Paris, 8-12 February 2010
26. Bovine spongiform encephalopathy (Chapter 11.6.)
The Code Commission received comments from Canada, the EU, Norway, People’s Republic of China, Switzerland and the USA.
The Code Commission reviewed comments on the description of tallow, as modified at the 77th General Session in May 2009. The Code Commission noted that some countries continue to raise concerns about the safety of tallow made from raw material from animals that have not passed ante and post mortem inspection. However, the Commission considered that the rationale provided at previous meetings is still relevant and no text modifications were made.
The Code Commission accepted a proposal from a Member to modify the wording of Article 11.6.1. and therefore deleted similar text proposed for Article 11.6.3. and Article 11.6.4.
The Code Commission referred to the SCAD comments from Members regarding new scientific data that raise the possibility that the tissues of the jejunum may harbour BSE infectivity and the possible need for new text in Article 11.6.14.
The Code Commission agreed with Members who commented that for countries not in the negligible risk category, the key issue for BSE risk management is the age of the cattle at the time of slaughter, not the BSE status of the country. Moreover, brains and eyes present a higher risk than vertebral column. The text of Article 11.6.14. was modified accordingly.
The Code Commission did not accept proposed text amendments from a Member regarding the definition of cattle subpopulations for surveillance purposes as the Commission considered that the points raised were adequately addressed in the existing text.
The Code Commission discussed the comments of Members regarding the investigation of BSE cases in cattle born after the feed ban. The Code Commission agreed with a Member’s argument that the finding of cases in such cattle does not imply that risk management is not effective. However, the investigation of cohorts of cattle born after the feed ban would normally be part of the epidemiological investigation of BSE cases in cattle born after the ban. The Code Commission made appropriate text amendments to Article 11.6.23.
The revised text is presented at Annex XXVIII of this report for adoption.
33. Scrapie (Chapter 14.9.)
The Code Commission received comments from Australia, Canada, the EU, Norway, New Zealand, People’s Republic of China, the USA and the IETS.
In response to a Member comment that the OIE should present the scientific rationale for stating that scrapie is not considered to present a risk to human health, the Code Commission called attention to the following:
Brown P., Cathala F., Raubertas R.F., Gajdusek D.C. & Castaigne P. (1987). The epidemiology of Creutzfeldt-Jakob disease: conclusion of a 15-year investigation in France and review of the world literature. Neurology, 37, 895–904.
Budka H. (2007). Portrait of Creutzfeldt-Jakob disease. In Hörnlimann B, Riesner D, Kretschmar H (editors) Prions in Humans and Animals. De Gruyter, Berlin, 195–203.
Harries Jones R., Knight R., Will R.G., Cousens S.N., Smith P.G. & Mathews W.B. (1988). Creutzfeldt-Jakob disease in England and Wales, 1980-1984: a case-control study of potential risk factors. Journal of Neurology, Neurosurgery and Psychiatry, 51, 1113–1119.
Hörnlimann B., van Keulen L., Ulvund M.J. & Bradley R. (2007). Portrait of scrapie in sheep and goat. In Hörnlimann B, Riesner D, Kretschmar H (editors) Prions in Humans and Animals. De Gruyter, Berlin, 222–232.
Kondo K. & Kuriowa Y. (1982). A case-control study of Creutzfeldt-Jakob disease: association with physical injuries. Annals of Neurology, 11, 377–381.
Van Dijn C.M., Delasniere-Laupretre N., Masullo C., de Silva R., Wientjens DPWM, Brandel J.-P., Weber T., Bonavita V., Zeidler M., Alperovitch A., Poser S., Granieri E., Hofman A. & Hill R.G. (1998). Case-control study of risk factors of Creutzfeldt-Jakob disease in Europe during 1993-95. The Lancet, 351, 1081–1085.
Zerr I. & Poser S. (2007). Epidemiology and risk factors of Creutzfeldt-Jakob disease. In Hörnlimann B, Riesner D, Kretschmar H (editors) Prions in Humans and Animals. De Gruyter, Berlin, 423–433.
In response to several Members questioning the sufficiency of evidence for the inclusion of semen as a safe commodity, the Code Commission removed semen from Article 14.9.1., modified Article 14.9.2. accordingly and re-instated Article 14.9.8. However, based on the fact that there is some evidence for the safety of semen, the Code Commission deleted 14.9.8. point 1(b), consistent with a Member’s recommendation.
Based on advice from the International Embryo Transfer Society (IETS) the Code Commission added ‘’in vivo derived sheep embryos handled in accordance with Chapter 4.7. of the Terrestrial Code‘’ to Article 14.9.1. and modified Article 14.9.2. and other articles in the chapter as appropriate.
The Code Commission modified Article 14.9.3. in response to Members’ comments.
