Tuesday, January 10, 2012

ESHRE position statement concerning prion detection in urinary gonadotropin formulations

ESHRE position statement concerning prion detection in urinary gonadotropin formulations


A recent laboratory evaluation, partly funded by a company producing recombinant human gonadotropin, questions the safety of urinary-derived human chorionic gonadotropin. Based on the detection of traces of normal prion protein in licensed urinary derived products, the authors surmise that these widely used gonadotropins might also harbor abnormally folded prion proteins that could result in cases of nosocomial transmission of Creutzfeldt-Jakob Disease (CJD).


The ESHRE task-force for transmissible viral diseases has reviewed the study but found no convincing evidence that would support the concern raised by Dorsselaer et al. Biological and epidemiological evidence argues against the possibility of CJD-transmission through urine-derived gonadotropins. Prion proteins are normally found in human urine and are not associated with CJD. Dorsselaer et al. did not document the detection of the CJD-associated abnormally folded form of prion proteins. The incidence of CJD is extremely rare (1 case / mio/year) and there is no indication that abnormal prion proteins are found in urine prior to the manifestation of the disease. As for urine donors, those contributing samples for hCG extraction, who are pregnant women, are in the age range far before the age of 50 years, when the vast majority of CJD cases are diagnosed. Those contributing samples for FSH extraction are in the menopausal age range, when eventual clinical manifestation of CJD can be diagnosed.


One particular nature of the transmission of prions associated with the development of the diseases is the association between the infectious dose and the latency from infection to disease development (Klöhn et al.). This is a fundamental difference to the transmission of a virus or a bacteria. Thus, low level exposure to the transmissible agent does not result in the development of overt disease during a lifetime. Since urine-derived products are pooled from large numbers of urine samples any specific protein from one individual donor would be diluted. Thus, even in the unlikely event that a young woman donor is shedding abnormal prion protein in her urine, the potentially transmissible agent is so far diluted that it makes transmission of CJD biologically unlikely event. This theoretical concept is supported by epidemiological evidence. Despite the use of urine derived gonadotropins for more than 50 years by millions of women worldwide, there is not a single case of CJD associated with these products. More importantly, the M/F sex ratio of CJD has remained stable at one (or slightly above at 1.05 in a large french survey 1998-2000;




Further evidence against the suspected possibility of CJD transmission through urine-derived gonadotropins is also summarized in a position statement of the Candadian Fertility and Andrology Society. Based on this careful evaluation of the facts, the ESHRE task force does fully support the use of urine-derived gonadotropins and will continue to follow the published evidence.


Pietro Vernazza, Enrico Semprini For the Task Force Viral Diseases in ART Petra De Sutter Special Interest Group Safety and Quality in ART


Reference


Klöhn PC, Stoltze L, Flechsig E, Enari M, Weissmann C. A quantitative, highly sensitive cell-based infectivity assay for mouse scrapie prions. Proc Nat Acad Sci 2003, vol 100 (20); 11666-11671.









here we go again...




Posted by flounder on 29 Mar 2011 at 15:12 GMT


again, many many thanks to PLOS for open access !


Nice work Dr. Cashman and Dr. Vandors et al !


THIS is not surprising at all, and the warning shots for this risk factor of exposure to TSE were shot over the bow of the boat over a decade ago, but politics and the industry put up a good PR media blackout, or best they could. now look how many have become needlessly exposed around the globe. before synthetic growth hormones, CJD was killing via human growth hormone, this has been proven time and time again through death. the hospitals, medical, surgical procedures are spreading the TSE prion disease and their many different strains around the globe, as we speak, and the insanity, along with exposure continues. ...


how, why, has this been allowed to happen again ?


how many will die due to this needless exposure ?


how many times does science have to repeat itself, before our officials act ?


how many dead is enough ?


please see reference sources below ;




more than 1500 women were treated with the injectable fertility drug, human pituitary gonadotrophin (hPG) between the 1960s and 1985. It created miracle children, infamous multiple births - and tragedy.


This Federal Government-sponsored hormone extract, made from pituitary glands sliced from the brains of bodies in morgues, has killed four women, all in Australia where the most use of this drug was made, in the years 1988, 1989, 1990 and 1991. One young man, among the 700-odd children who received hGH (human growth hormone) injections between 1967 and 1985 in Australia, has died.


