Familial prion disease with alzheimer disease-like tau pathology and clinical phenotype
Suman Jayadev MD1, David Nochlin MD2, Parvoneh Poorkaj PhD3, Ellen J. Steinbart RN, MA3, James A. Mastrianni MD, PhD4, Thomas J. Montine MD, PhD5, Bernardino Ghetti MD6,7, Gerard D. Schellenberg PhD8, Thomas D. Bird MD1,3,9, James B. Leverenz MD1,10,11,12,*
Article first published online: 17 MAR 2011
DOI: 10.1002/ana.22264
Abstract
Objective
To describe the Alzheimer disease (AD)-like clinical and pathological features, including marked neurofibrillary tangle (NFT) pathology, of a familial prion disease due to a rare nonsense mutation of the prion gene (PRNP).
Methods
Longitudinal clinical assessments were available for the proband and her mother. After death, both underwent neuropathological evaluation. PRNP was sequenced after failure to find immunopositive Aß deposits in the proband and the documentation of prion protein (PrP) immunopositive pathology.
Results
The proband presented at age 42 years with a 3-year history of progressive short-term memory impairment and depression. Neuropsychological testing found impaired memory performance, with relatively preserved attention and construction. She was diagnosed with AD and died at age 47 years. Neuropathologic evaluation revealed extensive limbic and neocortical NFT formation and neuritic plaques consistent with a Braak stage of VI. The NFTs were immunopositive, with multiple tau antibodies, and electron microscopy revealed paired helical filaments. However, the neuritic plaques were immunonegative for Aß, whereas immunostaining for PrP was positive. The mother of the proband had a similar presentation, including depression, and had been diagnosed clinically and pathologically as AD. Reevaluation of her brain tissue confirmed similar tau and PrP immunostaining findings. Genetic analysis revealed that both the proband and her mother had a rare PRNP mutation (Q160X) that resulted in the production of truncated PrP.
Interpretation
We suggest that PRNP mutations that result in a truncation of PrP lead to a prolonged clinical course consistent with a clinical diagnosis of AD and severe AD-like NFTs. Ann Neurol 2010;
http://onlinelibrary.wiley.com/doi/10.1002/ana.22264/abstract
I suggest it's a Transmissible Spongiform Encephalopathy i.e. prion disease. ...TSS
strictly NOT private and confidential $$$
Saturday, January 22, 2011
Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html
Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
http://betaamyloidcjd.blogspot.com/
TSS
Saturday, March 19, 2011
PRION DISEASE MAN AND ANIMAL SPREADING NORTH AMERICA, WHILE FEDERAL FUNDING TO BE AXED
REQUEST FOR CONTINUING FUNDING FOR THE NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER
SUMMARY STATEMENT
We wish to emphasize the critical need of maintaining funding for the CDC supported National Prion Disease Pathology Surveillance Center (the Center) at no less than 90% of the current 5.474M (FY2010 appropriation). The Center is the only organization in the United States that (1) monitors the possible occurrence of "mad cow" disease and other human prion diseases caused by eating prion contaminated elk and deer meat, blood transfusion, surgical instruments and other sources of prion infection; and (2) ensures that countries that import meat products from the United States continue to regard US meat as safe from mad cow disease and do not discontinue importation as has happened in the past.
REASONS FOR THE REQUEST
Based at Case Western Reserve University in Cleveland OH, the Center receives 100% of its funding for prion (mad cow) disease surveillance through the Centers for Disease Control (CDC). Continued funding for the Center in 2011 (Continuing Resolution) and 2012 (President's proposed Budget) is at grave risk. The Department of Health and Human Services has proposed zeroing out funding for the Center, for 2012. Loss of that funding would force the Center to shut down at a time in which prion affected cows (mad cows) and human cases of mad cow disease continue to be detected around the world including the US and most recently Canada from which the United States freely imports cattle.
The Center also plays a decisive role in resolving suspected cases or clusters of cases of food acquired prion disease such as mad cow disease or prion diseases possibly acquired from prion infected elk and deer. These cases often are magnified by the media and stir intense public alarm. To date, the Center has examined about 4,000 suspected incidents of prion diseases and has definitely confirmed presence and type of prion disease in nearly 2,300 cases.
The Center represents the last line of defense in safeguarding the US public health against prion diseases because the United States - unlike other countries such as Canada, the United Kingdom, other European Countries and Japan - does not have a robust animal prion surveillance system,
The Center plays a second important role: It offers assurance to the countries that import (or consider whether to import) meat from the United States that the United States is free of indigenous human mad cow disease. For example, South Korean health officials recently resumed importation of US beef to their country after a visit to the Center provided assurances regarding prion surveillance.
CONCLUSION
Therefore, the abolition or major reduction of funding to the Center would not only eliminate an important safety net to US public health, but it would also jeopardize the export of US beef by making the United States the only industrialized country lacking prion surveillance.
Pierluigi Gambetti M.D. Professor and Director National Prion Disease Pathology Surveillance Center Department of Pathology, Division of Neuropathology Case Western Reserve University Cleveland, OH Phone 216 368 0587 FAX 216 368 2546
http://www.cjdfoundation.org/atc.html
All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
problem solved $$$
Monday, March 21, 2011
Sheep and Goat BSE Propagate More Efficiently than Cattle BSE in Human PrP Transgenic Mice
http://nor-98.blogspot.com/2011/03/sheep-and-goat-bse-propagate-more.html
(updated 3/22/2011)...TSS
Bovine spongiform encephalopathy (BSE) cases confirmed in Canada in 2011
BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.
The following table lists individual animals confirmed to be infected with BSE in Canada in 2011.
Current as of: 2011-02-28
Date confirmed Location Animal type infected Age of animal February 18 Alberta Dairy cow 77 months
http://inspection.gc.ca/english/anima/disemala/rep/2011bseesbe.shtml
Saturday, March 12, 2011
Variant Creutzfeldt-Jakob Disease in a Canadian resident Infectious Diseases News Brief - March 11, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/variant-creutzfeldt-jakob-disease-in.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
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
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.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
TSS
SUMMARY STATEMENT
We wish to emphasize the critical need of maintaining funding for the CDC supported National Prion Disease Pathology Surveillance Center (the Center) at no less than 90% of the current 5.474M (FY2010 appropriation). The Center is the only organization in the United States that (1) monitors the possible occurrence of "mad cow" disease and other human prion diseases caused by eating prion contaminated elk and deer meat, blood transfusion, surgical instruments and other sources of prion infection; and (2) ensures that countries that import meat products from the United States continue to regard US meat as safe from mad cow disease and do not discontinue importation as has happened in the past.
REASONS FOR THE REQUEST
Based at Case Western Reserve University in Cleveland OH, the Center receives 100% of its funding for prion (mad cow) disease surveillance through the Centers for Disease Control (CDC). Continued funding for the Center in 2011 (Continuing Resolution) and 2012 (President's proposed Budget) is at grave risk. The Department of Health and Human Services has proposed zeroing out funding for the Center, for 2012. Loss of that funding would force the Center to shut down at a time in which prion affected cows (mad cows) and human cases of mad cow disease continue to be detected around the world including the US and most recently Canada from which the United States freely imports cattle.