The Code Commission changed the target prevalence of the surveillance system prescribed in Article 14.9.3., section 2 (b) from 0.1% of all chronic wasting conditions to 0.01% of the defined target population. This was based on consideration of a Member comment, in which information from a national scrapie surveillance programme was presented and relevant references provided, i.e.
Lynn T., Grannis J., Williams M., Marshall K., Miller R., Bush E. & Bruntz S. An evaluation of scrapie surveillance in the United States. Prev. Vet. Med., 2007 Sep 14, 81 (1-3):70–9. Epub 2007 May 7.
Wineland N.E., Detwiler L.A. & Salman M.D. 1998. Epidemiologic analysis of reported scrapie in sheep in the United States: 1117 cases (1947-1992). Journal of the American Veterinary Medical Association, 212; 713–718.
The target population was broadened after consideration of a Member comment, based on a published report, i.e.
Cappuchio et al., Clinical Signs and Diagnosis of Scrapie in Italy: A Comparative Study in Sheep and Goats, J. Vet. Med. A 48, 23–31 (2001).
Noting the absence of evidence suggesting that the feeding of meat and bone meal has been associated with the transmission of scrapie, the Code Commission did not accept Members’ requests to modify Article 14.9.3. point 3. The Code Commission considered that it was prudent and reasonable to maintain the existing text.
In relation to Article 14.9.4., the Code Commission did not accept a Member’s arguments that rams from scrapie-free flocks could safely be permitted to have brief contact with sheep of lesser status. There is scientific evidence that horizontal transmission of scrapie between adult sheep and from a contaminated environment may occur. The Member’s proposal that such risks could be managed by imposing quarantine of the rams returning after contact with sheep of lesser status was rejected as impractical, given the prolonged incubation period of scrapie.
The Code Commission deleted Article 14.9.14. on the basis that relevant considerations are covered elsewhere in the revised Chapter 14.9.
The revised text is presented at Annex XXXV of this report for adoption.
WHY does the O.I.E. recognize the U.S.A. and all of North America as a BSE controled risk, even though the G.A.O. and the O.I.G repeatedly reported of the failures and flaws of not only the BSE surveillance program in the USA, also the ruminant feed ban of August 4, 1997, where it still fails today in 2010 ?
URGENT DATA ON ATYPICAL BSE RISK FACTORS TO HUMANS AND ANIMALS OIE REFUSE TO ACKNOWLEDGE $
position: Post Doctoral Fellow Atypical BSE in Cattle
Closing date: December 24, 2009
Anticipated start date: January/February 2010
Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
18.173 page 189
Experimental Challenge of Cattle with H-type and L-type Atypical BSE
A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
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
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.
page 114 ;
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
Transmissible Spongiform Encephalopathy
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 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.''
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
Wednesday, March 31, 2010
Atypical BSE in Cattle
95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASES OF ANIMALS IN THE USA
another question, just how long have these atypical BSE TSEs been around in the bovine ???
let's look at another case of atypical BSE in Germany way back in 1992 ;
Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years
Date: April 26, 2007 at 1:08 pm PST 1992
NEW BRAIN DISORDER
3. WHAT ABOUT REPORTS OF NEW FORM OF BSE?
THE VETERINARY RECORD HAS PUBLISHED AN ARTICLE ON A NEW BRAIN DISORDER OF CATTLE DISCOVERED THROUGH OUR CONTROL MEASURES FOR BSE. ALTHOUGH IT PRESENTS SIMILAR CLINICAL SIGNS TO BSE THERE ARE MAJOR DIFFERENCES IN THE HISTOPATHOLOGY AND INCUBATION PERIODS BETWEEN THE TWO. MUST EMPHASISE THAT THIS IS NOT BSE.
4. IS THIS NEW BRAIN DISORDER A THREAT?
WE DO NOT EVEN KNOW WHETHER THE AGENT OF THIS DISEASE IS TRANSMISSIBLE. IN ANY CASE, CASES SO FAR IDENTIFIED HAD SHOWN SIMILAR SYMPTOMS TO THOSE OF BSE, AND THEREFORE HAVE BEEN SLAUGHTERED AND INCINERATED, SO THAT IF A TRANSMISSIBLE AGENT WERE INVOLVED IT WOULD HAVE BEEN ELIMINATED. .......
2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.
3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.
This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.
COLLINGE THREATENS TO GO TO MEDIA
NOW, how the U.S.D.A. explains this case, will be beyond me, but they explained their way out of Aretha N. Vinson's case, i mean they literally made the official anouncement that it was not nvCJD first, however no one ever did say what it was, another spontaneous event. so myself and others await the explaination of Irma Linda Andablo. i am sure it will be another spontaneous CJD case, of which the fact Mrs. Andablo worked for TYSON foods, "where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle", will be documented as nothing more than another mere coincidence of the obvious. ...TSS
March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed .
The key word here is diverse. What does diverse mean?