Jennifer Cooke is the author of Cannibals, Cows & the CJD Catastrophe (Random House Australia) which won the 1999 Eureka Science Book Prize, Australia’s most prestigious award for popular science writing.


Background of Australian Human Pituitary Hormone Program From 1967 until 1985 2,100 Australians were treated with human pituitary hormones under the Australian Human Pituitary Hormone Program (AHPHP).


In similar programs in overseas countries the majority of recipients of human pituitary hormones (hPH) were treated with human growth hormone (hGH) for short statue. In Australia the Australian Human Pituitary Hormone Program (AHPHP) treated approximately 1570 woman and about 60 men for infertility using human pituitary gonadotrophin (hPG). Approximately 660 Australian children were treated for short statue with human growth hormone (hGH).


Five Australians may so far have developed and died from health-care associated (iatrogenic) Creutzfeldt-Jakob disease (CJD) after hPH treatment . The program was suspended in 1985 following CJD deaths of recipients of hGH in the United States and England.


All those treated with hPH are at low risk of developing CJD. There is no way of knowing if batches received by recipients were contaminated. To date there is no test to show if recipients are incubating CJD.


The AHPHP was run under the auspices of the Commonwealth Department of Health. The hormones were manufactured by the then government-owned Commonwealth Serum Laboratories in Melbourne.


The AHPHP was conceived and operated by the Human Pituitary Advisory Committee (HPAC) until its activities ceased in 1985 and the committee was disbanded.


From 1992 intense media and political pressure followed news of the first two deaths from iatrogenic CJD as the families demanded an explanation. The then Minister for Health, Senator Graham Richardson, ordered an independent inquiry.


Associate Professor Margaret Allars, an administrative law expert from the University of Sydney conducted the inquiry into the use of Pituitary Derived Hormones in Australia and Creutzfeldt-Jakob Disease, which reported in June 1994.


The inquiry report made a number of recommendations concerning the care of recipients, the establishment of support services and the formation of a ministerial advisory council.


Recipients of hPH now live with a health status of being at “low risk” of CJD. Current infection control guidelines refer to “low risk” patients. Recipients and their families also live with anxiety linked to the threat of contracting a disease which can lie dormant for decades and for which there is no test, treatment or cure.








1: Dev Biol Stand 1996;88:237-41


Transmissible encephalopathies and biopharmaceutical production.


Robinson MM


USDA-ARS Animal Disease Research Unit, Washington State University, Pullman, USA.


The use of post-mortem tissues as sources for the production of biologicals, vaccines and feedstuffs has led to the transmission or generation of transmissible encephalopathies in some recipients. For example, the use of pituitary-derived human growth hormone and gonadotropins has resulted in the transmission of Creutzfeldt-Jakob disease to other humans [1], the use of formalin-inactivated sheep brain as a source for louping ill vaccine led to the transmission of scrapie to over 1,000 sheep from one vaccine lot [2], and the use of rendered products from ruminant carcasses in the domestic animal food chain led to the emergence and epizootic of bovine spongifrom encephalopathy in the United Kingdom [3]. Infection with transmissible encephalopathies by iatrogenic or other mechanisms is difficult to predict or control. The characteristics of these pathogens do not permit easy detection, clearance, or inactivation in routine biopharmaceutical production environments.


Publication Types: Review Review, tutorial


PMID: 9119144, UI: 97169782





PLUS, ARMOUR MADE A BOVINE THYROID MEDICATION SOME TIME BACK CALLED "THYRAR" MADE FROM DESSICATED BOVINE THYROID GLAND...






Creutzfeldt-Jakob Disease, CJD Support Group for short statured children of the 1970's and 1980's. Recommendations for Unapproved/Unregistered recipiants












SHORT REPORT


Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth hormone






the warning shots fired over the bow of the boat that were never heard ;




PITUITARY EXTRACT


This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...







NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE


snip...


I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.


snip...


The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...






B.S.E. and Veterinary Medicines


Thank you very much indeed for your letter of the 26th of January outlining to me the various steps that are proposing to take in order to reduce the risk from B.S.E. in veterinary medicines. It is, as you say, and extremely difficult problem. ....






Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)










(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)


PITUITARY EXTRACT


This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.


BEEF BRAIN AND BRAIN INFUSION BROTHS


Considered to be of great risk.






