Please include copies of any available documentation demonstrating that corrections have been made.

Your written reply should be directed to Scott A. Nabe, Compliance Officer, U.S. Food and Drug Administration, 22201 23rd Drive SE, Bothell, Washington 98021-4421. If you have any questions about this letter, please contact Mr. Nabe at (425) 483-4753.



Charles M. Breen District Director Seattle District

cc: Joy A. Kinyon, Division Manager, Aquaculture Feeds-General Feeds Rangen, Inc. PO Box 706 115-13th Avenue South Buhl, Idaho 83316



Monday, March 1, 2010



Tuesday, March 2, 2010

Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA


Monday, May 4, 2009

Back to the Past With New TSE Testing Agricultural Research/May-June 2009


I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;


''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''

Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA


I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS

Month Number of Tests

Feb 2009 -- 1,891

Jan 2009 -- 4,620



Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.


Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock

Project Number: 3625-32000-086-05 Project Type: Specific Cooperative Agreement

Start Date: Sep 15, 2004 End Date: Sep 14, 2009

Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.

Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.


Wednesday, February 11, 2009

Atypical BSE North America Update February 2009

Both of the BSE cases ascertained in the US native-born cattle were atypical cases (H-type), which contributed to the initial ambiguity of the diagnosis. 174, 185 In Canada, there have been 2 atypical BSE cases in addition to the 14 cases of the classic UK strain of BSE2: one was the H-type, and the other was of the L-type.198


source :

Enhanced Abstract Journal of the American Veterinary Medical Association January 1, 2009, Vol. 234, No. 1, Pages 59-72

Bovine spongiform encephalopathy

Jane L. Harman, DVM, PhD; Christopher J. Silva, PhD


Atypical BSE North America Update February 2009


Sunday, May 17, 2009




Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...


Sunday, September 6, 2009










Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$


Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy


Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008


QFC s Delayed Mad Cow Response Draws Lawsuit

Family claims QFC should have used customer database to warn those at risk sooner

March 05, 2004

SEATTLE A Bellevue, Wash. family today filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with mad cow disease.

The suit, filed in King County Superior Court, seeks to represent all Washington residents who purchased the potentially tainted meat, and asks the court to establish a medical monitoring fund.

Jill Crowson purchased the potentially tainted beef from a Bellevue QFC on Dec. 22 and 23, and used her Advantage Card, QFC s customer loyalty program. She served the meat to her husband over Dec. 25 and 26, and later heard of the recall in the newspaper.

Steve Berman, the attorney representing the Crowsons, asserts that since the company tracks purchases, it should have warned the Crowsons and many other customers who purchased the beef at approximately 40 stores across Washington.

If you lose your keys with an Advantage Card attached, QFC will return them to you free of charge, said Berman. If they can contact you over a lost set of car keys, why couldn t they contact you and tell you that the beef you purchased could kill you?

QFC is among the large number of grocers that track customer purchases through loyalty cards like the Advantage Card. Once a customer shares contact information including name, address and phone number they are given discounts on certain items.

Regardless of any discounts offered, the loyalty card tracks customers every purchase and stores them in a central database, the complaint states.

We contend that QFC knew which Advantage Card customers purchased the suspect meat, and could have easily called to warn them, said Berman. Instead, QFC used a series of spurious excuses to hide their failure to act.

On Dec. 23, the U.S. Department of Agriculture ordered the recall of approximately 10,410 pounds of raw beef that may have been infected with bovine spongiform encephalopathy (BSE), which if consumed by humans can lead to the always-fatal Cruetzfeldt-Jakobs Disease (vCJD).

According to the complaint, QFC at first mistakenly believed it did not have any of the affected beef and took no action to remove the product from its shelves. The store later removed the beef on Dec. 24, but then did little to warn those who earlier purchased the meat, the suit claims.

It wasn t until Dec. 27 that the grocery chain posted small signs with information about the recall, the complaint alleges.

The Crowsons contacted QFC when they suspected they had purchased the potentially tainted meat, but QFC would not confirm their suspicions for two more weeks, the suit states. According to Berman, the family had to file a written request before QFC would confirm their fears.

According to health experts, Cruetzfeldt-Jakobs Disease can have an incubation period of as long as 30 years. There is no test to determine if infection took place after possible exposure, nor is there any treatment once one is infected. The condition is always fatal.

If the court grants the suit class-action status, QFC would likely be compelled to turn over the names of those who purchased the potentially tainted beef.

The proposed class-action claims QFC violated provisions of the Washington Product Liability Act by failing to give adequate warning to consumers about the potentially dangerous meat.