If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP]
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
WHY does the O.I.E. fail to recognize any of the following transmission studies showing transmission of typical scrapie to many different species and to non-human primates, and still refuse to acknowledge these studies as any part of risk factor to humans from anyone of the over 20 strains of typical scrapie ?
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
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.
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)
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).
EMBO reports 4, 5, 530–533 (2003) doi:10.1038/sj.embor.embor827 AOP Published online: 11 April 2003
Widespread PrPSc accumulation in muscles of hamsters orally infected with scrapie
Achim Thomzig, Christine Kratzel, Gudrun Lenz, Dominique Krüger & Michael Beekes
Robert Koch-Institut, P26, Nordufer 20, D-13353 Berlin, Germany
To whom correspondence should be addressed Michael Beekes Tel: +49 30 4547 2396; Fax: +49 30 4547 2609; BeekesM@rki.de
Received 13 February 2003; Accepted 13 March 2003; Published online 11 April 2003.
Scrapie, bovine spongiform encephalopathy and chronic wasting disease are orally communicable, transmissible spongiform encephalopathies (TSEs). As zoonotic transmissions of TSE agents may pose a risk to human health, the identification of reservoirs for infectivity in animal tissues and their exclusion from human consumption has become a matter of great importance for consumer protection. In this study, a variety of muscles from hamsters that were orally challenged with scrapie was screened for the presence of a molecular marker for TSE infection, PrPSc (the pathological isoform of the prion protein PrP). Sensitive western blotting revealed consistent PrPSc accumulation in skeletal muscles from forelimb and hindlimb, head, back and shoulder, and in tongue. Previously, our animal model has provided substantial baseline information about the peripheral routing of infection in naturally occurring and orally acquired ruminant TSEs. Therefore, the findings described here highlight further the necessity to investigate thoroughly whether muscles of TSE-infected sheep, cattle, elk and deer contain infectious agents.
EMBO reports 4, 5, 530–533 (2003) doi:10.1038/sj.embor.embor827 AOP Published online: 11 April 2003
Nobel Lecture, December 13, 1976
ALSO, see in animal Scrapie;
New World monkeys : capuchin, spider, squirrel
Old World monkeys : cynomolgus macaque, rhesus
J Infect Dis. 1994 Apr;169(4):814-20.
Intracerebral transmission of scrapie to cattle.
Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, Robinson MM.
USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA 50010.
To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy.
PMID: 8133096 [PubMed - indexed for MEDLINE]
Second passage of a US scrapie agent in cattle
References and further reading may be available for this article. To view references and further reading you must purchase this article.
R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl
United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA
Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.
Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of “prion protein scrapie” (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.
Correspondence to: R. C. Cutlip, USDA, Agricultural Research Service, National Animal Disease Center, P.O. Box 70, 2300 Dayton Road, Ames, Iowa 50010, USA.
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
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. ........
Macaque Models of Human Infectious Disease
Macaques have served as models for more than 70 human infectious diseases of diverse etiologies, including a multitude of agents—bacteria, viruses, fungi, parasites, prions. The remarkable diversity of human infectious diseases that have been modeled in the macaque includes global, childhood, and tropical diseases as well as newly emergent, sexually transmitted, oncogenic, degenerative neurologic, potential bioterrorism, and miscellaneous other diseases. Historically, macaques played a major role in establishing the etiology of yellow fever, polio, and prion diseases. With rare exceptions (Chagas disease, bartonellosis), all of the infectious diseases in this review are of Old World origin. Perhaps most surprising is the large number of tropical (16), newly emergent (7), and bioterrorism diseases (9) that have been modeled in macaques. Many of these human diseases (e.g., AIDS, hepatitis E, bartonellosis) are a consequence of zoonotic infection. However, infectious agents of certain diseases, including measles and tuberculosis, can sometimes go both ways, and thus several human pathogens are threats to nonhuman primates including macaques. Through experimental studies in macaques, researchers have gained insight into pathogenic mechanisms and novel treatment and vaccine approaches for many human infectious diseases, most notably acquired immunodeficiency syndrome (AIDS), which is caused by infection with human immunodeficiency virus (HIV). Other infectious agents for which macaques have been a uniquely valuable resource for biomedical research, and particularly vaccinology, include influenza virus, paramyxoviruses, flaviviruses, arenaviruses, hepatitis E virus, papillomavirus, smallpox virus, Mycobacteria, Bacillus anthracis, Helicobacter pylori, Yersinia pestis, and Plasmodium species. This review summarizes the extensive past and present research on macaque models of human infectious disease.