The Center also plays a decisive role in resolving suspected cases or clusters of cases of food acquired prion disease such as mad cow disease or prion diseases possibly acquired from prion infected elk and deer. These cases often are magnified by the media and stir intense public alarm. To date, the Center has examined about 4,000 suspected incidents of prion diseases and has definitely confirmed presence and type of prion disease in nearly 2,300 cases.
The Center represents the last line of defense in safeguarding the US public health against prion diseases because the United States - unlike other countries such as Canada, the United Kingdom, other European Countries and Japan - does not have a robust animal prion surveillance system,
The Center plays a second important role: It offers assurance to the countries that import (or consider whether to import) meat from the United States that the United States is free of indigenous human mad cow disease. For example, South Korean health officials recently resumed importation of US beef to their country after a visit to the Center provided assurances regarding prion surveillance.
CONCLUSION
Therefore, the abolition or major reduction of funding to the Center would not only eliminate an important safety net to US public health, but it would also jeopardize the export of US beef by making the United States the only industrialized country lacking prion surveillance.
Pierluigi Gambetti M.D. Professor and Director National Prion Disease Pathology Surveillance Center Department of Pathology, Division of Neuropathology Case Western Reserve University Cleveland, OH Phone 216 368 0587 FAX 216 368 2546
http://www.cjdfoundation.org/atc.html
All Other Emerging and Zoonotic Infectious Diseases CDC‘s FY 2012 request of $52,658,000 for all other emerging and zoonotic infectious disease activities is a decrease of $13,607,000 below the FY 2010 level, which includes the elimination of Prion activities ($5,473,000), a reduction for other cross-cutting infectious disease activities, and administrative savings. These funds support a range of critical emerging and zoonotic infectious disease programs such Lyme Disease, Chronic Fatigue Syndrome, and Special Pathogens, as well as other activities described below.
http://www.cdc.gov/fmo/topic/Budget%20Information/appropriations_budget_form_pdf/FY2012_CDC_CJ_Final.pdf
problem solved $$$
Monday, March 21, 2011
Sheep and Goat BSE Propagate More Efficiently than Cattle BSE in Human PrP Transgenic Mice
http://nor-98.blogspot.com/2011/03/sheep-and-goat-bse-propagate-more.html
(updated 3/22/2011)...TSS
Bovine spongiform encephalopathy (BSE) cases confirmed in Canada in 2011
BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.
The following table lists individual animals confirmed to be infected with BSE in Canada in 2011.
Current as of: 2011-02-28
Date confirmed Location Animal type infected Age of animal February 18 Alberta Dairy cow 77 months
http://inspection.gc.ca/english/anima/disemala/rep/2011bseesbe.shtml
Saturday, March 12, 2011
Variant Creutzfeldt-Jakob Disease in a Canadian resident Infectious Diseases News Brief - March 11, 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/variant-creutzfeldt-jakob-disease-in.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
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
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.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
TSS
Saturday, March 12, 2011
Variant Creutzfeldt-Jakob Disease in a Canadian resident
Infectious Diseases News Brief - March 11, 2011
[Current Issue - Table of contents]
Variant Creutzfeldt-Jakob Disease in a Canadian resident Canadian Creutzfeldt-Jakob Disease Surveillance System, National Microbiology Laboratory, Public Health Agency of Canada Working closely with Canadian clinical specialists, the Public Health Agency of Canada’s Creutzfeldt-Jakob Disease Surveillance System (CJDSS) has identified a probable case of variant Creutzfeldt-Jakob disease (variant CJD, also called vCJD) in a Canadian resident. The diagnosis is supported by several lines of clinical, paraclinical and laboratory evidence, in keeping with internationally accepted surveillance case definitions for human prion disease.(1, 2) This is the second case of variant CJD reported in Canada to date. The first such case occurred in 2002, in an individual who is believed to have contracted the disease outside of Canada.(3) As explained in more detail below, evidence to date strongly indicates that (i) the risk exposure in the second case also occurred outside Canada; (ii) there are no negative implications for the safety of the Canadian food supply; and (iii) the case poses no secondary risks to the health of Canadians.
Variant CJD belongs to a group of rare, fatal degenerative brain disorders called prion diseases that affect humans and animals and can arise sporadically, genetically, or through infectious transmission.(4) Prion diseases are marked by brain tissue vacuolation (spongiform change), neuronal loss, and presence of a pathologically altered form of a host-encoded glycoprotein, PrP, that is considered to constitute the transmissible agent, or prion.(5) Among classic types of human prion disease, the most common and widespread is sporadic CJD, which occurs without an apparent infectious or genetic cause mostly in persons 50+ years of age and accounts for 80–90% of the remarkably uniform annual prion disease mortality of ~1–2 per million population.(6) Most of the remaining 10–20% of classic human prion diseases are caused by mutations in the PRNP gene that encodes PrP.(7) Fewer than 1% of classic cases of CJD are attributed to accidental transmission through surgical and medical procedures such as dura mater grafts, and use of therapeutic hormone preparations that were derived from prion-contaminated cadaveric pituitary tissue.(8)
Variant CJD is the only known zoonotic human prion disease, resulting from dietary exposure to a feedborne prion disease of cattle, bovine spongiform encephalopathy (BSE, also known as “mad cow disease”), that emerged internationally in the 1980s and 1990s.(9) Most human exposure to BSE is thought to have occurred before regulatory controls were implemented to control BSE in animals and to eliminate the inclusion of high-risk bovine tissues in human food.(10) A small number of secondary cases of variant CJD have also been linked to transfusion of fresh blood components (erythrocytes) from pre-symptomatic donors who later developed the disease.(11) By October 2010, a total of 222 definite and probable variant CJD cases had been reported worldwide in residents of 12 countries.(12) The total numbers of clinical cases of variant CJD that will ultimately emerge remains uncertain, as does the frequency of long-term asymptomatic carriage during which apparently healthy individuals could transmit infection for example through blood donation or invasive medical procedures.(13)
Importantly, based on extensive interviews with family members there is no indication that the current patient was ever a blood donor, received a blood transfusion, or underwent a surgical procedure that was not managed to prevent prion transmission as per the Public Health Agency of Canada’s CJD Infection Control Guidelines.(14) This indicates the absence of secondary risks to the health of Canadians as a result of this case. Health Canada issued directives to Canadian blood operators in 1999, 2000, 2001 and 2005, requiring deferral of blood donors with a history of residence and/or travel in the United Kingdom (UK), France and Western Europe in the period 1980-1996, as well as other criteria including receipt of blood transfusion in the UK, and has committed to review these deferral policies if new scientific information becomes available. Canada has also reported a small number of cases of BSE,(15) and Health Canada and the Canadian Food Inspection Agency have implemented regulations to prevent both the transmission of BSE in animal populations and human exposure to it. Given (i) these protective measures, (ii) the observation that acquired prion diseases have long incubation periods (years to often a decade or more), and (iii) the fact that the current patient experienced onset of symptoms just prior to immigrating to Canada in early 2010, the possibility of BSE exposure in this country can essentially be ruled out as the cause of illness. The patient was born in the Middle East, and also resided in several other countries before arriving in Canada. Apart from a few visits totalling less than three months in duration, there was no history of travel to the UK or Europe.