The suit seeks unspecified damages for the plaintiffs, as well as the establishment of a medical monitoring fund.


QFC's Delayed Mad Cow Response Draws Lawsuit

... subsidiary of Kroger , claiming the grocery store chain should ... beef potentially tainted with "mad cow disease ...
beef at approximately 40 stores across Washington. ...
www.forrelease.com/D20040305/sff005.P2.03042004214558.03634.html - 9k -

040307 Woman Sues QFC Over Mad-Cow Recall ...
Jakob disease, the human form of mad-cow, from eating ...
QFC is subject to the Washington Product Liability ...
been found in a slaughtered Yakima County dairy cow. ...
www.spcnetwork.com/mii/2004/040307.htm - 6k




QUALITY FOOD CENTERS, INC., an Ohio corporation Defendent

NO. 04-2-05608-0 SEA


The Court hereby GRANTS the defendant's motion to dismiss the plaintiff's claims based on a manufacturer's strict liability (Counts I and II) and DENIES the defendant's motion to dismiss the plaintiff's claim of negligence by a product seller (Count III).

DATED this 14th day of June, 2004



Date Filed: March 5, 2004 Court: King County Superior Court (Washington) Location: Seattle Ticker Symbol: NYSE:KR

Join This Suit Tell a Friend

Consumers filed a proposed class-action lawsuit against Quality Food Centers (QFC), a subsidiary of Kroger (NYSE: KR), claiming the grocery store chain should have used information gathered through its customer loyalty program to warn those who purchased beef potentially tainted with ?mad cow disease.? The USDA issued a recall notice for the meat on December 23, 2003. QFC sold the meat through its approximately 40 stores across Washington.

The suit claims that even though QFC had the ability to quickly warn every customer who purchased the potentially deadly meat if they used the QFC Advantage Card at the time of purchase, the grocery store neglected to do so.

The suit seeks to represent every consumer in Washington state who purchased the recalled meat from QFC.

Recent Updates

June 14, 2004 - the King County Superior Court gave the green light to a suit claiming QFC didn't do enough to warn customers about beef potentially tainted with 'mad cow disease,' finding enough questions about the beef and QFC's responsibility to explore in the courtroom.

Read the court order.


see full text ;



AS far as human transmission for CWD, you will just have to make your own minds up on that. In my opinion, there is as much evidence for transmission of cwd to humans, as there is for scrapie and BSE to humans. it's the friendly fire there from i.e. cwd exposure that concerns me the most, but the did not recall all this cwd positive elk meat FOR THE WELL BEING OF THE DEAD ELK ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

please see ;



PRODUCT a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; CODE Elk Meats with production dates of December 29, 30, and 31 RECALLING FIRM/MANUFACTURER Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009. Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing. REASON Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). VOLUME OF PRODUCT IN COMMERCE Unknown DISTRIBUTION NV, CA, TX, CO, NY, UT, FL, OK







Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.


Tuesday, August 04, 2009

Susceptibilities of Nonhuman Primates to Chronic Wasting Disease


Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


full text ;


From: TSS (216-119-163-189.ipset45.wt.net)


Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"


Cc: "Race, Richard (NIH)" ; ; "Belay,


Sent: Monday, September 30, 2002 9:22 AM


Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was

attached to your email), we did not say CWD in humans will present like

variant CJD.

That assumption would be wrong. I encourage you to read the whole

article and call me if you have questions or need more clarification

(phone: 404-639-3091). Also, we do not claim that "no-one has ever been

infected with prion disease from eating venison." Our conclusion stating

that we found no strong evidence of CWD transmission to humans in the

article you quoted or in any other forum is limited to the patients we


Ermias Belay, M.D.

Centers for Disease Control and Prevention

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


Sent: Sunday, September 29, 2002 10:15 AM

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV



Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most

serious because of rapid horizontal spread and higher prevalence than BSE in

UK, up to 15% in some populations. Also may be a risk to humans - evidence

that it is not dangerous to humans is thin.



Tuesday, August 04, 2009 Susceptibilities of Nonhuman Primates to Chronic Wasting Disease


Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains


In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.


CWD occurred principally in two locations, this one at Sybille and in a similar faccility at Fort Collins, Colorado, some 120 miles southwest. It was estimated that in total probably 60-70 cases of CWD have occurred.

It was difficult to gain a clear account of incidence and temporal sequence of events (-this presumably is data awaiting publication - see below) but during the period 1981-1984, 10-15 cases occurred at the Sybille facility.

The moribidity amongst mule deer in the facilities ie. those of the natural potentially exposed group has been about 90% with 100% mortality.


Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

see full text 33 pages ;



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