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
Then follow up with PNAS studies from which new scientist article written from;
SEE FULL TEXT AND STUDIES ON ATYPICAL NOR-98 SCRAPIE ;
WHY does the O.I.E. fail to recognize the atypical Scrapie as a Transmissible Spongiform Encephalopathy, and refuse to regulate trade of the atypical scrapie as with other Transmissible Spongiform Encephalopathy ?
especially since ;
Sent: Friday, April 16, 2010 11:38 AM
Subject: PRO-MED ATYPICAL SCRAPIE
Background ----------- "Retrospective studies have identified cases predating the initial identification of this form of scrapie, and epidemiological studies have indicated that it does not conform to the behaviour of an infectious disease, giving rise to the hypothesis that it represents spontaneous disease. However, atypical scrapie isolates have been shown to be infectious experimentally, through intracerebral inoculation in transgenic mice and sheep. [Many of the neurological diseases can be transmitted by intracerebral inoculation, which causes this moderator to approach intracerebral studies as a tool for study, but not necessarily as a direct indication of transmissibility of natural diseases. - Mod.TG]
"The 1st successful challenge of a sheep with 'field' atypical scrapie from an homologous donor sheep was reported in 2007.
"Results -------- "This study demonstrates that atypical scrapie has distinct clinical, pathological, and biochemical characteristics which are maintained on transmission and sub-passage, and which are distinct from other strains of transmissible spongiform encephalopathies in the same host genotype.
"Conclusions ------------ Atypical scrapie is consistently transmissible within AHQ homozygous sheep, and the disease phenotype is preserved on sub-passage."
Lastly, this moderator wishes to thank Terry Singletary for some of his behind the scenes work of providing citations and references for this posting. - Mod.TG]
The HealthMap/ProMED-mail interactive map of Australia is available at
THE O.I.E has failed terribly in protecting not only animal health, but also human health, by putting the cart before the horse so to speak. The O.I.E. made atypical scrapie a legal trading commodity, without any transmission studies to prove if it will or will not transmit to other species, especially man. THE O.I.E. did this all the while knowing that the atypical scrapie was ;
Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,
see also ;
All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
Monday, December 14, 2009
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
SEE FULL TEXT AND STUDIES ON ATYPICAL NOR-98 SCRAPIE ;
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
WHY does the O.I.E. still fail to recognize a potential risk from Chronic Wasting Disease (TSE) in cervids to animal and man ?
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
REPEAL THE B.S.E. MINIMAL RISK REGION (MRR) policy !
THEN, put back in place the B.S.E. G.B.R. Risk Assessments, and enhance them to include all T.S.E. i.e. the atypical strains.
REPEAL THE B.S.E. MINIMAL RISK REGION (MRR) policy !
The BSE MRR policy was shoved down the throat of every country by the O.I.E. and the U.S.D.A..
MOST every one of those Country's came down with BSE.
THE O.I.E. formula to detect B.S.E. is, and has been flawed. It was and is a policy set up for trade, NOT for human and animal health.
The BSE MRR policy made legal what the U.K. did, when the poisoned the globe with BSE. Except BSE has mutated and different strains have evolved, some that are more virulent than the c-BSE, all can transmit to humans (Kong et al 2009), all are in North America.
The BSE MRR policy was ratified while two cases of BSE were sitting on the shelf waiting to be confirmed (one was 7+ months later after an Act of Congress, and the other suspect sample that sat on a shelf for 4 months, which was not preserved correctly, which only IHC could be used, the least likely to detect BSE, was found inconclusive or negative), then the Alabama mad cow was confirmed. AFTER this, the USDA shut the testing program down to levels that would not detect BSE.
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
SEE FULL TEXT ;
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
Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY
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. ...
SEE FULL TEXT ;
IN A NUT SHELL ;
(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 the Central Bureau,
WHAT THE USA AND THE OIE DID, was make legal what the U.K. did when they poisoned the globe with mad cow disease. they knew what they were doing, but did it anyway. The BSE GBR risk assessments were put into place so that would never ever happen again. UNTIL they USA finally documented a case. UP until then, the USA would not accept products that may contain BSE from any country. ONCE the USA lost the 'gold card', the shoe was the on the other foot, and they literally left 2 suspect mad cow brain samples sit on a shelf for 7+ months and 4 months respectfully, all the while the BSE MRR policy was being legalized. ONCE made legal, and after an act of Congress, the one suspect Texas mad cow case that had sat up on a shelf for 7+ months was finally confirmed by Weybridge et al in the U.K., and the other, which the sample was not preserved correctly, was found after being a suspect, to be inconclussive and finally they termed it negative. Then the Alabama mad cow was confirmed and they had to shut the program down before they found anymore. ...TSS
England worried briefly about infecting other countries 27 Aug 00
correspondence obtained by Terry S. Singeltary Sr.
DEPARTMENT OF HEALTH AND SOCIAL SECURITY Richmond House, 79 Whitehall, London SWIA 2NS Telephone 01-210 3000 From the Chief Medical Officer Sir Donald Achson KBE DM DSc FRCP FFCM FFOM
Mr K C Meldrum Chief Veterinary Officer Ministry of Agriculture, Fisheries and Food Government Buildings Hook Rise South Tolworth Surbiton Surrey KT6 7NG 3 January 1990
Dear Mr Meldrum
BOVINE SPONGIFORM ENCEPHALOPATHY
You will recall that we have previously discussed the potential risks of BSE occurring in other countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.
