Eurosurveillance, Volume 17, Issue 15, 12 April 2012
Research articles
Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010
E Alcalde-Cabero1, J Almazán-Isla1, J P Brandel2, M Breithaupt3, J Catarino4, S Collins5, J Haybäck6, R Höftberger7, E Kahana8, G G Kovacs7,9, A Ladogana10, E Mitrova11, A Molesworth12, Y Nakamura13, M Pocchiari10, M Popovic14, M Ruiz-Tovar1, A L Taratuto15, C van Duijn16, M Yamada17, R G Will12, I Zerr3, J de Pedro Cuesta ()1 National Centre of Epidemiology - Consortium for Biomedical Research in Neurodegenerative Diseases (Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas – CIBERNED), Carlos III Institute of Health, Madrid, Spain Institut National de la Santé et de la Recherche Médicale (INSERM) UMRS 975, National CJD Surveillance Network, Assistance publique - Hôpitaux de Paris (APHP), National Reference Centre for CJD, Pitié-Salpêtrière Hospital Group, Paris, France Department of Neurology, National Reference Centre for TSE, Georg-August University, Göttingen, Germany Alameda Epidemiology and Health Statistics Department, Lisbon, Portugal Department of Pathology, University of Melbourne, Melbourne, Australia Institute of Neuropathology, Zurich University Hospital, Zurich, Switzerland Institute of Neurology, Vienna Medical University, Vienna, Austria Department of Neurology, Barzilai Medical Centre, Ashkelon, Israel National Reference Centre for Human Prion Diseases, Semmelweis University, Budapest, Hungary Department of Cell Biology and Neurosciences, Health Institute, Rome, Italy Department of Prion Diseases, Slovak Medical University Research Base, Bratislava, Slovakia National CJD Research and Surveillance Unit, Western General Hospital, Edinburgh, United Kingdom Department of Public Health, Jichi Medical University, Shimotsuke, Japan Institute of Pathology, Medical Faculty, University of Ljubljana, Ljubljana, Slovenia Department of Neuropathology/FLENI, Referral Centre for CJD and other TSEs, Institute for Neurological Research, Buenos Aires, Argentina National Surveillance of CJD, Erasmus MC, Rotterdam, The Netherlands Neurology Department, Kanazawa University Hospital, Kanazawa, Japan
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Citation style for this article: Alcalde-Cabero E, Almazán-Isla J, Brandel JP, Breithaupt M, Catarino J, Collins S, Haybäck J, Höftberger R, Kahana E, Kovacs GG, Ladogana A, Mitrova E, Molesworth A, Nakamura Y, Pocchiari M, Popovic M, Ruiz-Tovar M, Taratuto AL, van Duijn C, Yamada M, Will RG, Zerr I, de Pedro Cuesta J. Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010 . Euro Surveill. 2012;17(15):pii=20144. Available online: http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20144
Date of submission: 04 November 2011
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In 2009, a pathologist with sporadic Creutzfeldt–Jakob Disease (sCJD) was reported to the Spanish registry. This case prompted a request for information on health-related occupation in sCJD cases from countries participating in the European Creutzfeldt Jakob Disease Surveillance network (EuroCJD). Responses from registries in 21 countries revealed that of 8,321 registered cases, 65 physicians or dentists, two of whom were pathologists, and another 137 healthcare workers had been identified with sCJD. Five countries reported 15 physicians and 68 other health professionals among 2,968 controls or non-cases, suggesting no relative excess of sCJD among healthcare professionals. A literature review revealed: (i) 12 case or small case-series reports of 66 health professionals with sCJD, and (ii) five analytical studies on health-related occupation and sCJD, where statistically significant findings were solely observed for persons working at physicians' offices (odds ratio: 4.6 (95 CI: 1.2–17.6)). We conclude that a wide spectrum of medical specialities and health professions are represented in sCJD cases and that the data analysed do not support any overall increased occupational risk for health professionals. Nevertheless, there may be a specific risk in some professions associated with direct contact with high human-infectivity tissue.
snip...