In Canada, all human prion diseases are both legally reportable at the provincial/territorial level and nationally notifiable, and despite their rarity the public health importance and economic impacts of these diseases have maintained a need for timely diagnosis, reporting, and surveillance. To help meet these requirements the CJDSS has conducted prospective national surveillance of human prion diseases continuously since 1998, and working collaboratively with a network of health professionals sponsors detailed diagnostic and epidemiologic investigation of any suspected case of human prion disease in Canada. Supporting laboratory services are provided for autopsy, neuropathologic examination, molecular genetics, and biochemical testing for 14-3-3 protein in cerebrospinal fluid. Test results are reported directly to referring health professionals, with CJDSS case files maintained centrally to facilitate diagnostic assessment and final case classification. Full patient enrolment with the CJDSS takes place with written informed consent. The CJDSS surveillance protocol has been approved by the Health Canada Research Ethics Board (Certificate REB-2009-0036), and by numerous REBs at collaborating healthcare institutions. For further information on human prion diseases, available services and how to access them, interested health professionals are invited to contact the CJDSS toll-free, at 1-888-489-2999.
References 1.World Health Organization (WHO). WHO manual for surveillance of human transmissible spongiform encephalopathies including variant Creutzfeldt-Jakob disease. 2003. http://whqlibdoc.who.int/publications/2003/9241545887.pdf . 2.Heath CA, Cooper SA, Murray K et al. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010;67(6):761-770. 3.Jansen GH, Voll CL, Robinson CA et al. First case of variant Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2003;29(13):117-120. 4.Aguzzi A, Calella AM. Prions: protein aggregation and infectious diseases. Physiol Rev 2009;89(4):1105-1152. 5.Prusiner SB. Prions. Proc Natl Acad Sci USA 1998;95(23):13363-13383. 6.Ladogana A, Puopolo M, Croes EA et al. Mortality from Creutzfeldt-Jakob disease and related disorders in Europe, Australia, and Canada. Neurology 2005;64(9):1586-1591. 7.Kovacs GG, Puopolo M, Ladogana A et al. Genetic prion disease: the EUROCJD experience. Hum Genet 2005;118(2):166-174. 8.Brown P, Brandel JP, Preece M et al. Iatrogenic Creutzfeldt-Jakob disease: The waning of an era. Neurology 2006;67(3):389-393. 9.Bradley R, Collee JG, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 1. Folia Neuropathol 2006;44(2):93-101. 10.Collee JG, Bradley R, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 2. Folia Neuropathol 2006;44(2):102-110. 11.Lefrere JJ, Hewitt P. From mad cows to sensible blood transfusion: the risk of prion transmission by labile blood components in the United Kingdom and in France. Transfusion 2009;49(4):797-812. 12.European Creutzfeldt-Jakob Disease Surveillance Network. vCJD cases worldwide. http://www.eurocjd.ed.ac.uk/surveillance%20data%204.htm. 13.de Marco MF, Linehan J, Gill ON et al. Large-scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain. J Pathol 2010;222(4):380-387. 14.Public Health Agency of Canada. Infection control guidelines: classic Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2002;28S5:1-110. 15.Canadian Food Inspection Agency. BSE in North America. http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml
http://www.phac-aspc.gc.ca/ccdrw-rmtch/2011/ccdrw-rmtcs1011r-eng.php
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.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
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
TSS
[Current Issue - Table of contents]
Variant Creutzfeldt-Jakob Disease in a Canadian resident Canadian Creutzfeldt-Jakob Disease Surveillance System, National Microbiology Laboratory, Public Health Agency of Canada Working closely with Canadian clinical specialists, the Public Health Agency of Canada’s Creutzfeldt-Jakob Disease Surveillance System (CJDSS) has identified a probable case of variant Creutzfeldt-Jakob disease (variant CJD, also called vCJD) in a Canadian resident. The diagnosis is supported by several lines of clinical, paraclinical and laboratory evidence, in keeping with internationally accepted surveillance case definitions for human prion disease.(1, 2) This is the second case of variant CJD reported in Canada to date. The first such case occurred in 2002, in an individual who is believed to have contracted the disease outside of Canada.(3) As explained in more detail below, evidence to date strongly indicates that (i) the risk exposure in the second case also occurred outside Canada; (ii) there are no negative implications for the safety of the Canadian food supply; and (iii) the case poses no secondary risks to the health of Canadians.
Variant CJD belongs to a group of rare, fatal degenerative brain disorders called prion diseases that affect humans and animals and can arise sporadically, genetically, or through infectious transmission.(4) Prion diseases are marked by brain tissue vacuolation (spongiform change), neuronal loss, and presence of a pathologically altered form of a host-encoded glycoprotein, PrP, that is considered to constitute the transmissible agent, or prion.(5) Among classic types of human prion disease, the most common and widespread is sporadic CJD, which occurs without an apparent infectious or genetic cause mostly in persons 50+ years of age and accounts for 80–90% of the remarkably uniform annual prion disease mortality of ~1–2 per million population.(6) Most of the remaining 10–20% of classic human prion diseases are caused by mutations in the PRNP gene that encodes PrP.(7) Fewer than 1% of classic cases of CJD are attributed to accidental transmission through surgical and medical procedures such as dura mater grafts, and use of therapeutic hormone preparations that were derived from prion-contaminated cadaveric pituitary tissue.(8)
Variant CJD is the only known zoonotic human prion disease, resulting from dietary exposure to a feedborne prion disease of cattle, bovine spongiform encephalopathy (BSE, also known as “mad cow disease”), that emerged internationally in the 1980s and 1990s.(9) Most human exposure to BSE is thought to have occurred before regulatory controls were implemented to control BSE in animals and to eliminate the inclusion of high-risk bovine tissues in human food.(10) A small number of secondary cases of variant CJD have also been linked to transfusion of fresh blood components (erythrocytes) from pre-symptomatic donors who later developed the disease.(11) By October 2010, a total of 222 definite and probable variant CJD cases had been reported worldwide in residents of 12 countries.(12) The total numbers of clinical cases of variant CJD that will ultimately emerge remains uncertain, as does the frequency of long-term asymptomatic carriage during which apparently healthy individuals could transmit infection for example through blood donation or invasive medical procedures.(13)
Importantly, based on extensive interviews with family members there is no indication that the current patient was ever a blood donor, received a blood transfusion, or underwent a surgical procedure that was not managed to prevent prion transmission as per the Public Health Agency of Canada’s CJD Infection Control Guidelines.(14) This indicates the absence of secondary risks to the health of Canadians as a result of this case. Health Canada issued directives to Canadian blood operators in 1999, 2000, 2001 and 2005, requiring deferral of blood donors with a history of residence and/or travel in the United Kingdom (UK), France and Western Europe in the period 1980-1996, as well as other criteria including receipt of blood transfusion in the UK, and has committed to review these deferral policies if new scientific information becomes available. Canada has also reported a small number of cases of BSE,(15) and Health Canada and the Canadian Food Inspection Agency have implemented regulations to prevent both the transmission of BSE in animal populations and human exposure to it. Given (i) these protective measures, (ii) the observation that acquired prion diseases have long incubation periods (years to often a decade or more), and (iii) the fact that the current patient experienced onset of symptoms just prior to immigrating to Canada in early 2010, the possibility of BSE exposure in this country can essentially be ruled out as the cause of illness. The patient was born in the Middle East, and also resided in several other countries before arriving in Canada. Apart from a few visits totalling less than three months in duration, there was no history of travel to the UK or Europe.