I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminamts in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants [or zoo animals, including rare and endangered primates -- webmaster]. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.
I would be very interested to hear how you feel this gap in the present precautionary measures to eliminate BSE should be closed. We should be aiming at the global elimination of this new bovine disense. The export of our meat and bone meal is a continuing risk to other countries.
Yours Sincerely Donald Acheson
Copy: Dr Metters Dr Pickles
90/1.03/1.1 ============ BSE13/3 0083
Dr Pickles From: Dr J S Metters DCM0 International, Prevention and Community Services 7 June 1990 Copies to: Dr McInnes Miss Pease Mr Otley
1. I spoke to Mr Capstick yesterday. Among other things, he told me that MAFF are now considering the labelling of animal foodstuffs, and in particular what detail would be required if such labelling was made compulsory. Apparently our freedom of action is constrained by EC Directives [total garbage, MAFF wants to keep exporting -- webmaster], and there is also concern about the level of detail that should be included in any foodstuff labels.
2. Mr Capstick suggested that this was not an area that DH had a particular interest. I countered by saying that we supported the principle of labelling of animal foodstuffs, particularly when these were going for export.
3. I also thanked him for keeping us informed, in a way that I hope encourage further communication of MAFF's internal deliberations.
J S METTERS Room 509 Richmond House Ext. 5591 92/YdeS 90/6.7/5.1
see singeltary comments 2000 ;
MY comments/questions are as follows ;
1. SINCE the first Harvard BSE Risk Assessment was so flawed and fraught with error after the PEER REVIEW assessment assessed this fact, how do you plan on stopping this from happening again, will there be another peer review with top TSE Scientist, an impartial jury so-to-speak, to assess this new and updated Harvard BSE/TSE risk assessment and will this assessment include the Atypical TSE and SRM issues ?
*** Suppressed peer review of Harvard study October 31, 2002 ***
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
2.1 Import of cattle from BSE-Risk2 countries
An overview of the data on live cattle imports is presented in table 1 and is based on data as provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to the USA. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC July 2000 and updated January 2002).
• According to the country dossier, 323 cattle were imported directly from the UK, all between 1980 and 1989, and 10 via Canada in 90, 91 and 92. According to Eurostat, 327 cattle were imported from UK. Of these cattle 96% were beef breeding cattle, 4% were dairy cattle. After 1989 an import stop for UK cattle was in effect.
• Cattle imported from the UK were traced-back in 1995. This trace back exercise provided the details on which the assessment of the HRS of the import risk assessment is based. The animals still alive in 1995 (117 cattle) have been purchased, diagnostic samples were taken, and the carcasses were incinerated. These animals were not taken into account for the external challenge. All these animals tested negative for BSE (histopathology and IHC). Of these 117 cattle 52 came from UK-herds in which one or more cases of BSE later on developed.
• For 173 cattle imported from the UK in the 80s, information on their final use is, according to the HRS, lacking and it is indicated that it is possible that some of these animals could have been rendered. In the HRS it is also noted that these animals were imported before the peak of the epidemic and none came from a birth cohort in which a BSE case is known to be developed. However, based on realistic worst case assumptions it has to be assumed that they created a risk if rendered for feed.
• EU export data show that from the EU (excluding UK), 1,663 cattle were exported to the USA since 1980; according to the CD only 460 cattle have been imported from the EU.
• According to the CD, 162 cattle were imported from Ireland between 1980 and 1988 (according to Eurostat 233). The trace back of these animals showed that 22 were found as being excluded from rendering in the US system and 4 were born in US quarantine and were therefore not taken into account for the external challenge.
• According to the CD, 6 cattle from Belgium (Eurostat also 6), 46 from Germany (Eurostat 430), 3 from Austria (Eurostat 0) and 8 from Italy (Eurostat 21) have been imported. The 40 breeding-cattle imported from these countries in 1996 and 1997 were all traced back and none of them entered the US system.
• According to Eurostat, 12 cattle from Denmark and 558 cattle from the Netherlands were imported to the USA. These imports were not indicated in the CD.
• Additionally according to the CD, 235 cattle have been imported from France (403 according to Eurostat) and 103 cattle from Switzerland (48 according to other sources).
• The discrepancy in the EU export data and the import data in the CD (See table 1) can in some cases, be explained by the use of the fiscal year data (from October to September) in the CD.
• Between 235.000 and 1.7 Million (CD and Other sources) cattle per year are imported to the USA from Canada. According to the CD, feeder/slaughter cattle represent typically more around 80% of the imported cattle from Canada; therefore, only 20% of the imported cattle have been taken into account.