Results
Individualised occupational data from national CJD surveillance teams
Health professionals among registered sCJD cases A total of 202 health professionals were listed among 8,321 cases of sCJD registered by 21 respondent countries participating in EuroCJD (Table 1). Of these, 65 (32%) were physicians and 137 were other healthcare workers. The highest numbers by medical speciality were general practitioners (n=9), surgeons (n=7), internists (n=7), dentists (n=4), ophthalmologists (n=3) and pathologists (n=2). The proportion of physicians or dentists among all registered sCJD cases was 65/8,321 (0.8%).
snip...
Discussion
Despite a number of case reports of sCJD in physicians and technicians, the findings of this EuroCJD survey do not suggest an increased risk of sCJD in health professionals, nor do analytical studies show a clear excess risk for health-related professions. Methodological limitations of analytical studies in which occupational data were frequently provided by informants who were probably aware of the sCJD diagnosis [3-7,26] argue in favour of a cautious interpretation of the positive association reported for persons working at physicians’ offices [19]. Consequently, the main finding of this literature review and complementary EuroCJD observation is that health professionals, including medical staff, are not at greater risk of developing sCJD. However, this cannot exclude the possibility that there may be an occupational risk in specific circumstances, for example, for people in contact with high-risk central nervous system tissue, and appropriate precautions, as recommended by national authorities, should therefore be followed, particularly regarding laboratory work.
Although in some studies occupation was specifically analysed [19,25] and occupation may be the subject of specific inquiry in some surveillance systems, a limitation of some registries and scientific studies is that occupation may not have been systematically recorded. When occupation was recorded, it is unlikely that a framework for consistent occupational data collection was used, so that neither registries nor case–control studies have incorporated the classic epidemiological double approach. Recording of occupation may not identify specific chemical or biological exposures, which would require data for professions (job titles, medical specialisations) being cross-referenced with branches of activity (laboratory, administrative or clinical patient-contact work). The lack of registered surveillance data that combine profession with activity (e.g. contact with human tissue), when compared with the descriptions from previous case reports and the incident in Spain, illustrates the limits of the validity of available data for analytical purposes and precludes formal use of statistical testing. Although our study does not provide evidence of an excess risk of sCJD in health professionals, the fact that the data collected were mainly linked to medical speciality rather than actual activity might have concealed an excess risk of sCJD for some specific health professionals.
A case–control study seeking to examine the putative occupational risk posed by surgical injuries should have a biologically clear working hypothesis and a custom-tailored methodology. Matrices designed by linking medical speciality and surgical/forensic-anatomical/pathological activity, in which the health professional can come into direct contact with high human-infectivity tissue by accident might not provide a sufficient background for analysis, without appropriate control being made for the influence of PRNP genotype, surgical or laboratory work history and long latency. Assuming that among non-cases or controls the proportion of medical specialities with potential exposure (surgeons, forensic surgeons and other surgical specialists, pathologists) may be low, i.e. approximately 1 per 1,000 (based on the figures of 3/2,968 in Table 2), the study size that would afford the necessary statistical power for a proper examination of the specific practices of health professions is higher than that provided by existing CJD registries in any one country. Since complementary analyses would be needed for professional and activity categories defined in terms of temporal references that have not been explored to date, such as ‘ever employed’ or ‘currently employed’, as well as duration of employment, requirements for study size and collaboration would be even higher.
In conclusion, a wide spectrum of medical specialities and health professions are represented in sCJD registries. Although selection due to higher ascertainment may lie behind the case reports of certain professions involved in clinical management or care of patients with sCJD, the biological significance of these observations remains uncertain and available data do not indicate an increased risk of sCJD in health professionals. However, the methodological issues mentioned above indicate the need for caution in drawing conclusions from the data and large-scale studies with specific causal hypotheses are needed in order for further research to be undertaken into the potential link between health professions and sCJD.
snip...please see full text ;
http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=20144
Friday, February 10, 2012
Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive
http://creutzfeldt-jakob-disease.blogspot.com/2012/02/creutzfeldt-jakob-disease-cjd-biannual.html
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 ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html
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.
http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html
Saturday, February 12, 2011
Another Pathologists dies from CJD, another potential occupational death ?
another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ???
http://creutzfeldt-jakob-disease.blogspot.com/2011/02/another-pathologists-dies-from-cjd.html
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html
Pathologist dies of suspected Creutzfeldt-Jakob (Mad cow) disease
29 March, 2009 03:33:00
Creutzfeldt-Jakob disease (mad cow) research pathologist Antonio Ruiz Villaescusa died Sat., March 28, from the disease. Colleagues suspect he may have contracted the disease from exposure to infected human tissue, according to the Barcelona Reporter newspaper.