In Canada, all human prion diseases are both legally reportable at the provincial/territorial level and nationally notifiable, and despite their rarity the public health importance and economic impacts of these diseases have maintained a need for timely diagnosis, reporting, and surveillance. To help meet these requirements the CJDSS has conducted prospective national surveillance of human prion diseases continuously since 1998, and working collaboratively with a network of health professionals sponsors detailed diagnostic and epidemiologic investigation of any suspected case of human prion disease in Canada. Supporting laboratory services are provided for autopsy, neuropathologic examination, molecular genetics, and biochemical testing for 14-3-3 protein in cerebrospinal fluid. Test results are reported directly to referring health professionals, with CJDSS case files maintained centrally to facilitate diagnostic assessment and final case classification. Full patient enrolment with the CJDSS takes place with written informed consent. The CJDSS surveillance protocol has been approved by the Health Canada Research Ethics Board (Certificate REB-2009-0036), and by numerous REBs at collaborating healthcare institutions. For further information on human prion diseases, available services and how to access them, interested health professionals are invited to contact the CJDSS toll-free, at 1-888-489-2999.
References 1.World Health Organization (WHO). WHO manual for surveillance of human transmissible spongiform encephalopathies including variant Creutzfeldt-Jakob disease. 2003. http://whqlibdoc.who.int/publications/2003/9241545887.pdf . 2.Heath CA, Cooper SA, Murray K et al. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010;67(6):761-770. 3.Jansen GH, Voll CL, Robinson CA et al. First case of variant Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2003;29(13):117-120. 4.Aguzzi A, Calella AM. Prions: protein aggregation and infectious diseases. Physiol Rev 2009;89(4):1105-1152. 5.Prusiner SB. Prions. Proc Natl Acad Sci USA 1998;95(23):13363-13383. 6.Ladogana A, Puopolo M, Croes EA et al. Mortality from Creutzfeldt-Jakob disease and related disorders in Europe, Australia, and Canada. Neurology 2005;64(9):1586-1591. 7.Kovacs GG, Puopolo M, Ladogana A et al. Genetic prion disease: the EUROCJD experience. Hum Genet 2005;118(2):166-174. 8.Brown P, Brandel JP, Preece M et al. Iatrogenic Creutzfeldt-Jakob disease: The waning of an era. Neurology 2006;67(3):389-393. 9.Bradley R, Collee JG, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 1. Folia Neuropathol 2006;44(2):93-101. 10.Collee JG, Bradley R, Liberski PP. Variant CJD (vCJD) and bovine spongiform encephalopathy (BSE): 10 and 20 years on: Part 2. Folia Neuropathol 2006;44(2):102-110. 11.Lefrere JJ, Hewitt P. From mad cows to sensible blood transfusion: the risk of prion transmission by labile blood components in the United Kingdom and in France. Transfusion 2009;49(4):797-812. 12.European Creutzfeldt-Jakob Disease Surveillance Network. vCJD cases worldwide. http://www.eurocjd.ed.ac.uk/surveillance%20data%204.htm. 13.de Marco MF, Linehan J, Gill ON et al. Large-scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain. J Pathol 2010;222(4):380-387. 14.Public Health Agency of Canada. Infection control guidelines: classic Creutzfeldt-Jakob disease in Canada. Can Commun Dis Rep 2002;28S5:1-110. 15.Canadian Food Inspection Agency. BSE in North America. http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml
http://www.phac-aspc.gc.ca/ccdrw-rmtch/2011/ccdrw-rmtcs1011r-eng.php
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.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
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
TSS
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
We write to you regarding Japan's interest in joining the Trans-Pacific Partnership (TPP) negotiations.
We appreciate your Administration's efforts to expand the presence of U.S. businesses and exports in the vital Asia-Pacific region through the TPP. Expanded trade is needed for economic growth, as well as for the continued competitiveness of our businesses, workers, farmers, and ranchers. Further expanding our market access in important economies of this region will provide significant opportunities for our exporters and will favorably reorient the region economically and geopolitically towards the United States.
It is also encouraging that the leaders of the Japanese government have expressed their interest in joining the TPP and thus eliminating their tariff and non-tariff trade barriers to U.S. goods and services. However, given Japan's historical intransigence in allowing market access for American agricultural goods, we write to express reservations regarding Japan's inclusion in these negotiations until certain conditions are met. In addition to prohibitively high tariffs on many agricultural goods, Japan has discriminated against U.S. beef imports with restrictions that are inconsistent with international standards and not based on scientific criteria.
As you know, Japan closed its market to U.S. beef in December of 2003, after the discovery of a Canadian-born cow infected with bovine spongiform encephalopathy (BSE) in the United States. At that time, Japan was the largest export market for U.S. beef, valued at $1.4 billion. Since then, Japan has had restrictions in place on U.S. beef imports and currently only allows imports of beef from cattle aged 20 months and younger.
The United States has spent years putting in place an effective system of interlocking safeguards that has successfully prevented BSE from becoming established in our country. The U.S. Department of Agriculture's Animal and Plant Health Inspection Service has aggressively enhanced our BSE surveillance system since 1990, testing at levels forty times higher than recommended by the World Organization for Animal Health (OIE). As a result, out of a U.S. cattle inventory numbering nearly 100 million head every year, there have only been three confirmed cases of BSE since 2003-the one imported Canadian cow and two atypical cases of cattle born in the U.S. prior to our 1997 feed ban-and none since 2006 (In contrast, Japan, with an annual cattle inventory of only 4.5 million head, has had thirty-six cases of BSE since 2003). Because of these efforts, the United States has been classified as a controlled risk country by the OlE, which indicates that U.S. beef products are completely safe for export and consumption. Incidentally, this is the same BSE risk status classification as that of Japan.
American farmers and ranchers produce the highest quality agricultural products in the world. When given the opportunity to compete on a level playing field, they will thrive, creating more jobs and revenue at home while providing foreign customers affordable access to our products across the world. Japan's agricultural sector stands in stark contrast as one of the most highly protected in the world. If Japan asks for inclusion in the TPP negotiations, we encourage you to press Japanese leaders to immediately relax its restrictions on u.s. beef to be fully consistent with OlE guidelines and reopen its market. At the very least, Japan should agree to immediately relax its age restrictions to 30 months and address other issues necessary to achieve a commercially-viable, science-based import protocol, while also laying a clear pathway for eventual full OlE compliance. Likewise, we would have serious reservations with any TPP agreement submitted to Congress that includes Japan if it has not made commitments to fully complete this process, as well as eliminate tariff and non-tariff barriers on its TPP partners' agricultural exports.
Trade agreements must solidify economic relations and foster mutual trust. Japan's past actions pose serious concerns that require your consideration and leadership in addressing; future commitments must ensure that Japan will abide by internationally-accepted, science-based trading standards that will be vigorously enforced.