• From Japan, 242 animals from a special beef breed were imported. These animals were traced, and were mostly excluded from the US rendering system. At most 39 of these animals have been rendered.
2.2 Import of MBM or MBM-containing feedstuffs from BSE-Risk countries
An overview of the data on MBM imports is presented in table 2 and is based on data provided in the country dossier (CD) and corresponding data on relevant exports as available from BSE risk countries that exported to the USA. Only data from risk periods are indicated, i.e. those periods when exports from a BSE risk country already represented an external challenge, according to the SSC opinion on the GBR (SSC, July 2000 and updated January 2002).
• The CD reports import of 5 tons of MBM from the UK. According to Eurostat, 63 tons have been exported from the UK to the USA between 1980 and 1996; however, according the updated MBM statistics from the UK (August 2001) 24 tons of MBM were exported from the UK to the USA between 1980 and 1996; 39 tons exported in 1989 were not confirmed by the updated UK export statistic and therefore not taken into account. A further 38 tons were exported in 1997-1998 and 39 tons in 1999. As it was illegal to export mammalian meat meal, bone meal and MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. Therefore, these imports were not taken into account.
• According to the CD, MBM was imported from Denmark, France, Italy and the Netherlands. It was claimed but not substantiated that these imports were not from ruminant origin, and therefore did not contribute to the BSE risk of the USA.
• The Eurostat export statistics indicated additional exports from Belgium, Greece, Ireland and Spain.
• Very large amounts of MBM (CD and other sources) between 18.000 and 44.000 tons annually were imported from Canada.
country imported 2038 (other sources) or 1128 (CD) live cattle from BSE risk countries other than Canada, of which 327 (other sources) or 323 (CD) came from the UK. From Canada the imports were >500,000 animals per year. The numbers shown in table 1 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported cattle did not enter the domestic BSE-cattle system, i.e. were not rendered into feed. In the case of the USA, all the animals for which tracing information showed that they were not rendered were excluded from the external challenge. MBM imports:
In total the country imported 689 tons MBM (CD) or 2,230 tons MBM (other sources) from BSE risk countries other than Canada, of which 5 tons (CD) or 101 tons (other sources) were exported from the UK (UK export data). From Canada, the imports were about 30 000 tons per year. The numbers shown in table 2 are the raw import figures and are not reflecting the adjusted imports for the assessment of the external challenge. Broken down to 5 year periods the resulting external challenge is as given in table 3. This assessment takes into account the different aspects discussed above that allow to assume that certain imported MBM did not enter the domestic BSE/cattle system or did not represent an external challenge for other reasons. As it was illegal to export mammalian MBM from UK since 27/03/1996, exports indicated after that date should only have included non-mammalian MBM. In the case of the USA imported MBM from UK in 1989 and between 1997 and 1999 was not taken into account.
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
please see full text ;
“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.
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)
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.
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Canada Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (0.1Mb)
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 to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. 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 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.
A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. 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 Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.
Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Mexico Question number: EFSA-Q-2003-083
Adopted: 1 July 2004 Summary (108 KB)
Report (168 KB)
Annex (251 KB)
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 Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.
EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.
Overview of GBR assessments covering 2000-2006: list of countries and their GBR level of risk (64 KB)
Published: 20 August 2004 Last updated: 8 September 2004
Thursday, April 8, 2010
FINAL REPORT OF A MISSION CARRIED OUT IN THE UNITED KINGDOM FROM 19 TO 29 JANUARY 2010 IN ORDER TO EVALUATE MEASURES CONCERNING BSE DG(SANCO) 2010-8344 - MR FINAL
1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY other Countries list in PDF file)
USA -------- TOTALS ''8'' TONS CANADA -- TOTALS ''29'' TONS
1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA
USA ------- TOTALS ''358'' TONS
CANADA --TOTALS ''24'' TONS
BONE-IN BEEF AND VEAL
USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons above?)
UK EXPORT OF LIKE CATTLE TO USA AND CANADA
1986 TO 1996 USA TOTAL = 1297
1986 TO 1996 CAN TOTAL = 299
UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987
CANADA -- 64,526 KG
UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED OR FROZEN OTHER THAN LIVER DEC 1987 YTD
USA -- 45,943 KG
UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988
CANADA -- 4,163 KG
PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE TO DEC 1988
USA -------- 28,609 KG CANADA -- 22,044 KG
MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989
USA -------- 17,880 KG MEXICO---- 33,444 KG
BONELESS MEAT OF BOVINE 1989
USA --------111,953 KG CANADA---1,800 KG MEXICO --- 1,143,387 KG
EDIBLE OFFAL OF BOVINE ANIMALS 1989
USA -------- 19,980 KG MEXICO--- 31,244 KG
MEAT OF BOVINE ANIMALS BONELESS 1990
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.???