COMMERCIAL IN CONFIDENCE


MEDICINES ACT - VETERINARY PRODUCTS COMMITTEE


5 BLANK PAGES. ...TSS


7. Any Other Business






TWA LITTLE STATEMENT 331


8 June 1988 Internal CVL meeting to discuss the implications of BSE to Biologicals Products containing bovine extracted material (Annex 6). (YB 88/06.08/11.1-11.2) Following a detailed review of situation the following recommendations were made:


1. Specific concern over use of pituitary gland products by veterinary surgeons and companies. Paper to be produced for Tolworth (Veterinary Medicines Division).


2. Urgent review of all products both immunological and pharmaceutical for possible inclusion of ingredients of bovine origin.


3. Draft guidelines to be presented in full to the National Office of Animal Health (NOAH), the trade body representing the Veterinary Medicines part of the pharmaceutical industry, at next meeting on 11 July 1988






TWA LITTLE minute


2. We have identified one problem over where we are unable to act and this is the use of gonadotrophins in embryo transfer work. Some veterinary surgeons are quite legally using this exemption from the Medicines Act contained in Section 9(2) to prepare gonadotrophins from pituitary glands from various species, including cattle. These hormones are used to stimulate superovulation in donor cows.














COMMERCIAL IN CONFIDENCE


3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy


It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.


and then another 3 + pages of blank space. ...TSS






COMMERCIAL IN CONFIDENCE


BSE - CURRENT POSITION WITH VETERINARY LICENCED PRODUCTS (MA.1968)


There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).


1) Vaccines






NOT FOR PUBLICATION


another 6 pages of blank space. ...TSS














COMMERCIAL IN CONFIDENCE






COMMERCIAL IN CONFIDENCE


Medicines Act - Veterinary Products Committee






COMMERCIAL IN CONFIDENCE






MANAGEMENT IN CONFIDENCE


CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS






Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001


Date: Tue, 9 Jan 2001 16:49:00 -0800


From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.


[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?


[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]


[host Richard] could you repeat the question?


[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?


[not sure whom ask this] what group are you with?


[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.


[not sure who is speaking] could you please disconnect Mr. Singeltary


[TSS] you are not going to answer my question?


[not sure whom speaking] NO


from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;


[unknown woman] what group are you with?


[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?


at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.


snip...full text ;








COMMERCIAL IN CONFIDENCE


NOT FOR PUBLICATION


COMMITTEE ON SAFETY OF MEDICINES


another 6 pages or so that are blank. ...TSS










COMMERCIAL IN CONFIDENCE


NOT FOR PUBLICATION


COMMITTEE ON SAFETY OF MEDICINES


WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY


7.2.1. Products with bovine brain/lymphoid tissue as ingredients and administered by injection...[111]


7.2.2 Products with bovine ingredients (other than brain/lymphoid tissue) and administered by injection...[135]


7.2.3 Tissue implants, open wound dressings, surgical materials, dental and opthalmic products with bovine ingredients...[27]


7.2.4. Products with bovine ingredients and administered topically...[5]


7.2.5 Products with bovine ingredients and administered orally...[9]


7.2.6 Products with other animal/insect/bird ingredients and administered:


a. by injection a: 117


b. by topically b: 6


c. orally c: 8


7.2.7 Products with materials produced from animal material by chemical processes, eg stearic acid, gelatin and lanolin...[156]


With two exceptions, the replies to date have not given any immediate cause for concern, although 176 products do not conform to the CSM/VPC guidelines.


8. The first exception was from which gave very limited information about a very large number of homoepathic medicines with material obtained from cattle and a number with material from the brain. Of these, 53 were injectable products of which 20 were derived from cattle brain. A list of these products is attached as Appendix 1 to Annex D. The second exception relates to the product, 'Surgical Catgut', which is sourced from UK bovine intestines and will contain lymphoid material...


see full text ;






please see ;


Sunday, December 16, 2007


Risk factors for sporadic Creutzfeldt-Jakob disease


Increased risk was not associated with surgical categories chosen a priori but was confined to the residual category other surgery, in which the increase in risk appeared most marked for three subcategories: skin stitches, nose/throat operations, and removal of growths/cysts/moles.


snip...


which the increase in risk appeared most marked for three subcategories:


skin stitches, nose/throat operations, and removal of growths/cysts/moles.


10 January 1990


Other US BSE risks: the imported products picture


24 Jul 00 Trade Statistics: UK to US


Compiled by Terry S.Singeltary Sr of Bacliff, Texas


[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?


Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.


Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]


10 January 1990


NOT FOR PUBLICATION


COMMITTEE ON SAFETY OF MEDICINES


WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY


SURGICAL CATGUT SUTURES


2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to License Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licensed catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K.


IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;


3006.10.0000: STERILE SURGICAL CATGUT, SIMILAR STERILE SUTURE MATERIALS AND STERILETISSUE ADHESIVES FOR SURGICAL WOUND CLOSURE; AND SIMILAR STERILE MATERIAL


U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)


<--- Dec 1998 ---> <--- 1998 YTD --->


Country Quantity Value Quantity Value


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


WORLD TOTAL . . . . . . . 10,801 3,116 143,058 40,068


Belgium . . . . . . . . . --- --- 107 14


France . . . . . . . . . 81 49 2,727 1,132


Switzerland . . . . . . . --- --- 1,357 1,693


United Kingdom . . . . . 1,188 242 35,001 5,564








see url now available at ;








Part II


2.1 Bovine Small Intestine


This is the largest single category, comprising 9 product licenses for surgical catgut, held by 3 Companies ;






2.2 Skin


Bovine dermal collagen is present in 2 products for correction of tissue contour deformities by injection and 4 implantable haemostates.


Source USA, USA, W Germany, W. Germany, France. ...






UPDATE ON SURGICAL CATGUT


MAY 1990






40,000 human heart valves a year from BSE herds


Sun, 3 Sep 2000.


Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas








The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.




TIP740203/l 0424 CONFIDENTIAL


snip...


The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.


8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.



snip...








5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.


see all 76 pages ;






EXPORT OF BRITISH BIOLOGICAL PHARMACEUTICALS


1. Please see the attached note of a recent meeting in Brussels. For Dr. Purford should read Dr. Purves (I think). If the Germans get their way, and it looks as if they might, because of worries about BSE we could end up with a ban on certain bovine materials being exported from the UK for pharmaceutical manufacture. Thse materials include cell cultures of bovine origin (? and also any cultures which have been fed bovine nutrient material), bovine serum, and fetal calf serum.


2. Whilst export of these raw materials may be very limited, it is only a small step to include in this export ban any finished product made from such materials. This would include virtually all biologicals and vaccines. This could have very serious effects on the export trade of British Manufacturers of biologicals because even where they source their bovine ingredients outside the UK it might be impossible or at least very difficult to bypass any export ban.


3. Our own line is that we have not used regulations to restrict the use of British bovine material for non-food use, although certain offals cannot be used for human consumption. ...






Export of British 'Biological' Pharmaceuticals










No papers were presented by our American guests and none covered the subject of pharmaceuticals. ...






STANDING COMMITTEE MEETING ON BSE


Thanks for your note. I am disappointed not to have been informed about this meeting in advance and am surprised that Dr. Tyrrell was not involved either. I find it insulting to be told the proceedings were in confidence and find your excuse about only hosting the meeting unconvincing.






The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.



TIP740203/l 0424 CONFIDENTIAL


Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4


snip...


89/06.19/8.1 BSE3/1 0191 Hr J Maslin (MAFF) Ref: Maslin3g


From: Dr H Pickles Med SEB/B Date: 3 July 1989


CATTLE BY-PRODUCTS AND BSE


I was interested to see the list of by-products sent to the HSE. Those of particular concern included:


* small intestines: sutures (I thought the source was ovine but you are checking this)


* spinal cord: pharmaceuticals


* thymus: pharmaceuticals


Are you able to give me more information on which UK manufacturers use these materials? Our proposed ban on bovine offal for human consumption would not affect these uses, I assume.


snip...see full text ;















USDA allows diseased animals into human food supply


Mon, 14 Aug 2000. Information provided by Terry S. Singeltary Sr. Farm Sanctuary web site


In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - Report of a visit to the USA - April-May 1989 - G A H Wells [head of England's main veterinary lab -- webmaster]


2. Meeting with USDA, BSE Task Force










MAD COW DISEASE BSE CJD CHILDREN VACCINES


Sunday, May 18, 2008


MAD COW DISEASE BSE CJD CHILDREN VACCINES


TIP740203/l 0424 CONFIDENTIAL








2011




Friday, March 25, 2011


Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach






Saturday, December 3, 2011


Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies


Volume 17, Number 12—December 2011






Thursday, December 22, 2011


Risk of Prion Disease Transmission through Bovine-Derived Bone Substitutes: A Systematic Review


Clin Implant Dent Relat Res. 2011 Dec 15. doi: 10.1111/j.1708-8208.2011.00407.x. [Epub ahead of print]






Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases?