Very truly yours,
http://johanns.senate.gov/public/?a=Files.Serve&File_id=81e2e8dc-c839-4558-8c37-951f02ad9930
(PLEASE SEE LIST OF SENATORS above THAT ARE REFUSING TO ACKNOWLEDGE THE MOST RECENT SCIENCE ON TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY AKA MAD COW DISEASE AND RISK FROM THE ATYPICAL TSE AND THE SPORADIC CJD, SEE THE LIST OF SENATORS THAT ARE IGNORING THE CONSTANT MAD COW FEED VIOLATIONS SINCE THE PARTIAL AND VOLUNTARY MAD COW FEED BAN WAS PUT IN PLACE IN AUGUST OF 1997, AND SEE THE LIST OF SENATORS THAT TURN THEIR HEADS THE OTHER WAY, EVERY TIME ANOTHER MAD COW IS COVERED UP, OR ATTEMPTED TO BE COVERED UP. PLEASE SEE THESE LIST OF SENATORS, and then see the most up to date science on TSE. then ask yourself, do you blame Japan ???...TSS)
Johanns et al @ the USDA and the OIE are the very reason we have spread mad cow disease all around the globe, again, except this time they made it legal while trying to cover up the Texas mad cow and that Alabama mad cow. the OIE BSE MRR policy is nothing more than a legal instrument to trade Transmissible Spongiform Encephalopathy globally, and legally. Johanns et al should be prosecuted for this $$$
Canada, U.S.A., and Mexico, have been swapping cattle, cattle by-products, and feed, like two lovers swapping spit, and in doing so, in my opinion, have been swapping Transmissible Spongiform Encephalopathy aka mad cow disease of all strains. THE FDA mad cow feed firewall that the USDA et al claim protects us, that firewall was breached long ago. actually, it was nothing but ink on paper. sporadic CJD of unknown phenotype is rising in Canada and the USA. North America has more documented cases of the prion disease aka TSE in more documented species in the wild than anybody in the world, most all of which has been rendered and fed to livestock producing animals for human and animals, at some point in time. NO spontaneous, naturally occurring TSE, has ever been documented in the field, in any species.
I think of one thing when i think of mad cow and cjd there from in the USA. i think of Tobacco and Asbestos, and how many decades the public was lied to about those products. the after effects and death there from was also a long incubating disease, diseases that you could forget about after consumption, for a while. just something to ponder. ...
i have watched these mad cow folly's by the Industry, USDA, FDA, et al daily now for almost 14 years. yes, i am angry, i am mad as hell, but these are the facts as i have come to know them. they are not pretty. in fact, very disturbing. ...time will tell. sporadic CJD is on the rise....oh, and the latest on sporadic CJD first, just so you ya know ;
***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
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
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
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
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Saturday, March 5, 2011
ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Greetings,
WITH more and more atypical Transmissible Spongiform Encephalopathy cases showing up in more and more species here in North America, and the enormous monumental amount of banned mad cow protein in commerce since the infamous partial and voluntary mad cow feed ban inked on paper, with tons and tons crossing back and forth between the USA, Canada, and Mexico, it just does not surprise me of all these "PENDING CLASSIFICATIONS" of human TSE in Canada, and the USA. UK c-BSE transmitted to humans became nvCJD. WE now have atypical strains of BSE in cattle. Mission Texas experiments long ago showed that transmitted USA sheep scrapie to USA bovine, produced a TSE much different than the UK typical c-BSE. SO why would human TSE in the USA look like UK human TSE ? The corruption is mind boggling. The UK saw a suspicious TSE in humans, and science linked it to cattle. North America is awash with human and animal TSE, CJD is rising in young and old, with the same pathology and same symptoms, and none of it is related to the other. isn't that nice. who, what, bestowed such miracles upon North America $
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
snip...
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Tuesday, January 1, 2008
BSE OIE USDA
Subject: OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA
Date: May 14, 2007 at 9:00 am PST
OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
they did not want to find BSE, and never intended to. ...tss
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Tuesday, January 1, 2008
BSE OIE USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ? they could not have found a mad cow if they were standing beside the stumbling and staggering bovine $$$, using the diagnostic criteria they were using, AND TOLD SO, but they kept on doing it anyway. ...
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Christopher J. Johnson1, Debbie McKenzie2, Joel A. Pedersen3, Judd M. Aiken4
1Prion Research Laboratory, USGS National Wildlife Health Center, Madison, Wisconsin, USA 2Centre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada 3Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin, USA 4Centre for Prions and Protein Folding Diseases, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta, Canada
Ingestion of prion-contaminated materials is postulated to be a primary route of prion disease transmission. Binding of prions to soil (micro)particles dramatically enhances peroral disease transmission relative to unbound prions, and it was hypothesized that micrometer– sized particles present in other consumed materials may affect prion disease transmission via the oral route of exposure. Small, insoluble particles are present in many substances, including soil, human foods, pharmaceuticals, and animal feeds. It is known that meat and bone meal (MBM), a feed additive believed responsible for the spread of bovine spongiform encephalopathy (BSE), contains particles smaller than 20 ìm and that the pathogenic prion protein binds to MBM. The potentiation of disease transmission via the oral route by exposure to MBM or three micrometer-sized mineral feed additives was determined. Data showed that when the disease agent was bound to any of the tested materials, the penetrance of disease was increased compared to unbound prions. Our data suggest that in feed or other prion– contaminated substances consumed by animals or, potentially, humans, the addition of MBM or the presence of microparticles could heighten risks of prion disease acquisition.
SNIP...
CONCLUSIONS
Should prions be present in animal feed, their association with MBM or insoluble particles such as those tested (viz. Mte, Kte, and SiO2) could substantially increase the risk of disease acquisition compared to consumption of prions alone. While care needs to be exercised when extrapolating results from laboratory rodent models to ruminants, these data may explain how MBM produced BSE transmission despite the presumably low titers of infectious agent present in cattle feed (Taylor et al., 1995). In addition, inorganic particles in commercial feeds or mineral licks may pose a previously unrecognized risk of enhancing TSE transmission to domestic and wildlife species from agents contaminating these materials or infectivity shed onto feed or licks.
Following consumption, (sub)micrometersized particles can be absorbed by the gut. Goblet cells (Doyle-McCullough et al., 2007), M cells in Peyer’s patches (Florence, 1997), and persorptive mechanisms at the tips of broken intestinal villi (Hillyer & Albrecht, 2001; Volkheimer, 2001) all contribute to intestinal particle uptake. Increased uptake of particlebound prions might explain enhanced oral transmissibility. Alternatively, aluminosilicates may increase residence time of agent in the digestive system (Bringe & Schultz, 1969; Collings et al., 1980; Quisenberry, 1968) and elevate exposure time at sites of conversion. Further investigation into these mechanisms, the effect of digestive processes on bound prions, and alterations of agent physicochemical properties upon binding is warranted.
It is noteworthy that microparticles find widespread use as human food and pharmaceutical additives in Western diets (Lomer et al., 2000, 2004). The average daily consumption dietary microparticles from food, pharmaceuticals, and dentifrices is approximately 40 mg (approximately 1012 particles) per person (Powell et al., 2007). The extent to which microparticles in the human diet influence prion disease acquisition is currently unknown, but these data suggest that microparticle consumption needs to be investigated as a potential risk factor in human TSE acquisition.
SEE FULL TEXT ;
http://www.informaworld.com/smpp/content~content=a931920802~db=all~jumptype=rss
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Monday, January 17, 2011
MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011
January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html
Friday, January 7, 2011
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.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/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Friday, February 04, 2011
NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico
----- Original Message -----
From: Terry S. Singeltary Sr.
