COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on BSE beef Bellinger, Singeltary, FRIDAY, 5 FEBRUARY 2010
COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA
COMMONWEALTH OF AUSTRALIA
Proof Committee Hansard
RRA&T 2 Senate Friday, 5 February 2010
RURAL AND REGIONAL AFFAIRS AND TRANSPORT
[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 Decemberlast 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.
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—
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 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-the shelves 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.
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—Sorry to interrupt you. We had better clarify it, because there are people out there that are hanging on every word that is said in here so they can photocopy it and flick it around the country. So we had better get it very, very clear.
Mr Bellinger—They are.
Senator STERLE—They are?
Mr Bellinger—Yes.
Senator STERLE—You are saying they are an arm of the WTO?
Mr Bellinger—They are under the WTO umbrella.
Senator STERLE—Okay, but not an arm of the WTO.
Senator O’BRIEN—They are under the WTO umbrella—underneath and therefore controlled by. That is what your implication is.
Senator HEFFERNAN—OIE—
Senator STERLE—Hang on. Chair—
CHAIR—Senator Sterle has the call.
Senator STERLE—I just want to clarify: they are not an arm of the WTO?
Mr Bellinger—An arm or an umbrella—it is hard to define.
Senator HEFFERNAN—The OIE’s advice is provided by the WTO.
Senator STERLE—Senator Heffernan, you have had your turn.
CHAIR—Senator Heffernan, Senator Sterle has the call.
Senator STERLE—Thank you, Chair. Also, you have said Robert Zoellick is head of the WTO?
Mr Bellinger—The WTO, yes.
Senator STERLE—I am led to believe he is head of the World Bank.
Mr Bellinger—I stand corrected.
Senator STERLE—We will clarify that. You mentioned the interview you did on a local radio station about meat off the shelves. What this committee does know is that that is policy. A hundred and fifty-two countries are signed up to that policy that if there is an outbreak, regardless of where the outbreak is, all meat has to be taken off the shelves, and that is previous government policy.
Mr Bellinger—Excuse me, Senator Sterle. You are saying that 152 countries have this policy as well as Australia?
Senator STERLE—There are 152 under the WTO. If there is an outbreak, regardless of where the outbreak is, all the meat must come off the shelves.
Mr Bellinger—But there was no meat off the shelves in the United States or Japan when an outbreak occurred. Why wasn’t there?
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.
Mr Carter—There is no country in the world that has taken its meat off the shelves. Senator STERLE—Let us get it very clear. Regardless of whether they have or they have not, that is the protocol.
Senator HEFFERNAN—No, it is not.
Senator STERLE—It is. This is what we have been led to believe.
Mr Carter—But they are irrelevant protocols because they are not implementable.
Mr Bellinger—So you are saying that the United States and Japan have broken protocol?
Senator STERLE—No, I am not saying that. You are the ones who are saying they have not done it. I do not know. So do not put words in my mouth. I just want to address this very clearly. Under previous government policy, regardless of where the outbreak was—and fortunately we did not have it here—all meat had to come off the shelves.
Senator HEFFERNAN—That is not right.
Senator STERLE—I am not asking you, Senator Heffernan; I am asking the witnesses.
Mr Carter—I would like to ask you, Senator Sterle.
Senator STERLE—No, you get to answer the questions here.
Mr Carter—You said it was the policy—
snip...
CHAIR—That is okay. It has all been submitted to us, so we can go through and read the submission. But thank you very much for that.
Senator BACK—Dr Steel, thanks again for the work you have done. Can I take you to page 69 of our proceedings. It is a response dated 20 January to you from Dr Andy Carroll, and I think this really goes to the sense of the whole thing. You had written to him expressing the concerns you have raised here. His response says:
In regard to chronic wasting disease (CWD) of deer and scrapie of sheep and goats, there is no evidence that these diseases can naturally infect cattle grazing on the same pastures as infected deer, sheep or goats. There is also no evidence that people can be infected by CWD or scrapie by consumption of meat … DAFF veterinarians working on transmissible spongiform encephalopathy issues are aware of the CWD research conducted by Dr. Elizabeth Williams—
and my colleague at the University of California. Are you satisfied that the integrity of animal health, beef health, in Australia and the integrity of human health is adequately answered and met? Are you happy now as a result of that paragraph?