Ruiz headed the department of pathology at the University Hospital in Madrid and was studying whether the disease is passed on to people who have been exposed to infected tissue.
The head of the pathology department at the Fundación Alcorcón, Dr. Radish, will perform an autopsy to clarify the cause of death and the final results will be announced in about a month, according to the Spanish news site.
Ruiz was recognized internationally for his study in the fields of neuropathology and anatomopatología, and devoted much of his professional life to the study of human transmissible spongiform encephalopathy.
Creutzfeldt-Jakob disease is a rare and invariably fatal brain disorder, according to the National Institute of Neurological Disorders and Stroke. There is currently no single diagnostic test for the disease. The only way to confirm a Creutzfeldt-Jakob disease diagnosis is by brain biopsy or autopsy.
http://www.fleshandstone.net/healthandsciencenews/ruiz.html
http://www.barcelonareporter.com/index.php?/news/comments/pathologist_dies_of_suspected_creutzfeldt-jakob_mad_cow_disease/
gabinetedecomunicacion@fhalcorcon.es
e-mail: fpinedo@fhalcorcon.es e-mail: mpdominguez@fhalcorcon.es
Dr. Alberto Rábano Gutiérrez. Fundación Hospital Alcorcón. Madrid
http://www.neuroprion.org/en/np-event-prion-2008.html
Friday, February 11, 2011
Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD
http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J,
UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html
Monday, March 29, 2010
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
URGENT, PLEASE NOTE ;
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.
She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.- Physician Discharge Summary, Parkland Hospital, Dallas Texas Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence. She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers. The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
Monday, March 29, 2010
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html
Thursday, September 02, 2010
NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human Rights The Disclosure Dilemma
http://creutzfeldt-jakob-disease.blogspot.com/2010/09/neurosurgery-and-creutzfeldt-jakob.html
Thursday, August 12, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/08/usa-blood-products-collected-from-donor.html
Sunday, August 01, 2010
Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010
http://vcjdtransfusion.blogspot.com/2010/08/blood-product-collected-from-donors.html
http://vcjdtransfusion.blogspot.com/
Thursday, July 08, 2010
Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/07/nosocomial-transmission-of-sporadic.html
Thursday, July 08, 2010
GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/07/global-clusters-of-creutzfeldt-jakob.html
Wednesday, June 02, 2010
CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated: May 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/cjd-annex-h-update-after-death.html
Tuesday, May 11, 2010
Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments
http://creutzfeldt-jakob-disease.blogspot.com/2010/05/current-risk-of-iatrogenic.html
Tuesday, May 04, 2010
Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/05/review-of-human-pituitary-trust-account.html
Tuesday, March 16, 2010
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/transmissible-spongiform-encephalopathy.html
Monday, August 17, 2009
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/transmissible-spongiform-encephalopathy.html
Monday, July 20, 2009
Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD) risk in neurosurgery and eye surgery units
http://vcjdtransfusion.blogspot.com/2009/07/pre-surgical-risk-assessment-for.html
Friday, July 17, 2009
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/revision-to-pre-surgical-assessment-of.html
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
Thursday, January 29, 2009
Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research
http://creutzfeldt-jakob-disease.blogspot.com/2009/01/medical-procedures-and-risk-for.html
Wednesday, August 20, 2008
Tonometer disinfection practice in the United Kingdom: A national survey
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/tonometer-disinfection-practice-in.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
Monday, December 31, 2007
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation
http://creutzfeldt-jakob-disease.blogspot.com/2007_12_01_archive.html
Subject: CJD: update for dental staff
Date: November 12, 2006 at 3:25 pm PST
1: Dent Update. 2006 Oct;33(8):454-6, 458-60.