To: President.BenShelly
Cc: sroanhorse ; opvp.nelson ; alaughing; georgehardeen; pressoffice
Sent: Thursday, February 03, 2011 12:15 PM
Subject: NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico
Greetings Honorable People of the Great Navajo Nation, and the Honorable President Ben Shelly,
I send this to you with great concern. ...
http://scrapie-usa.blogspot.com/2011/02/nmlb-and-usda-allow-scrapie-prion.html
Received October 28, 2010. Accepted January 4, 2011. Copyright © 2011, The American Society for Biochemistry and Molecular Biology
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, James A. Mastrianni4 and Claudio Soto5,*
http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long
Our findings demonstrate that cervid PrPSc, upon strain adaptation by serial passages in vitro or in cervid transgenic mice, is capable of converting human PrPC to produce PrPSc with unique biochemical properties, likely representing a new human prion strain. The newly generated CWD-huPrPSc material has been inoculated into transgenic mice expressing human PrP to study infectivity and disease phenotype and this data will be published elsewhere. ...end
http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Wednesday, March 02, 2011
CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010
http://chronic-wasting-disease.blogspot.com/2011/03/cwd-in-nebraska-is-increasing-with-51.html
Monday, February 28, 2011
South Dakota finds 25 more cases of Chronic Wasting Disease
Latest Chronic Wasting Disease Testing Results
http://chronic-wasting-disease.blogspot.com/2011/02/south-dakota-finds-25-more-cases-of.html
Thursday, February 10, 2011
CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer - Updated 2/07/2011
http://chronic-wasting-disease.blogspot.com/2011/02/cwd-illinois-update-february-2011.html
Thursday, February 10, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-found-in-white.html
Tuesday, February 22, 2011
Chronic wasting disease spreads farther west in Alberta
http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-spreads-farther.html
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley...
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
SEE FULL TEXT AND MORE HERE ;
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
IF ANY OF YOU WANT TO SEE THE CREDIBILITY OF THE O.I.E., (or the lack of credibility) i urge you to read this, and you will see what an industry laden group they really are. the O.I.E. protects one thing, and one thing only, they protect their own, THE INDUSTRY ;
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
snip...
Greetings,
Thank for your support to the OIE objectives for a safe world.
NOT !
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."
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...
please see full text ;
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
*** Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Saturday, June 19, 2010
U.S. DENIED UPGRADED BSE STATUS FROM OIE
http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html
Monday, April 12, 2010
Senator Kay Bailey Hutchison says NO to safer food and S. 510 FDA Food Safety Modernization Act of 2009
http://fdafailedus.blogspot.com/2010/04/senator-kay-bailey-hutchison-says-no-to.html
U.S. Department of State
Cases Regarding the Border Closure due to BSE Concerns
Several Canadian claimants have submitted notices of arbitration under the UNCITRAL Arbitration Rules alleging that the United States has violated NAFTA Chapter Eleven by closing the border to the importation of Canadian cattle after the discovery in 2003 of a case of bovine spongiform encephalopathy (BSE or mad cow disease) in a cow in Alberta, Canada. Claimants are Canadian citizens and corporations that own and operate cattle feeding, feedlot and transportation businesses in Canada, which they allege were damaged by the border closure.
Claimants allege that the border closure violates NAFTA Article 1102 (national treatment). The notices of arbitration seek damages of varying amounts, ranging from CAN$38,000 to CAN$95 million. The total amount of damages sought by claimants is approximately US$235 million.
On January 28, 2008, the tribunal issued its Award on Jurisdiction, dismissing the claims against the United States in their entirety. The tribunal’s award, and other documents in the case, appear below.
-01/28/08 Award on Jurisdiction [575 Kb] -10/10/07 Transcript of the Hearing on the Preliminary Issue - Day Two [166 Kb] -10/09/07 Transcript of the Hearing on the Preliminary Issue - Day One [260 Kb] -08/03/07 Procedural Order No. 3 [26 Kb] -07/05/07 Claimants' Rejoinder on the Preliminary Issue [849 Kb] -05/01/07 U.S. Reply on the Preliminary Issue [245 Kb] -03/01/07 Article 1128 Submission of Mexico [47 Kb] -01/30/07 Claimants' Response on the Preliminary Question [2303 Kb] -12/01/06 U.S. Memorial on the Preliminary Issue [167 Kb] -11/07/06 Procedural Order No. 2 [62 Kb] -10/20/06 Procedural Order No. 1 [122 Kb] -06/02/05 Jim McNall Notice of Arbitration [393 Kb] -06/02/05 Leslie Smith Notice of Arbitration [393 Kb] -06/02/05 Michael Sears Notice of Arbitration [393 Kb] -06/02/05 Rex Vandenberg Notice of Arbitration [393 Kb] -06/02/05 Richard Hiebert Notice of Arbitration [392 Kb] -06/02/05 Rod Oosterbroek Notice of Arbitration [392 Kb] -06/02/05 TER Cattle Notice of Arbitration [393 Kb] -05/20/05 Andrew Oosterbroek Notice of Arbitration [392 Kb] -05/20/05 Brad Hopkins Notice of Arbitration [396 Kb] -05/20/05 Brent Byers Notice of Arbitration [395 Kb] -05/20/05 Brent Fisher Notice of Arbitration [393 Kb] -05/20/05 Byron Sedore Notice of Arbitration [394 Kb] -05/20/05 Chris Irwin Notice of Arbitration [394 Kb] -05/20/05 Cornelius Van Hal Notice of Arbitration [392 Kb] -05/20/05 Darren Johnston Notice of Arbitration [394 Kb] -05/20/05 Dave Knapp Notice of Arbitration [394 Kb] -05/20/05 David Hewitt Notice of Arbitration [394 Kb] -05/20/05 Donald Procter Notice of Arbitration [394 Kb] -05/20/05 George Adams Notice of Arbitration [392 Kb] -05/20/05 Glen Thompson Notice of Arbitration [392 Kb] -05/20/05 Graham Alexander Notice of Arbitration [394 Kb] -05/20/05 Helmut Friesen Notice of Arbitration [393 Kb] -05/20/05 James Wiskerke Notice of Arbitration [392 Kb] -05/20/05 Joseph Daunt Notice of Arbitration [394 Kb] -05/20/05 Keith Kerr Notice of Arbitration [394 Kb] -05/20/05 Ken Andreychuk Notice of Arbitration [396 Kb] -05/20/05 Kevin Freiburger Notice of Arbitration [394 Kb] -05/20/05 Larry Brodersen Notice of Arbitration [392 Kb] -05/20/05 Lee Robson Notice of Arbitraiton [450 Kb] -05/20/05 Maria Vanden Elzen Notice of Arbitration [413 Kb] -05/20/05 Murray Johnston Notice of Arbitration [395 Kb] -05/20/05 NFL Holdings Notice of Arbitration [456 Kb] -05/20/05 Paul Gowing Notice of Arbitration [394 Kb] -05/20/05 Paul