PRION www.landesbioscience.com


please see more on Aerosols and TSE prion disease here ;






Monday, January 2, 2012


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






Sunday, July 03, 2011


J. Virol. doi:10.1128/JVI.05111-11 Copyright © 2011,American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.


Prion Disease Detection, PMCA Kinetics, and IgG in Urine from Naturally/Experimentally Infected Scrapie Sheep and Preclinical/Clinical CWD Deer




Thursday, June 09, 2011


Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission






Wednesday, March 18, 2009


Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay






Sunday, December 06, 2009


Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer






THEN YOU have water that has been contaminated from a CWD-endemic area ;




Wednesday, October 14, 2009


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area






ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;









Tuesday, September 02, 2008


Detection of infectious prions in urine (Soto et al Available online 13 August 2008.)






Wednesday, January 5, 2011


ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011


Prions


David W. Colby1,* and Stanley B. Prusiner1,2






UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010






Saturday, May 14, 2011


Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction






Tuesday, May 31, 2011


Chronic Wasting Disease


DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011






Saturday, November 12, 2011


Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease


Fri, 22 Sep 2006 09:05:59 –0500






Monday, June 27, 2011


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates






EFSA Journal 2011 The European Response to BSE: A Success Story


This is an interesting editorial about the Mad Cow Disease debacle, and it’s ramifications that will continue to play out for decades to come ;


Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip…


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as “sporadic” CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


snip…











see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;







Wednesday, August 24, 2011


There Is No Safe Dose of Prions








Wednesday, August 24, 2011




All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD










Thursday, December 08, 2011


A case of Iatrogenic Creutzfeldt Jakob Disease (iCJD) in a patient who had received a German-manufactured human dura mater graft 23 years ago







Monday, December 12, 2011


Second iatrogenic CJD case confirmed Korea







Monday, December 26, 2011


Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites







Tuesday, November 08, 2011


Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011


Original Paper


Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.











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Friday, January 6, 2012

OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease

Greetings,


Once again I must disclose my sincere disgust with the O.I.E.




ONCE again the OIE has proven itself to be nothing more than a National Brokerage Organization for all strains of Transmissible Spongiform Encephalopathy. A failed organization, one that’s only purpose is to protect trade.


OIE SEEMS TO HAVE nothing to do with protecting human or animal health, in my opinion.


OIE has proven this time and time with relations to animal Transmissible Spongiform Encephalopathy TSE Prion disease typical and atypical.


By the time the OIE recognizes a disease such as TSE as a threat to humans or animals, it’s years, decades too late.


THIS is the exact same thing that happened with Bovine Spongiform Encephalopathy BSE TSE prion disease. Because of the OIE and it’s BSE regulations and testing, BSE spread around the globe.


This will happen with CWD in cervids, as it did with BSE in cattle and Scrapie in sheep, especially and so foolishly for exempting the atypical TSE prion disease, all because of trade and the almighty dollar.


The OIE is nothing more than a ship of fools in my opinion, who’s absolute purpose is to protect trade, and the almighty dollar, to hell with human and animal health.


IN terms of BSE TSE prion disease and the OIE, there never was no ‘prevention’, it was simply never test enough to find.


This manual proves once again just this, in my opinion. ...




OIE Training Manual on Wildlife Diseases and Surveillance






TO REDUCE TESTING OF BSE IN THE USA TO ONLY 40,000 A YEAR, is simply not scientific regardless of what the OIE BSE testing protocol calls for. ALL one has to do is look at the countries above that all went down with BSE, that all went by the infamous OIE BSE testing protocols. THEN and only then, after the USA finally fumbled the 'BSE FREE' golden egg and accidently had to document a case or two of mad cow, low and behold, what next? yep, you guessed it, time to move the goal post in the middle of the football game, GWs and his sleeping partners at the OIE, gave birth to the BSE MRR policy, the legal trading of all strains of TSE globally was born. ...


SNIP...