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: firstname.lastname@example.org (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
Wednesday, April 16, 2008
MBM, greaves, meat offal, live cattle, imports from UK to USA vs Canada
AS i said before, one OAI can result in tons of banned suspect mad cow feed into commerce. plus, in my opinion, a VAI could lead to the same as an OAI if regulations were not followed, as not labeling pet food, and selling pet food as feed for ruminants.
Animal Proteins Prohibited in Ruminant Feed & Cattle Materials Prohibited in All Animal Feed
Nonprohibited Materials: These feed materials CAN be fed to ruminants.
A. The following protein products derived from mammals, including ruminants, are exempt from the Ruminant Feed Ban rule and CAN be fed to ruminants: Blood and blood products Milk products (milk and milk protein) Pure porcine (pork) protein Pure equine (horse) protein Gelatin Inspected meat products, such as plate waste, which have been cooked and offered for human food and further heat processed for animal feed.
B. The following non-mammalian protein products are not included in from the Ruminant Feed Ban rule and CAN be fed to ruminants: Poultry protein Vegetable protein Marine (fish) protein
C. The following materials CAN be fed to ruminants because they are not protein or tissue: Oil Recovered cooking oils from restaurants and food processors Amino Acids **Tallow ** and Tallow Derivatives Dicalcium Phosphate
** SEE Table 3 TALLOW STANDARDS**
Prohibited Materials: The products listed below, unless from the materials in Table 1, CANNOT be fed to ruminants because they may carry the BSE infective agent. *(See exceptions on page 3)
Animal By-Product Meal
Hydrolyzed Leather Meal
Bone Meal, Cooked
Meat and Bone Meal
Bone Meal, Steamed
Meat and Bone Meal Tankage
Cooked Bone Marrow
Dehydrated Food Waste
Meat Meal Tankage
Meat Protein Isolate
Distressed Pet Food
Mechanically Separated Bone Marrow
Dried Meat Solubles
Restaurant Food Waste
Salvage Pet Food
Food Processing Waste
Stock / Broth
Glandular Meal and Extracted Glandular Meal
Tallow exceeding 0.15% Insoluble Impurities
Unborn calf Carcasses
AGR PUB 631-282 (N/10/09) Page 1 of 8 21 CFR 589.2000 21 CFR 589.2001
Tallow with Insoluble Impurities level of 0.15% or LESS CAN be used in Ruminant and Non-Ruminant Feed
Tallow with MORE than 0.15% Insoluble Impurities
labeled “Do Not Feed To Cattle Or Other Ruminants”. CANNOT be used in Ruminant Feed
Can be used in Non-Ruminant Feed Tallow with MORE than 0.15% Insoluble Impurities
labeled “Do Not Feed To Animals”. CANNOT be used in any animal feed.
Cattle Materials Prohibited in Animal Feed (CMPAF)
1. The entire carcass of BSE-positive cattle.
2. The brains and spinal cords of cattle 30 months of age and older.
3. The entire carcass of cattle that are 30 months of age or older from which brains and spinal cords were not effectively removed or excluded from animal feed.
4. Mechanically separated beef derived from materials described in 2 and 3 above.
5. Tallow that exceeds 0.15% insoluble impurities derived from materials described in 2 and 3 above.
Title 21 CFR 589.2000 BSE - Feed Rule prohibits feeding most mammalian protein to all ruminants.
Title 21 CFR 589.2001 - Enhanced BSE Feed Rule prohibits feeding certain materials from cattle (CMPAF) to all animals.
LABELING – Cautionary Statement:
Non-Prohibited Materials: No cautionary label requirements.
Prohibited Materials: Must be labeled “Do Not Feed To Cattle Or Other Ruminants”.
CMPAF: Must be labeled “Do Not Feed To Animals”.
CMPAF: In addition to labeling, CMPAF must be marked with an agent that can be readily detected on visual inspection.
AGR PUB 631-282 (N/10/09) Page 2 of
SEE THE DEFINITIONS REFERENCES HERE ;
definition of RUMINANT ;
Physiologically, a ruminant is a mammal of the order Artiodactyla that digests plant-based food by initially softening it within the animal's first stomach, then regurgitating the semi-digested mass, now known as cud, and chewing it again. The process of rechewing the cud to further break down plant matter and stimulate digestion is called "ruminating". Ruminating mammals include cattle, goats, sheep, giraffes, bison, yaks, water buffalo, deer, camels, alpacas, llamas, wildebeest, antelope, pronghorn, and nilgai. Taxonomically, the suborder Ruminantia includes all those species except the camels, llamas, and alpacas, which are Tylopoda. Therefore, the term 'ruminant' is not synonymous with Ruminantia. The word "ruminant" comes from the Latin ruminare, which means "to chew over again".
we also feed cattle cervids with CWD. cervid are ;
cervid (sûrvd) Any of various hoofed mammals of the family Cervidae, which includes the deer and elk. Male cervids typically grow antlers that are shed yearly.