Dr Steel—Definitely not. It is a bit like the radar people at Pearl Harbour thinking, ‘Oh, it’s the boys coming in,’ if you do not anticipate. There are three principles in science:
presupposition, evidence and logic, and I do not think this new policy has any of these qualities at all.
snip...
Please refer to Page 9,BACKGROUND AND HISTORY,section 28, in which he states that “ Scrapie has been transmitted to mice and other experimental animals in the laboratory.” He does not say that it has been transmitted to cattle. That is an incredibly important transmission, even though it is experimental. I know that CWD and scrapie do not directly affect humans, and that is the position as it is. But there have been transmission experiments and I have referred to how vCJD was discovered by using these interspecies transmissions. Again, Professor Mathews omits Scrapie experimental infection to cattle, a domestic animal which has carried BSE to cause vCJD. To quote my submission again: All of a group of nine cattle … succumbed easily to Scrapie … This is what happens: in repeated transmissions—even though it is experimental—these become amplified and the survival times get shorter and shorter. Scrapie and CWD are highly infectious. Direct animal-to-animal transmission occurs with scrapie and CWD via body fluids—saliva and urine—in normal animals, even a year before being confirmed by the rapid test. That is incredible. This is all with this new technology. As I say in my submission:
In Table 1 BSE’s “Experiment transmission to” heading, are listed “mice, sheep and goats” but Professor Mathews makes no mention in the Review of the following important “back-cross” information from sheep to BSE in cattle. Why is it important? This information is about the changes that occur when Atypical cattle isolates of BSE acquire strain features— and purists would say, ‘What do you mean by strain?’ but let us use ‘strain’— similar to the classical BSE agent when propagated in mice expressing SHEEP prions. Professor Mathews does not—
CHAIR—Dr Steel, I am sorry, but we are going to have to move to questions or we are going to run out of time.
Dr Steel—Yes, I have not got through it because—
CHAIR—That is okay. It has all been submitted to us, so we can go through and read the submission. But thank you very much for that.
Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry
***> Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Prion Conference 2023
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
"Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material."
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."
=====end
Cattle with the EK211 PRNP polymorphism are susceptible to the H-type bovine spongiform encephalopathy agent from either E211K or wild type donors after oronasal inoculation
Justin J. Greenleea, Eric D. Cassmanna, S. Jo Moorea,b, and M. Heather West Greenleec
aVirus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA; bOak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, US; cDepartment of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, US
Aims: In 2006, a case of H-type bovine spongiform encephalopathy (H-BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Material and Methods: Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with the H-BSE agent from either the US 2004 case (wild type donor; n = 3) or from the US 2006 case with the E211K polymorphism (n = 4). Cattle were observed daily throughout the course of the experiment for the development of clinical signs. When signs were noted, animals were euthanized and necropsied. Cattle were confirmed positive for abnormal BSE prions by enzyme immunoassay (EIA; Idexx HerdChek BSE Ag Test), anti-PrP immunohistochemistry (IHC) on brainstem, and microscopic examination for vacuolation.
Results: Three-out-of-four (75%) calves with the EK211 genotype developed clinical signs of H-BSE including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and were euthanized. Two of the positive EK211 steers received H-BSE US 2004 inoculum (Incubation Period (IP): 59.3 and 72.3 months) while the other positive steer received the E211K H-BSE inoculum (IP: 49.7 months). EIA confirmed that abundant misfolded protein (O.D. 2.57–4.0) in the brainstem, and IHC demonstrated PrPScthroughout the brain. All wild type recipient cattle and a single EK211 steer remained asymptomatic for the duration of the experiment (approximately 7 years post-inoculation) and no abnormal prion protein was detected in these cattle by EIA.
Conclusions: This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. Cattle with the EK211 genotype are oronasally susceptible to small doses of the H-BSE agent from either EK211 or EE211 (wild type) donors. Wild-type EE211 cattle remained asymptomatic for the duration of the experiment with this small dose (0.1 g) of inoculum. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Funded by: US Department of Agriculture
How in the hell do you make a complete recall of 27,694,240 lbs of feed that was manufactured from materials that may have been contaminated with mammalian protein, in one state, Michigan, 2006? Wonder how much was fed out?
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim’s" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006.
FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006.
Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
???