CJD: update for dental staff.
http://seac992007.blogspot.com/2008/06/seac-2008-one-hundredth-meeting-of.html
Saturday, January 16, 2010
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al
Evidence For CJD/TSE Transmission Via Endoscopes
From Terry S. Singletary, Sr flounder@wt.net 1-24-3
http://creutzfeldt-jakob-disease.blogspot.com/2010/01/evidence-for-cjd-tse-transmission-via.html
2011 TO 2012 UPDATE
Saturday, December 3, 2011
Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies
Volume 17, Number 12—December 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/candidate-cell-substrates-vaccine.html
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html
Thursday, December 29, 2011
Aerosols An underestimated vehicle for transmission of prion diseases?
PRION http://www.landesbioscience.com/
please see more on Aerosols and TSE prion disease here ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
Sunday, February 12, 2012
National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas
http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
http://www.youtube.com/watch?v=zf3lfz9NrT4
http://www.youtube.com/watch?v=c0tWkNvhO4g
http://www.youtube.com/watch?v=zf3lfz9NrT4&feature=results_main&playnext=1&list=PL780BE2AF0B62A944
full text with source references ;
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68
Comment from Terry Singeltary Document ID: APHIS-2008-0010-0008 Document Type: Public Submission This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products Docket ID: APHIS-2008-0010 RIN:0579-AC68
Topics: No Topics associated with this document View Document: More
Document Subtype: Public Comment Status: Posted Received Date: March 22 2012, at 12:00 AM Eastern Daylight Time Date Posted: March 22 2012, at 12:00 AM Eastern Daylight Time Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight Time Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fdd617 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: CJD TSE PRION Submitter's Representative: CONSUMERS
Comment: comment submission Document ID APHIS-2008-0010-0001 Greetings USDA, OIE et al, what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY. what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $ I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons. North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading. IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, they I would regard that to be highly suspicious. IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again. I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002. THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible. I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor. SEE REFERENCE SOURCES IN ATTACHMENTS
SEE Terry S. Singeltary Sr. Attachment WORD FILE ;
http://www.regulations.gov/#!documentDetail;D=APHIS-2008-0010-0008
http://www.regulations.gov/#!docketDetail;D=APHIS-2008-0010
Sunday, March 11, 2012
APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations
http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/aphis-proposes-new-bovine-spongiform.html
L-BSE, TME, AND SPORADIC CJD aka mad cow disease in North America
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...
http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1
http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf
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...
http://www.neuroprion.org/en/np-neuroprion.html
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1 Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain; 5Health Canada; Ottawa, ON Canada†Presenting author; Email: emmanuel.comoy@cea.fr
The epidemiology of Transmissible mink encephalopathy (TME) indicates an alimentary origin. Several inter-species transmission experiments have not succeeded in establishing with certainty any natural reservoir of this prion strain, although both ovine and bovine sources have been suspected. Cattle exposed to TME develop a spongiform encephalopathy that is distinct from classical Bovine Spongiform Encephalopathy (c-BSE).
Inoculation of c-BSE to cynomolgus macaque provided early evidence of a possible risk to humans, and remains an important model to define the risk of both primary (oral transmission from cattle to primate) and secondary (intravenous intra-species transmission) exposures. We have also evaluated the transmissibility of other cattle prion strains to macaques, including L- and H- atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.
BSE-L induced a neurological disease distinct from c-BSE. Peripheral exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted TME also induced a rapid disease in cynomolgus macaque. The clinical features, lesion profile, and biochemical signature of the induced disease was similar to the features observed in animals exposed to BSE-L, suggesting a link between the two prion strains. Secondary transmissions to a common host (transgenic mouse overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in primates induced diseases with similar incubation periods: like the c-BSE strain, these cattle strains maintained their distinctive features regardless of the donor species and passages.
If the link between TME and BSE-L is confirmed, our results would suggest that BSE-L in North America may have existed for decades, and highlight a possible preferential transmission of animal prion strains to primates after passage in cattle.
=====================end...tss====================
link url not available, please see PRION 2011 ;
http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf
Volume 13, Number 12–December 2007 Research
Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model
Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and†Montana State University, Bozeman, Montana, USA
Abstract
Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profiles, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.
snip...