MacIntyre Notice of Arbitration [394 Kb] -05/20/05 Peter Schwenk Notice of Arbitration [448 Kb] -05/20/05 Peter Vander Heyden Notice of Arbitration [415 Kb] -05/20/05 Robert Emerson Notice of Arbitration [394 Kb] -05/20/05 Robert Laidlaw Notice of Arbitration [393 Kb] -05/20/05 Ron Coulter Notice of Arbitration [393 Kb] -05/20/05 Ross McCall Notice of Arbitration [394 Kb] -05/20/05 Ryan Kasko Notice of Arbitration [393 Kb] -05/11/05 Barry Hillman Notice of Arbitration [392 Kb] -05/11/05 Ben Gardiner Notice of Arbitration [416 Kb] -05/11/05 Bernie Loman Notice of Arbitration [392 Kb] -05/11/05 Blair Bieman Notice of Arbitration [394 Kb] -05/11/05 Blake Holtman Notice of Arbitration [393 Kb] -05/11/05 Bruce Groenenboom Notice of Arbitration [403 Kb] -05/11/05 Butch Martin Notice of Arbitration [441 Kb] -05/11/05 Dale Pallister Notice of Arbitration [394 Kb] -05/11/05 Darwin Ullery Notice of Arbitration [412 Kb] -05/11/05 Dave Gardiner Notice of Arbitration [415 Kb] -05/11/05 Dave Johnston Notice of Arbitration [415 Kb] -05/11/05 Dave Matthies, Notice of Arbitration [421 Kb] -05/11/05 David Millsap Notice of Arbitration [394 Kb] -05/11/05 Doug Briggs Notice of Arbitration [394 Kb] -05/11/05 Doug Nieboer Notice of Arbitration [392 Kb] -05/11/05 Doug Shelswel Notice of Arbitration [394 Kb] -05/11/05 Ed Stronks Notice of Arbitration [413 Kb] -05/11/05 Eric Thacker Notice of Arbitration [394 Kb] -05/11/05 Eve t Kraayenbrink Notice of Arbitration [415 Kb] -05/11/05 Firmin Declercq Notice of Arbitration [392 Kb] -05/11/05 Frank Zettler Notice of Arbitration [395 Kb] -05/11/05 G. Lee Hochstein Notice of Arbitration [374 Kb] -05/11/05 George Alton Notice of Arbitration [394 Kb] -05/11/05 George Maxwell Notice of Arbitration [394 Kb] -05/11/05 Glen Armitage Notice of Arbitration [392 Kb] -05/11/05 Grant Nelson Notice of Arbitration [393 Kb] -05/11/05 Harry Duban Notice of Arbitration [393 Kb] -05/11/05 Harry Vandersteen Notice of Arbitration [393 Kb] -05/11/05 Harry Welsch Notice of Arbitration [393 Kb] -05/11/05 Henry Van Hall Notice of Arbitration [392 Kb] -05/11/05 Herb Groenenboom Notice of Arbitration [392 Kb] -05/11/05 Herbert Serfas Notice of Arbitration [403 Kb] -05/11/05 Herman Stroeve Notice of Arbitration [449 Kb] -05/11/05 Ian MacLean Notice of Arbitration [394 Kb] -05/11/05 Jim Steed Notice of Arbitration [394 Kb] -05/11/05 Joe Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Schooten Notice of Arbitration [392 Kb] -05/11/05 John Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Vander Heyden Notice of Arbitration [392 Kb] -05/11/05 Julie Coe Notice of Arbitration [394 Kb] -05/11/05 Keith Scott Notice of Arbitration [392 Kb] -05/11/05 Larry Lehrbass Notice of Arbitration [394 Kb] -05/11/05 Leighton Kolk Notice of Arbitration [392 Kb] -05/11/05 Lloyd Sproule Notice of Arbitration [391 Kb] -05/11/05 Louis Ypma Notice of Arbitration [392 Kb] -05/11/05 Marty Wren Notice of Arbitration [392 Kb] -05/11/05 Mary Conlin Notice of Arbitration [395 Kb] -05/11/05 Murray Brodhagen Notice of Arbitration [394 Kb] -05/11/05 Nick Popovic Notice of Arbitration [394 Kb] -05/11/05 Paul Adams Notice of Arbitration [392 Kb] -05/11/05 Renus Van Hal Notice of Arbitration [392 Kb] -05/11/05 Richard Visser Notice of Arbitration [392 Kb] -05/11/05 Rients Wever Notice of Arbitration [392 Kb] -05/11/05 Robert Cooke Notice of Arbitration [415 Kb] -05/11/05 Robert Vander Heyden Notice of Arbitration [393 Kb] -05/11/05 Ryan Gibson Notice of Arbitration [392 Kb] -05/11/05 Steve McKague Notice of Arbitration [394 Kb] -05/11/05 Stuart Alton Notice of Arbitration [394 Kb] -05/11/05 Ward Takeda Notice of Arbitration [393 Kb] -05/11/05 Wayne Beattie Notice of Arbitration [394 Kb] -05/11/05 Wilfred Haines Notice of Arbitration [415 Kb] -03/16/05 Cor Van Raay Notice of Arbitration [396 Kb] -03/16/05 Joe Groenenboom Notice of Arbitration [392 Kb] -03/16/05 John Vander Heyden Notice of Arbitration [393 Kb] -03/16/05 Larry Nolan Notice of Arbitration [393 Kb] -03/16/05 Theodorus de Boer Notice of Arbitration [392 Kb]
http://www.state.gov/s/l/c14683.htm
TEST, TEST, TEST !!! why is that so difficult to do $$$ USDA did not do it correctly during the june 2004 enhanced BSE cover-up program, so why did they shut the testing numbers down so low they could not find anymore cases ??? could it be they are afraid of what they would find. ....
this is just how i view this ongoing nightmare since the death of my mother to the heidenhain variant of creutzfeldt jakob disease confirmed on 12/14/97.
i just made a promise to her i would not let this issue be swept under the rug like asbestos and tobacco was $$$
TSS
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
----- Original Message -----
From: noreply@whitehouse.gov
To: flounder9@verizon.net
Sent: Wednesday, March 09, 2011 6:37 PM
Subject: Message Notification
Dear Friend,
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Thank You! Thank you for contacting the White House.
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http://www.whitehouse.gov/thank-you
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
We write to you regarding Japan's interest in joining the Trans-Pacific Partnership (TPP) negotiations.
We appreciate your Administration's efforts to expand the presence of U.S. businesses and exports in the vital Asia-Pacific region through the TPP. Expanded trade is needed for economic growth, as well as for the continued competitiveness of our businesses, workers, farmers, and ranchers. Further expanding our market access in important economies of this region will provide significant opportunities for our exporters and will favorably reorient the region economically and geopolitically towards the United States.
It is also encouraging that the leaders of the Japanese government have expressed their interest in joining the TPP and thus eliminating their tariff and non-tariff trade barriers to U.S. goods and services. However, given Japan's historical intransigence in allowing market access for American agricultural goods, we write to express reservations regarding Japan's inclusion in these negotiations until certain conditions are met. In addition to prohibitively high tariffs on many agricultural goods, Japan has discriminated against U.S. beef imports with restrictions that are inconsistent with international standards and not based on scientific criteria.
As you know, Japan closed its market to U.S. beef in December of 2003, after the discovery of a Canadian-born cow infected with bovine spongiform encephalopathy (BSE) in the United States. At that time, Japan was the largest export market for U.S. beef, valued at $1.4 billion. Since then, Japan has had restrictions in place on U.S. beef imports and currently only allows imports of beef from cattle aged 20 months and younger.