M A M M A L I A N P R O T E I N F E E D I N G B A N
(this is not and has not taken place in the USA...TSS)
IN my opinion, I believe a total mammalian feed ban (NOT PARTIAL), is warranted, especially here in the USA. we have CWD in cervid (two documented strains to date), we have atypical and typical Scrapie in sheep and Scrapie in goats, BSE and atypical BSE here in the USA. WE have TME in mink (two documented strains to date), and nobody is looking at TSE in the feline and or canine species, and you know why. because all this is fed back to livestock for human and animal consumption over the years, decades. we also have many TSE strains in humans. daa.
>> An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented. <<<
Number of active firms inspected – 1,041 Number of active firms handling materials prohibited from use in ruminant feed – 485 (47% of those active firms inspected) Of the 485 active firms handling prohibited materials, their most recent inspection revealed that: 1 firm (0.2%) was classified as OAI
Total number of active renderers, feed mills, and protein blenders inspected – 6,671 Number of active renderers, feed mills, and protein blenders processing with prohibited materials – 460 (6.9%) Of the 460 active renderers, feed mills, and protein blenders processing with prohibited materials, their most recent inspection revealed that: 1 firm (0.2%) was classified as OAI
Number of active firms inspected – 24,675 Number of active firms handling materials prohibited from use in ruminant feed – 8,285 (34% of those active firms inspected) Of the 8,285 active firms handling prohibited materials, their most recent inspection revealed that: 1 firm (0%) was classified as OAI
Number of active firms whose initial inspection has been reported to FDA – 29,535 Number of active firms handling materials prohibited from use in ruminant feed – 8,885 (30% of those active firms inspected) Of the 8,885 active firms handling prohibited materials, their most recent inspection revealed that: 1 firm (0.01%) was classified as OAI
SRMS to humans 2010 ;
North Dakota Firm Recalls Whole Beef Head Products That Contain Prohibited Materials
Recall Release CLASS II RECALL FSIS-RC-023-2010 HEALTH RISK: LOW
Congressional and Public Affairs (202) 720-9113 Catherine Cochran
WASHINGTON, April 5, 2010 - North American Bison Co-Op, a New Rockford, N.D., establishment is recalling approximately 25,000 pounds of whole beef heads containing tongues that may not have had the tonsils completely removed, which is not compliant with regulations that require the removal of tonsils from cattle of all ages, the U.S. Department of Agriculture's Food Safety and Inspection Service (FSIS) announced today.
Tonsils are considered a specified risk material (SRM) and must be removed from cattle of all ages in accordance with FSIS regulations. SRMs are tissues that are known to contain the infective agent in cattle infected with Bovine Spongiform Encephalopathy (BSE), as well as materials that are closely associated with these potentially infective tissues. Therefore, FSIS prohibits SRMs from use as human food to minimize potential human exposure to the BSE agent.
Monday, April 5, 2010
Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
please see full text ;
for example, one bad apple equals how much banned potential mad cow protein in commerce, and this is what i am talking about, where simply a mislabeling i.e. VAI could lead too, much less a OAI. ...TSS
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
and all this was confirmed here ;
C O N F I R M E D
----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Thursday, November 05, 2009 9:25 PM
Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
Thursday, November 12, 2009
BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
THIS IS A NO BRAINER, BUT FEEDING BLOOD MEAL TO CATTLE IS ABOUT AS STUPID AS FEEDING MEAT AND BONE MEAL TO CATTLE (RUMINANTS AND MAMMALS) if you want to stop all TSE. ...TSS
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
Monday, October 26, 2009
MAD COW DISEASE, AND U.S. BEEF TRADE
MAD COW DISEASE, CJD, TSE, SOUND SCIENCE, COMMERCE, AND SELLING YOUR SOUL TO THE DEVIL
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E.
Posted: Wed Dec 19, 2007 3:47 pm Post subject: OIE
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.
Saturday, April 10, 2010
TOYOTA VS MAD COW DISEASE USA OIE BSE MRR IMPORT AND EXPORT TRADE WARS
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN
''they don't wanna know, the dont' care''
watch and listen to video here, turn it up ;
I find it appauling that in 2010, the O.I.E. is still going by science on Transmissible Spongiform Encephalopathy that is decades old. New emerging strains of Transmissible Spongiform Encephalopathy have emerged, in different species, along with new science that shows these new strains of T.S.E. are more virulent than the c-B.S.E. MOST every Country that went by the O.I.E. B.S.E. guidelines, most all came down with B.S.E. THE O.I.E. has now shown they are nothing more than a National Trading Brokerage for all strains of animal T.S.E. AS i said before, O.I.E. 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. ...
still disgusted in Bacliff, Texas USA 77518
Terry S. Singeltary Sr.