Conclusion
These studies provide experimental evidence that the Stetsonville TME agent is distinct from typical BSE but has phenotypic similarities to L-type BSE in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for a bovine source of TME infection than typical BSE. In the scenario that a ruminant TSE is the source for TME infection in mink, this would be a second example of transmission of a TSE from ruminants to non-ruminants under natural conditions or farming practices in addition to transmission of typical BSE to humans, domestic cats, and exotic zoo animals(37). The potential importance of this finding is relevant to L-type BSE, which based on experimental transmission into humanized PrP transgenic mice and macaques, suggests that L-type BSE is more pathogenic for humans than typical BSE (24,38).
http://www.cdc.gov/eid/content/13/12/1887.htm?s_cid=eid1887_e
PLEASE NOTE *
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...
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
PLoS One. 2012; 7(2): e31449.
Published online 2012 February 21. doi: 10.1371/journal.pone.0031449
PMCID: PMC3283643
Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy
The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3283643/?tool=pubmed
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html
WHICH CAME FIRST, THE CART OR THE HORSE ???
Minnesota
CAPTIVE CWD CONFIRMED 2002
FREE RANGING CWD CONFIRMED 2011
http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm
Colorado
Captive CWD discovered 1967
Free ranging CWD discovered 1981
PLEASE STUDY THIS MAP !
SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS
http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
SNIP...
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).
SNIP...
Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, SNIP...SEE FULL TEXT ;
*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***
Saturday, February 18, 2012
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
CDC Volume 18, Number 3—March 2012
http://wwwnc.cdc.gov/eid/article/18/3/11-0685_article.htm
see much more here ;
http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html
Sunday, January 22, 2012
Chronic Wasting Disease CWD cervids interspecies transmission
http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html
Thursday, January 26, 2012
The Risk of Prion Zoonoses
Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html
Thursday, January 26, 2012
Facilitated Cross-Species Transmission of Prions in Extraneural Tissue
Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659
http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html
Thursday, February 16, 2012
Bovine Spongiform Encephalopathy BSE
31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012
http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html
Thursday, February 23, 2012
EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME
http://madcowusda.blogspot.com/2012/02/eight-former-secretaries-of-agriculture.html
Sunday, March 11, 2012
APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations
http://transmissiblespongiformencephalopathy.blogspot.com/2012/03/aphis-proposes-new-bovine-spongiform.html
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
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>
Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/direct.php?id=20101206.4364
> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <
don’t forget the children...
PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.
who will watch our children for CJD for the next 5+ decades ???
WAS your child exposed to mad cow disease via the NSLP ???
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
http://downercattle.blogspot.com/
DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? you can check and see here ;
http://www.fns.usda.gov/fns/safety/pdf/Hallmark-Westland_byState.pdf
Friday, March 09, 2012
Experimental H-type and L-type bovine spongiform encephalopathy in cattle: observation of two clinical syndromes and diagnostic challenges
Research article
http://bse-atypical.blogspot.com/2012/03/experimental-h-type-and-l-type-bovine.html
Tuesday, February 28, 2012
The 27th Colloque Médecine et Recherche of the Fondation Ipsen in the Alzheimer Disease series: “Proteopathic Seeds and Neurodegenerative Diseases”
Press release
>>> This opens up the possibility of an environmental causation for the many patients with a neurodegenerative disease who do not have hereditary links (Jucker; Soto; Westermark). <<<
snip...
where would have been today, IF INDUSTRY AND TRADE WOULD NOT HAVE RULED OVER POLICY MAKING FOR TSE PRION DISEASE $$$
WHAT ABOUT IATROGENIC ALZHEIMERS ?
IS ALZHEIMERS JUST A LOW DOSE TSE ?
IF the following work would have been pursued 2 decades ago, where would we have been today ???
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC.
2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion.
93/01.05/4.1
http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832
121/YdeS
92/11.4/1.2
http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
Wednesday, January 18, 2012
Government seeking $1T campaign against Alzheimer's
http://betaamyloidcjd.blogspot.com/2012/01/government-seeking-1t-campaign-against.html
Tuesday, October 4, 2011
De novo induction of amyloid-β deposition in vivo
Molecular Psychiatry advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
http://betaamyloidcjd.blogspot.com/2011/10/de-novo-induction-of-amyloid-deposition.html
snip...see full text ;
http://betaamyloidcjd.blogspot.com/2012/02/27th-colloque-medecine-et-recherche-of.html
TSS
layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net