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
FOR IMMEDIATE RELEASE P01-05 January 30, 2001
Print Media: 301-827-6242 Broadcast Media: 301-827-3434 Consumer Inquiries: 888-INFO-FDA
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
SATURDAY, MAY 20, 2023
***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
MAY 19, 2023
2 weeks before the announcement of this recent mad cow case in the USA, i submitted this to the APHIS et al;
***> APPRX. 2 weeks before the recent mad cow case was confirmed in the USA, in Tennessee, atypical L-Type BSE, I submitted this to the APHIS et al;
Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission May 2, 2023
''said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical''...
big outbreak of spontaneous mad cow disease evidently, around the same time, strange;
WEDNESDAY, NOVEMBER 08, 2023
Ireland Atypical BSE confirmed November 3 2023
TUESDAY, NOVEMBER 14, 2023
Ireland Atypical BSE case, 3 progeny of case cow to be culled
SUNDAY, JULY 16, 2023
Switzerland Atypical BSE detected in a cow in the canton of St. Gallen
WAHIS, WOAH, OIE, REPORT Switzerland Bovine Spongiform Encephalopathy Atypical L-Type
Switzerland Bovine Spongiform Encephalopathy Atypical L-Type
Switzerland - Bovine spongiform encephalopathy - Immediate notification
Monday, March 20, 2023
WAHIS, WOAH, OIE, REPORT United Kingdom Bovine Spongiform Encephalopathy Atypical H-Type
BRAZIL BSE START DATE 2023/01/18
BRAZIL BSE CONFIRMATION DATE 2023/02/22
BRAZIL BSE END DATE 2023/03/03
SPAIN BSE START DATE 2023/01/21
SPAIN BSE CONFIRMATION DATE 2023/02/03
SPAIN BSE END DATE 2023/02/06
NETHERLANDS BSE START DATE 2023/02/01
NETHERLANDS BSE CONFIRMATION DATE 2023/02/01
NETHERLANDS BSE END DATE 2023/03/13
PLEASE NOTE, USDA ET AL ONLY TESTING <25k CATTLE FOR MAD COW DISEASE, woefully inadequate, yet USDA just documented a case Atypical L-Type BSE, the most virulent strain to date...
Monday, May 22, 2023
***> BSE TSE Prion MAD COW TESTING IN THE USA COMPARED TO OTHER COUNTRIES?
FRIDAY, DECEMBER 22, 2023
The Mad Cow That Stole Christmas, 20 Years Later
Wednesday, May 24, 2023
***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
USA 50 State Emergency BSE Conference Call 2001
Monday, November 13, 2023
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
NOW, BE AWARE, OIE AND USDA HAVE NOW MADE ATYPICAL SCRAPIE AND ATYPICAL BSE A LEGAL TRADING COMMODITY, WITH NO REPORTING OF SAID ATYPICAL CASES, EXCEPT FOR A VOLUNTARY NOTE ON ANNUAL REPORT...i don't make this stuff up...terry
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
Transmission of scrapie prions to primate after an extended silent incubation period
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
==============
PRION 2015 CONFERENCE
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 1933-690X
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications
Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE.
***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $ 5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip... R. BRADLEY
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.
snip...
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
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously. snip... 76/10.12/4.6
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)
C. J. GIBBS jun. & D. C. GAJDUSEK 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).
Detection of classical BSE prions in asymptomatic cows after inoculation with atypical/Nor98 scrapie
* Marina Betancor, Belén Marín, Alicia Otero, Carlos Hedman, Antonio Romero, Tomás Barrio, Eloisa Sevilla, Jean-Yves Douet, Alvina Huor, Juan José Badiola, Olivier Andréoletti & Rosa Bolea * Veterinary Research volume 54, Article number: 89 (2023)
Abstract
The emergence of bovine spongiform encephalopathy (BSE) prions from atypical scrapie has been recently observed upon experimental transmission to rodent and swine models. This study aimed to assess whether the inoculation of atypical scrapie could induce BSE-like disease in cattle. Four calves were intracerebrally challenged with atypical scrapie. Animals were euthanized without clinical signs of prion disease and tested negative for PrPSc accumulation by immunohistochemistry and western blotting. However, an emergence of BSE-like prion seeding activity was detected during in vitro propagation of brain samples from the inoculated animals. These findings suggest that atypical scrapie may represent a potential source of BSE infection in cattle.
