Thursday, January 05, 2012

Comparative analysis of Japanese and foreign L-type BSE prions

Short Communication


Comparative analysis of Japanese and foreign L-type BSE prions


Volume 6, Issue 1 January/February/March 2012


Kentaro Masujin, Ritsuko Miwa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama View affiliations


L-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE. To characterize the Japanese L-type BSE prion, we conducted a comparative study of the Japanese and foreign L-type BSE isolates. The L-type BSE isolates of Japan, Germany, France and Canada were intracerebrally inoculated into bovinized prion protein-overexpressing transgenic mice (TgBoPrP). All the examined L-type BSE isolates were transmitted to TgBoPrP mice, and no clear differences were observed in their biological and biochemical properties. Here, we present evidence that the Japanese and Canadian L-type BSE prions are identical to those from the European cases.







Tuesday, December 15, 2009

Intraspecies transmission of L-type-like bovine spongiform encephalopathy detected in Japan

NOTE






Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION


Date: August 24, 2005 at 2:47 pm PST August 24, 2005







Wednesday, August 20, 2008


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


SNIP...


IN CONFIDENCE


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.





SEE ;





COLLINGE THREATENS TO GO TO MEDIA





SEE ;





2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.


3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.


snip...


This minute is re-issued with a wider distribution. The information contained herein should NOT be disseminated further except on the basis of ''NEED TO KNOW''.


R Bradley




SEE ;





IN CONFIDENCE


BSE ATYPICAL LESION DISTRIBUTION




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1983


BSE CONSULTANT


APPROVAL OF MATERIAL FOR PUBLICATIONS


All material for publication including written works to be published in scientific journals, books, proceedings of scientific meetings, abstracts of verbally delivered papers and the like should be scrutinized for risk to the Ministry before dispatch to the publishers.............


full text;




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- 10 -


19. On 18th February, 1987 (YB87/2.18/1.1) I reported to Dr Watson and Dr Shreeve on a further case which we had received from Truro VIC. The brain had shown neuronal vacuolation and in brain extracts there were fibrils that were similar in size and appearance to SAFs from sheep with scrapie. The Virology Department was studying the brain further and considering a transmission study. A few weeks before this, I had discussed the possibility of a transmission study with Michael Dawson, a research officer in the Virology Department and an expert in viral diseases in sheep, and we were considering carefully the safety aspects. In my note I raised the question of whether we should disclose the information we had more widely to the VIS because this may assist in getting any other cases referred to CVL but there was the difficulty that we knew very little about the disorder and would be unable to deal with queries that might be raised.


20. On 23rd February, 1987 (YB87/2.23/1.1) I sent Mr Wells a note asking him to prepare a statement for publication in Vision, the in-house newsheet prepared by the VIS for the SVS, setting out details of what we had discovered. On 24th February, 1987 (YB87/2.25/2.1) Gerald Wells indicated in a note to me that he had discussed the proposed article with Mr Dawson and they both believed that it could be damaging to publish anything at that stage. They believed cases would be referred to CVL in any event because they were unusual and they did not feel "Vision" was an appropriate publication because its confidentiality was questionable and might lead to referrals to veterinary schools rather than CVL. Gerald Wells was also concerned about the resources available in his section to deal with referred cases. I replied (YB87/2.25/2.1) indicating a draft statement was needed by the Director before a decision on publication could be made. Gerald Wells prepared a draft statement (YB87/3.2/2.1) and sent it to me on 2nd March, 1987. In his cover note (YB87/3.2/1.1) he commented that he believed the distribution of any statement about the new disease outside of CVL to be premature because there was so little information available about the new disease. I passed on a copy of Gerald Wells' note to Dr Watson (YB87/3.2/3.1). I discussed the matter of publication with Dr Watson. No decision had been taken to publish any material at that stage and I sent a note to Gerald Wells letting him know the position and confirming that his views and those of Michael Dawson would be taken into account when a decision was taken.