9/13/2005


Page 12 of 17


SEE SLIDES IN PDF FILE;








4. WHAT does USDA/FDA ET AL intend to do about the risks of atypical BSE/TSE in cattle now that infectivity shows in tissue samples other than CNS in Japan, the fact now that the last Texas mad cow and that last mad cow in Alabama were indeed of the atypical strain, the fact that the studies long ago in Mission, Texas of USA sheep scrapie transmission to the USA bovine, which proved an 'atypical tse' in the USA bovine, the fact also that USDA/FDA are still floundering on the last SRM regulations, but with the BASE strain now in cattle that is not similar to nvCJD, but very similar to the sporadic CJD, and sporadic CJD has tripled in the last few years in the USA. WHAT do you plan to do to protect human health from these atypical strains of TSE, in relations to SRMs ?


5. THE 2004 Enhanced BSE surveillance program, that tested all those cows, but then we found just how terribly flawed the program was, from testing protocols, to testing the most likely to have BSE i.e. high risk, to the geographical distribution of the testing and high risk areas, to letting the tissue samples of one mad cow sit on a shelf for 7+ months and then having to have an act of Congress to ever get that cow finally confirmed, to that other Texas mad cow they decided to not even bother testing at all, just rendered that very suspect cow, to suspect to test evidently, back to that Alabama mad cow that they could only give a guess as to age with dentition where we all know that the age of that cow was so close to 10 years it could have been 9 years 7 months to 10 years 3 months, thus possibly being an BAPB i.e. USA 'born after partial ban', to all those rabies suspect cows that did not have rabies, and DID NOT get tested for BSE/TSE in that June 2004 enhanced surveillance program, even though the common lay person knows the suspect rabies negative cows are suppose to be BSE/TSE tested, how does one correct all these blatant failures and will they be corrected?


IT never was about human/animal health, but all about commodities and futures. ... MISSION ACCOMPLISHED $$$


ENFAMOUS NON-SPECIES CODING SYSTEM BY FDA ET AL, another handy tool for importing/exporting all strains of TSE ;


Docket Management


Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305


Comment Number: EC –254


Accepted - Volume 11


Page 94 of 98


8/3/2006






ONE FINAL THOUGHT ;


OPINION






> > > New methodology, under the auspices of the OIE, is under construction within the EU and EFSA and the Panel recommended that once these classifications had been finalised they should harmonised with those used in the EFSA BSE QRA guidance document. The Panel anticipated that this harmonisation may have a knock-on impact on the QRA calculations, conclusions and recommendations and that, again, future Panel members should review this, and other, inputs of the QRA and address this impact using their “self-tasking mandate” option. < < <




GOD HELP US!


sample survey via oie for bse is about 400 test via 100 million cattle, if i am not mistaken. MOST countries that went by these OIE guidelines all eventually went down with BSE. ...TSS






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


Page 95 of 98


8/3/2006


WHAT ABOUT RISK FACTORS TO HUMANS FROM ALL OTHER TSEs, WITH RELATIONS TO SRMs ???


a.. BSE OIE


SNIP...SEE FULL TEXT ;






Transmissible Spongiform Encephalopathy and the O.I.E.


OIE Terrestrial Animal Health Standards Commission / September 2010


The EU takes note of the fact that atypical scrapie is not an OIE listed disease. Nevertheless, it will remain notifiable in the EU. Moreover it must be stressed that any emergence of this disease should be notified to the OIE by Members and that scientific data should continue to be gathered.


snip...


Zoonotic Potential


Has transmission to humans been proven? (with the exception of artificial circumstances) AND


Is human infection associated with severe consequences? (death or prolonged illness)







P.4.23


Transmission of atypical BSE in humanized mouse models


Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA


Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.


Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.


Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.*** The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.


Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.


Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.






P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS


Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA


Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C.*** The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.


III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)






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 ;


.....snip


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


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


END...TSS


Thursday, December 04, 2008 2:37 PM


"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS




BSE-H is also transmissible in our humanized Tg mice.


The possibility of more than two atypical BSE strains will be discussed.


Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.









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


"The origin of atypical BSE is not yet determined. According to EFSA's scientific opinion published in 2008, all the cases of atypical BSE were reported with birth dates before the real feed ban in January 2001 in Europe. Therefore, the possibility of those atypical cases attributing to the contaminated feeds, just as in classical BSE, cannot be completely denied."


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



atypical BSE TSE cases have been around for a long long time, so yes indeed MBM or SRM could very well and most likely did contain atypical TSE of all strains in the USA, and the typical strains as well, of all species. the North America and the USA has typical and atypical BSE, typical and atypical Scrapie, and two strains now of Chronic Wasting Disease, call them typical and atypical, or call them what you want, all this has been rendered and fed to food producing livestock for humans and animals for years in the USA. these are the facts, like them or not. please see ;


1992


IN CONFIDENCE


BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367)





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 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. ...