Snip…
Further in vivo experiments challenging different mouse lines have been started in order to confirm the infectivity of the PMCA products obtained in this study. However, in conclusion, our findings show that the propagation of atypical scrapie in cattle leads to the emergence of BSE-like seeding activity. This is a concerning issue with far-reaching implications for public health and food safety. The possibility of interspecies transmission of prion diseases and the emergence of new prion strains highlight the critical need for continued surveillance and monitoring of these diseases in both animal and human populations. Early detection of prion diseases is crucial, and highly sensitive detection techniques such as PMCA can play an important role in this regard.
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Disease phenotype of classical sheep scrapie is changed upon experimental passage through white-tailed deer
Author item Kokemuller, Robyn item MOORE, S.JO - Oak Ridge Institute For Science And Education (ORISE) item Bian, Jifeng item WEST GREENLEE, HEATHER - Iowa State University item Greenlee, Justin
Submitted to: PLoS Pathogens Publication Type: Peer Reviewed Journal Publication Acceptance Date: 11/9/2023 Publication Date: 12/4/2023 Citation: Kokemuller, R., Moore, S., Bian, J., West Greenlee, H.M., Greenlee, J.J. 2023. Disease phenotype of classical sheep scrapie is changed upon experimental passage through white-tailed deer. PLoS Pathogens. https://doi.org/10.1371/journal.ppat.1011815. DOI: https://doi.org/10.1371/journal.ppat.1011815 Interpretive Summary: Transmissible spongiform encephalopathies (TSEs) are a group of fatal diseases caused by the accumulation of misfolded prion protein in the brain. Ruminant species such as sheep, deer, and elk can get prion diseases. In sheep the disease is called scrapie. In deer and elk, the disease is called chronic wasting disease (CWD). The source of CWD is unknown, but one possibility is that scrapie jumped from sheep to deer. When we experimentally exposed white-tailed deer to the sheep scrapie agent, all deer developed scrapie. The purpose of the current experiment was to determine if sheep can get scrapie derived from white-tailed deer. Some sheep developed scrapie after oronasal exposure to the scrapie agent from white-tailed deer. Passage through white-tailed deer results in a scrapie isolate with different strain properties than the original inoculum. The detection of new strain properties was an unexpected result that will be the subject of further studies. These results indicate that sheep could be susceptible to the scrapie agent after passage through deer if exposed to the agent in natural or agricultural settings, which could be a confounding factor to the scrapie eradication program. National and state regulatory and wildlife officials should consider this information when developing plans to reduce or eliminate TSEs.
Technical Abstract: Transmissible spongiform encephalopathy (TSE) agents have strain variations that influence disease phenotype and may affect the potential for interspecies transmission. Since deer and sheep may use the same grazing land, it is important to understand the potential transmission of TSEs between these species. The US scrapie isolate (No.13-7) had a 100% attack rate in white-tailed deer after oronasal challenge. The purpose of this study was to determine if sheep are susceptible to oronasal challenge with the scrapie agent from white-tailed deer. Suffolk lambs of various prion protein genotypes were challenged by the oronasal route with a 10% brain homogenate from scrapie-affected white-tailed deer. Sheep were euthanized and necropsied upon development of clinical signs or at the end of the experiment (72 months post-inoculation). Tissues were tested for PrPSc by enzyme immunoassay, western blot, and immunohistochemistry. The first sheep (2/2) to develop clinical signs at approximately 29 months post-inoculation (MPI) had the VRQ/VRQ genotype. One of the two sheep with the ARQ/ARQ genotype also developed clinical signs at 48 MPI. This is in contrast to the original No.13-7 inoculum that has a faster incubation period in sheep with the ARQ/ARQ genotype compared to sheep of the VRQ/VRQ genotype. The shorter incubation period in VRQ/VRQ sheep than ARQ/ARQ sheep after passage through deer indicates a phenotype change. This is important because scrapie infected deer could transmit disease to sheep resulting in new scrapie strain properties. This work raises the concern that scrapie infected deer could serve as a confounding factor to scrapie eradication programs as the scrapie agent from deer is transmissible to sheep by the oronasal route.