- 11 -


21. In March, 1987 serious consideration was given to possible transmission (e.g. to hamsters) and other experiments (other than the collection of epidemiological data by the VIS and clinicopathology which had been in progress since the first cases were recognised in November, 1986).


22. On 23rd April, 1987 I sent a report (YB87/4.23/1.1) to Dr Watson and Dr Shreeve informing them that nine control brains were being examined for SAFs and a cow which appeared to be affected with BSE had been purchased for observation. The cow had come from the farm where the original cases had developed and had arrived at CVL on 22nd April, 1987.


23. On 15th May, 1987 Dr Watson informed me that the proposed "Vision" draft would be circulated to VICs in England and Wales if it was approved by management. On 22nd May, 1987 I was copied in on a note (YB87/5.22/2.1) from B.M Williams, (who I believe was Head of the VIS at this time but retired shortly after this), to Dr Watson. This confirmed that the draft prepared for publication in Vision was approved but that the final paragraph should be amended to make it clear that knowledge of the new disease should not be communicated to other research institutes or university departments. At a meeting with Dr Watson on 2nd June, 1987 he informed me that no communication should be made with NPU until after the meeting with the CVO on 5th June, 1987 (see my note of 3rd June, 1987 – YB87/6.3/1.1). We needed much more data and information to answer inevitable queries. ...




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*This case study accompanies the IRGC report “Risk Governance Deficits: An analysis and illustration of the most common deficits in risk governance”.


The Bovine Spongiform Encephalopathy (BSE) Epidemic in the United Kingdom


By Belinda Cleeland1


SNIP...


A6 Misrepresenting information about risk


From the very beginning of the BSE outbreak, not only was knowledge misrepresented by the British government, but in some cases it was even withheld. For example, after the initial diagnosis of BSE by the SVS in late 1986, there was an embargo placed on the sharing, or making public, of any BSE-related information that ran until mid-1987. Also, up until at least 1990, outside scientists that requested access to BSE data to conduct further studies were denied, despite the fact the improved scientific understanding of the disease had the greatest potential to minimise the impact of the epidemic. Even government scientists within the CVL have acknowledged that there was a culture of suppressing information, to the point that studies revealing damaging evidence (e.g. that there was a causal link between BSE and the new encephalopathy found in cats) were denied publication permission [Ashraf, 2000].


The withholding of such information allowed the government to publicly assert that BSE was just like another version of scrapie – not transmissible to humans – and that there was “clear scientific evidence that British beef is perfectly safe” [UK House of Commons, 1990].2 This was certainly a misrepresentation of the knowledge held at the time, and one that was only possible due to the suppression of some scientific findings and recommendations. Of course, the main reason for this misrepresentation of knowledge was the protection of agricultural and industrial interests – the specific stakeholder favoured in this case was the British beef industry, which stood to lose billions of pounds if a large number of its animals had to be slaughtered, if export bans were put in place, or if costly regulations were implemented.


To protect the interests of the beef industry, the government would assert on many occasions that British beef was safe to eat and that regulatory controls already implemented would prevent any 2 This comment was made by the Agriculture Minister to the House of Commons.


contaminated material from entering the food chain. This was also a misrepresentation of knowledge, as the government was fully aware that their measures were not designed to eliminate exposure, but only to diminish the risk [van Zwanenberg & Millstone, 2002:161].


What’s more, many uncertainties relating to the transmissibility of the disease were either down-played or ignored, resulting in an overstatement of certainty that British beef was completely safe to eat and that BSE was not transmissible to humans. The way uncertainty was dealt with in this case was the result of a number of factors, including the desire to protect specific stakeholder interests.


One crucial factor was the underlying element of risk political culture in the UK that linked the identity of the actor to the consistency of his policy positions. This led to consistency of position being prioritised over accuracy [Dressel, 2000], and resulted in the government insisting on the absence of risk to the population, maintaining this public position despite mounting evidence to the contrary. Although aware of them, policy-makers chose not to overtly acknowledge the levels of uncertainty and the complexity of the risks involved with BSE and its spread because the ramifications of these were too great for the interests they were trying to safeguard.