Tuesday, November 17, 2009


SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1





NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS


"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"


2009







''THE LINE TO TAKE'' ON IBNC $$$ 1995 $$$


1995


page 9 of 14 ;


30. The Committee noted that the results were unusual. the questioned whether there could be coincidental BSE infection or contamination with scrapie. Dr. Tyrell noted that the feeling of the committee was that this did not represent a new agent but it was important to be prepared to say something publicly about these findings. A suggested line to take was that these were scientifically unpublishable results but in line with the policy of openness they would be made publicly available and further work done to test their validity. Since the BSE precautions were applied to IBNC cases, human health was protected. Further investigations should be carried out on isolations from brains of IBNC cases with removal of the brain and subsequent handling under strict conditions to avoid the risk of any contamination.


31. Mr. Bradley informed the Committee that the CVO had informed the CMO about the IBNC results and the transmission from retina and he, like the Committee was satisfied that the controls already in place or proposed were adequate. ... snip... see full text









Wednesday, July 28, 2010


Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report






Tuesday, November 02, 2010


BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992






Wednesday, February 16, 2011


IN CONFIDENCE


SCRAPIE TRANSMISSION TO CHIMPANZEES


IN CONFIDENCE






Sunday, April 18, 2010


SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010






Monday, April 25, 2011


Experimental Oral Transmission of Atypical Scrapie to Sheep


Volume 17, Number 5-May 2011






Thursday, June 2, 2011


USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California






Monday, June 20, 2011 2011


Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA






Thursday, July 14, 2011


Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)






Wednesday, October 12, 2011


White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation






Saturday, December 18, 2010


OIE Global Conference on Wildlife Animal Health and Biodiversity – Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011


I see again that the OIE has done little to help eradicate all animal TSE from the globe, and in fact in my opinion, have help enhance the spread of BSE and other animal TSE globally by their industry friendly regulations. I tried to warn the OIE in 2002 about CWD and the potential, but very real threat of CWD to humans. I was told that they were seriously considering this. what happened ? NOW, the OIE and the USDA collaborate to make legal the trading of all strains of atypical BSE legal, and in fact have done so with the atypical scrapie, when science has made perfectly clear the risk factors to humans and other species. I have said it once (see below), and i will say again ;


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


JUST about every country that went by the infamous O.I.E. B.S.E. guidelines, most all came down with B.S.E. ...TSS


NOW, some history on the failed OIE BSE/TSE policy, and why the OIE allowed BSE and other TSE to spread around the globe $$$


SNIP...


i proposed to OIE years ago to include CWD. but with these new atypical case of TSE showing up in cattle and sheep, it will be interesting to see how the OIE handles the USA demands on weakening the BSE/TSE regs for exporting countries;


Date: Fri, 12 Jul 2002 16:11:42 –0700


Reply-To: B S E-l


Sender: Bovine Spongiform Encephalopathy


From: TSS


Subject: CWD/USA — CWD/OIE?


snip...


Greetings List Members,


speaking with someone at the OIE about my concerns with CWD and the non-testing for TSEs in USA cattle, i find it very sad that the OIE does not follow CWD related issues. BUT, they voice my same concerns and said changes are in the makings. sadly, the changes will take about 2 years?


snip...


''I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee.''


snip...


two years is a very long time, on an issue of such importance to both humans and animals...


kind regards, terry




snip...




PAGE 25 Transmission Studies Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret...






Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.


snip...






and why do we not want to do TSE transmission studies on chimpanzees $




snip...


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.


snip...


R. BRADLEY






same reason CJD/TSE is not reportable Nationally in the USA. same reason no CJD questionnaire exists in the USA that is issued to all victims and families of victims asking real questions pertaining to route and source of agent. no autopies for all demented of young AND OLD! same reason the USA is steadfast refusing to this day to rapid TSE test all cattle for human/animal consumption. the USA simply does not want to know$


hell, we should just retain it all, and just play like it has not happened for the next 40 years as well. hmm, something else to ponder ;


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man


so, when/where is our first case transmission study of TSE on man going to be? i wish to witness this and have a few suggestions for our first human guinea-pigs ;-)


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




END...TSS


C H A P T E R 2 . 3 . 1 3 .