Research Project: Elucidating the Pathobiology and Transmission of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
Author item Cassmann, Eric item QI, XU - Case Western Reserve University (CWRU) item KONG, QINGZHONG - Case Western Reserve University (CWRU) item Greenlee, Justin
Submitted to: Meeting Abstract Publication Type: Abstract Only Publication Acceptance Date: 3/15/2023 Publication Date: 5/30/2023 Citation: Cassmann, E.D., Qi, X., Kong, Q., Greenlee, J.J. 2023. The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons (abstract). Meeting Abstract. 4th International Chronic Wasting Disease Symposium, May 30-June 3, 2023, Denver, Colorado. Interpretive Summary:
Technical Abstract: The aim of this study was to evaluate the zoonotic potential of the raccoon passaged chronic wasting disease (CWD) agent in humanized transgenic mice in comparison with the North American CWD agent from the original white-tailed deer (WTD) host. Pooled brain (GG96) from CWD positive deer was used to intracranially inoculate two WTD and one raccoon. Brain homogenates (10% w/v) from the raccoon and the WTD were used to intracranially inoculate transgenic mice (Tg40h) expressing the methionine 109 human prion protein. Brains and spleens were collected from mice at experimental endpoints of clinical disease or approximately 700 days post-inoculation. Tissues were divided and homogenized or fixed in 10% buffered neutral formalin. Immunohistochemistry, enzyme immunoassay, and western blot were used to detect misfolded prion protein (PrPSc) in tissue. Tg40h mice inoculated with the raccoon passaged CWD agent from WTD exhibited a 100% (12/12) attack rate with an average incubation period of 605 days. PrPSc was detected in brain tissue by enzyme immunoassay with an average optical density of 3.6/4.0 for positive brains. PrPSc also was detected in brain tissue by western blot and immunohistochemistry. No PrPSc was detected in the spleens of mice inoculated with the raccoon passaged CWD agent. Humanized mice inoculated with the CWD agent from WTD did not have detectable PrPSc using conventional immunoassay techniques. These results demonstrated that the host range of the CWD agent from WTD was expanded in our experimental model after one passage through raccoons.
2023
OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
4. Definitions of meat-and-bone meal (MBM) and greaves
TUESDAY, NOVEMBER 28, 2023
EFSA TSE Report 2022 First published 28 November 2023 The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2022
THURSDAY, DECEMBER 7, 2023
Chronic Wasting Disease CWD TSE Prion Cervid Update By State December 2023 (Long Version)
(Short Version)
FRIDAY, DECEMBER 08, 2023
TEXAS CWD TSE PRION DIRE CONSEQUENCES ARE HERE!
FRIDAY, FEBRUARY 16, 2024
Texas TPWD CWD TSE Prion Positives Jump To 637 Confirmed Cases To Date
TUESDAY, JANUARY 16, 2024
CIDRAP launches international effort to prepare for possible chronic wasting disease spillover
MONDAY, FEBRUARY 05, 2024
Mad Cow Scaremongers, The Center For Consumer Freedom Team, Terry Singeltary Sr Revisited 2024
Tuesday, May 30, 2023
World Organisation for Animal Health 90th General Session of the World Assembly of Delegates BSE TSE Prion 2023
Professor John Collinge on tackling prion diseases, sCJD accounts for around 1 in 5000 deaths worldwide
MONDAY, SEPTEMBER 11, 2023
Professor John Collinge on tackling prion diseases
“The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide.”
There is accumulating evidence also for iatrogenic AD. Understanding prion biology, and in particular how propagation of prions leads to neurodegeneration, is therefore of central research importance in medicine.
MONDAY, DECEMBER 18, 2023
Change in Epidemiology of Creutzfeldt-Jakob Disease in the US, 2007-2020
TUESDAY, DECEMBER 12, 2023
CREUTZFELDT JAKOB DISEASE TSE PRION DISEASE UPDATE USA DECEMBER 2023
SUNDAY, NOVEMBER 26, 2023
The role of environmental factors on sporadic Creutzfeldt-Jakob disease mortality: evidence from an age-period-cohort analysis
22 years ago;
2001 Singeltary on CJD
February 14, 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr
Author Affiliations
JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
MONDAY, JANUARY 29, 202
Iatrogenic Alzheimer’s disease in recipients of cadaveric pituitary-derived growth hormone
''The clinical syndrome developed by these individuals can, therefore, be termed iatrogenic Alzheimer’s disease, and Alzheimer’s disease should now be recognized as a potentially transmissible disorder.''
Monday, January 29, 2024
iatrogenic Alzheimer’s disease, Alzheimer’s disease should now be recognized as a potentially transmissible disorder
Iatrogenic Alzheimer’s disease in recipients of cadaveric pituitary-derived growth hormone
Terry S. Singeltary Sr.
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