B1 Responding to early warnings


The incorporation of rendered meat and bone meal into animal feed creates a number of risks related to the transmission, recycling and amplification of pathogens. Such risks were recognised well before the emergence of BSE. In the US in the mid-1970s, concerns that scrapie may be linked to CJD (although there is no evidence that scrapie is transmissible to humans) led to some regulations being placed on the incorporation of sheep or goat carcasses into human and animal foods [van Zwanenberg & Millstone, 2002:158]. In the UK, too, the Royal Commission on Environmental Pollution recommended in 1979 that minimum processing standards be implemented by the rendering industries in order to minimise the potential for disease spread [RCEP, 1979]. The incoming Thatcher government withdrew these proposed regulations, preferring to let industry decide for itself what standards to use. In retrospect, the failure to act at this point to mitigate the general risk of disease transmission may have had a crucial impact on the later outbreak of BSE, given that the disease “probably originated from a novel source in the early 1970s” [BSE Inquiry, 2000b].


Early warnings that BSE might be transmissible to humans were, in fact, observed by scientists and government officials throughout the period from 1986 (the time of first diagnosis in cattle) to 1995 (when vCJD was first observed in humans). Such observations are noted in, for example, the minutes of a meeting of the National Institute for Biological Standards and Control in May 1988, where the probability of transmission of BSE to humans is assessed as more than remote. The diagnosis in 1990 of a domestic cat with a previously unknown spongiform encephalopathy resembling BSE indicated that the disease could infect a wider range of hosts. Responses to such early warnings of potential dangers to human health were either too weak or came too late. This may have been partly a result of an ‘unwillingness to know’ due to the economic harm this knowledge would cause the UK beef industry (related to deficit A6); and partly due to institutional capacities and procedures (related to deficits B5, 9 and 10).






Tuesday, July 28, 2009


MAD COW COVER-UP USA MASKED AS SPORADIC CJD






SEE THE VIDEO NOW AT THE BOTTOM OF THE BLOG BELOW ;





Tuesday, July 14, 2009


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


WHERE did we go wrong $$$





MY GOD, HOW MANY CASES GOT INTO THE FOOD CHAIN ??? IATROGENIC THERE FROM ??? ATYPICAL BSE MORE VIRULENT, HOW MANY MORE WILL DIE NEEDLESSLY IN THE YEARS AND DECADES TO COME. ...TSS



Friday, December 23, 2011




Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

Volume 18, Number 1—January 2012 Dispatch


Wednesday, January 4, 2012


A Bovine Prion Acquires an Epidemic Bovine Spongiform Encephalopathy Strain-Like Phenotype on Interspecies Transmission





Tuesday, November 15, 2011


Alternative BSE Risk Assessment Methodology of Imported Beef and Beef Offal to Japan Journal of Veterinary Medical Science


Advance Publication





Monday, January 2, 2012


EFSA Minutes of the 6th Meeting of the EFSA Scientific Network on BSE-TSE Brussels, 29-30 November 2011





Saturday, June 25, 2011


Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque


"BSE-L in North America may have existed for decades"





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


snip...


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





2011 Monday, September 26, 2011


L-BSE BASE prion and atypical sporadic CJD






Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS RegulationsComments


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


Page 1 of 98






FSIS RFEPLY TO TSS ;


Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:




Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:






Saturday, June 19, 2010


U.S. DENIED UPGRADED BSE STATUS FROM OIE






Friday, August 20, 2010


USDA: Animal Disease Traceability August 2010






Friday, November 18, 2011


country-of-origin labeling law (COOL) violates U.S. obligations under WTO rules WT/DS384/R WT/DS386/R










Saturday, April 10, 2010


TOYOTA VS MAD COW DISEASE USA OIE BSE MRR IMPORT AND EXPORT TRADE WARS





TSS

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