BOVINE SPONGIFORM ENCEPHALOPATHY


Article 2.3.13.1.


SNIP...please see full text ;






putting the cart before the horse OIE TSE policy. ...TSS




Monday, November 30, 2009


USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE






Friday, February 11, 2011


Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues






Sunday, December 12, 2010


EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010






Thursday, December 23, 2010


Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002–2009 Volume 17, Number 1–January 2011






Thursday, November 18, 2010


Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep






Sunday, October 3, 2010


Scrapie, Nor-98 atypical Scrapie, and BSE in sheep and goats North America, who's looking ?










Saturday, January 29, 2011


Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate


Jpn. J. Infect. Dis., 64 (1), 81-84, 2011






Thursday, February 10, 2011


Chronic Wasting Disease Found In A White-Tailed Deer In Maryland










CWD Maryland Emergency Response Plan 2011












Thursday, February 10, 2011


CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer – Updated 2/07/2011






Wednesday, February 09, 2011


CWD Minnesota deer feeding ban covering Dodge, Goodhue, Olmsted, and Wabasha counties will become effective Feb. 14, 2011






Tuesday, January 25, 2011


Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island






UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010






Tuesday, January 25, 2011


Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions


Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.


Reference List


snip...


please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!!






Tuesday, January 25, 2011


Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions






PLEASE NOTE ;


there are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;


P35


ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD


Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5


The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.






PPo3-7:


Prion Transmission from Cervids to Humans is Strain-dependent


Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA


Key words: CWD, strain, human transmission


Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.


Acknowledgement Supported by NINDS NS052319 and NIA AG14359.




PPo2-27:


Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions


Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA


Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.




PPo2-7:


Biochemical and Biophysical Characterization of Different CWD Isolates


Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany


Key words: CWD, strains, FT-IR, AFM


Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.








CJD9/10022


October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,


CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT


Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all. ...end






UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010






snip... see full text ;


Tuesday, January 25, 2011


Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions






2011-2012


EFSA Journal 2011 The European Response to BSE: A Success Story


This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;


Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip...


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


snip...









see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;






Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases?


PRION www.landesbioscience.com


please see more on Aerosols and TSE prion disease here ;






Saturday, December 31, 2011


Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation






please see this game farm that was shut down, and the incredible infection rate ;



Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011






Wednesday, December 21, 2011


CWD UTAH San Juan deer hunting unit






Monday, November 14, 2011


WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011






Wednesday, November 16, 2011


Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011






Sunday, November 13, 2011


COLORADO CWD CJD TSE PRION REPORTING 2011






Monday, June 27, 2011


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates






Friday, December 23, 2011


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


Volume 18, Number 1—January 2012 Dispatch






Saturday, December 3, 2011 Isolation of Prion with BSE Properties from Farmed Goat


Volume 17, Number 12—December 2011






COLLINGE THREATENS TO GO TO MEDIA







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.








COLLINGE THREATENS TO GO TO MEDIA







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








IN CONFIDENCE


BSE ATYPICAL LESION DISTRIBUTION








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;






- 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. ...












*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 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 $$$









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-2006-0041-0006 Public Submission Title Comment from Terry S Singletary Sr Views Add Comments How To Comment


snip...


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....


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










Monday, January 2, 2012


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






Thursday, January 05, 2012


Comparative analysis of Japanese and foreign L-type BSE prions






Friday, December 23, 2011


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


Volume 18, Number 1—January 2012 Dispatch




Wednesday, May 25, 2011


O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 2011


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


From: Terry S. Singeltary Sr.


To: BSE-L@LISTS.AEGEE.ORG


Cc: trade@oie.int ; oie@oie.int ; f.diaz@oie.int ; scientific.dept@oie.int ; cjdvoice@yahoogroups.com ; BLOODCJD@YAHOOGROUPS.COM


Sent: Tuesday, May 24, 2011 2:24 PM


Subject: O.I.E. Terrestrial Animal Health Standards Commission and prion (TSE) disease reporting 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"






Saturday, November 19, 2011


Novel Prion Protein in BSE-affected Cattle, Switzerland






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






Wednesday, March 31, 2010


Atypical BSE in Cattle


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.


This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.




Thursday, August 12, 2010


Seven main threats for the future linked to prions


First threat


The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.


***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.


Second threat


snip...






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, July 23, 2011


CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE




Saturday, November 6, 2010


TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU


Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation




Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>


Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)






Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis








full text with source references ;




TSS
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