The United States has spent years putting in place an effective system of interlocking safeguards that has successfully prevented BSE from becoming established in our country. The U.S. Department of Agriculture's Animal and Plant Health Inspection Service has aggressively enhanced our BSE surveillance system since 1990, testing at levels forty times higher than recommended by the World Organization for Animal Health (OIE). As a result, out of a U.S. cattle inventory numbering nearly 100 million head every year, there have only been three confirmed cases of BSE since 2003-the one imported Canadian cow and two atypical cases of cattle born in the U.S. prior to our 1997 feed ban-and none since 2006 (In contrast, Japan, with an annual cattle inventory of only 4.5 million head, has had thirty-six cases of BSE since 2003). Because of these efforts, the United States has been classified as a controlled risk country by the OlE, which indicates that U.S. beef products are completely safe for export and consumption. Incidentally, this is the same BSE risk status classification as that of Japan.
American farmers and ranchers produce the highest quality agricultural products in the world. When given the opportunity to compete on a level playing field, they will thrive, creating more jobs and revenue at home while providing foreign customers affordable access to our products across the world. Japan's agricultural sector stands in stark contrast as one of the most highly protected in the world. If Japan asks for inclusion in the TPP negotiations, we encourage you to press Japanese leaders to immediately relax its restrictions on u.s. beef to be fully consistent with OlE guidelines and reopen its market. At the very least, Japan should agree to immediately relax its age restrictions to 30 months and address other issues necessary to achieve a commercially-viable, science-based import protocol, while also laying a clear pathway for eventual full OlE compliance. Likewise, we would have serious reservations with any TPP agreement submitted to Congress that includes Japan if it has not made commitments to fully complete this process, as well as eliminate tariff and non-tariff barriers on its TPP partners' agricultural exports.
Trade agreements must solidify economic relations and foster mutual trust. Japan's past actions pose serious concerns that require your consideration and leadership in addressing; future commitments must ensure that Japan will abide by internationally-accepted, science-based trading standards that will be vigorously enforced.
Very truly yours,
http://johanns.senate.gov/public/?a=Files.Serve&File_id=81e2e8dc-c839-4558-8c37-951f02ad9930
(PLEASE SEE LIST OF SENATORS above THAT ARE REFUSING TO ACKNOWLEDGE THE MOST RECENT SCIENCE ON TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY AKA MAD COW DISEASE AND RISK FROM THE ATYPICAL TSE AND THE SPORADIC CJD, SEE THE LIST OF SENATORS THAT ARE IGNORING THE CONSTANT MAD COW FEED VIOLATIONS SINCE THE PARTIAL AND VOLUNTARY MAD COW FEED BAN WAS PUT IN PLACE IN AUGUST OF 1997, AND SEE THE LIST OF SENATORS THAT TURN THEIR HEADS THE OTHER WAY, EVERY TIME ANOTHER MAD COW IS COVERED UP, OR ATTEMPTED TO BE COVERED UP. PLEASE SEE THESE LIST OF SENATORS, and then see the most up to date science on TSE. then ask yourself, do you blame Japan ???...TSS)
Johanns et al @ the USDA and the OIE are the very reason we have spread mad cow disease all around the globe, again, except this time they made it legal while trying to cover up the Texas mad cow and that Alabama mad cow. the OIE BSE MRR policy is nothing more than a legal instrument to trade Transmissible Spongiform Encephalopathy globally, and legally. Johanns et al should be prosecuted for this $$$
Canada, U.S.A., and Mexico, have been swapping cattle, cattle by-products, and feed, like two lovers swapping spit, and in doing so, in my opinion, have been swapping Transmissible Spongiform Encephalopathy aka mad cow disease of all strains. THE FDA mad cow feed firewall that the USDA et al claim protects us, that firewall was breached long ago. actually, it was nothing but ink on paper. sporadic CJD of unknown phenotype is rising in Canada and the USA. North America has more documented cases of the prion disease aka TSE in more documented species in the wild than anybody in the world, most all of which has been rendered and fed to livestock producing animals for human and animals, at some point in time. NO spontaneous, naturally occurring TSE, has ever been documented in the field, in any species.
I think of one thing when i think of mad cow and cjd there from in the USA. i think of Tobacco and Asbestos, and how many decades the public was lied to about those products. the after effects and death there from was also a long incubating disease, diseases that you could forget about after consumption, for a while. just something to ponder. ...
i have watched these mad cow folly's by the Industry, USDA, FDA, et al daily now for almost 14 years. yes, i am angry, i am mad as hell, but these are the facts as i have come to know them. they are not pretty. in fact, very disturbing. ...time will tell. sporadic CJD is on the rise....oh, and the latest on sporadic CJD first, just so you ya know ;
***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
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
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
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
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
Saturday, March 5, 2011
ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
Greetings,
WITH more and more atypical Transmissible Spongiform Encephalopathy cases showing up in more and more species here in North America, and the enormous monumental amount of banned mad cow protein in commerce since the infamous partial and voluntary mad cow feed ban inked on paper, with tons and tons crossing back and forth between the USA, Canada, and Mexico, it just does not surprise me of all these "PENDING CLASSIFICATIONS" of human TSE in Canada, and the USA. UK c-BSE transmitted to humans became nvCJD. WE now have atypical strains of BSE in cattle. Mission Texas experiments long ago showed that transmitted USA sheep scrapie to USA bovine, produced a TSE much different than the UK typical c-BSE. SO why would human TSE in the USA look like UK human TSE ? The corruption is mind boggling. The UK saw a suspicious TSE in humans, and science linked it to cattle. North America is awash with human and animal TSE, CJD is rising in young and old, with the same pathology and same symptoms, and none of it is related to the other. isn't that nice. who, what, bestowed such miracles upon North America $
Archive Number 20100405.1091 Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
snip...
[Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
http://whqlibdoc.who.int/publications/2003/9241545887.pdf
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
CANADA CJD UPDATE 2011
CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011
3. Final classification of 49 cases from 2009, 2010, 2011 is pending.
snip...
http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf
USA 2011
USA
National Prion Disease Pathology Surveillance Center
Cases Examined1
(November 1, 2010)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 87 51 43 7 1 0
1999 121 73 65 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 13
2005 344 194 157 36 1 0
2006 383 197 166 29 0 24
2007 377 214 187 27 0 0
2008 394 231 205 25 0 0
2009 425 258 215 43 0 0
2010 333 213 158 33 0 0
TOTAL 38315 22656 1907 328 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.
I also urge you to again notice these disturbing factors in lines 5 and 6 ;
5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
========end=====tss=====2011
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE) Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
http://www.usda.gov/oig/webdocs/sarc070619.pdf
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.html
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
Tuesday, January 1, 2008
BSE OIE USDA
Subject: OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA
Date: May 14, 2007 at 9:00 am PST
OIE BSE RECOMMENDATION FOR USA, bought and paid for by your local cattle dealers i.e. USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
they did not want to find BSE, and never intended to. ...tss
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Tuesday, January 1, 2008
BSE OIE USDA
STATEMENT BY DR. RON DEHAVEN REGARDING OIE RISK RECOMMENDATION
March 9, 2007
http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ? they could not have found a mad cow if they were standing beside the stumbling and staggering bovine $$$, using the diagnostic criteria they were using, AND TOLD SO, but they kept on doing it anyway. ...
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Christopher J. Johnson1, Debbie McKenzie2, Joel A. Pedersen3, Judd M. Aiken4
1Prion Research Laboratory, USGS National Wildlife Health Center, Madison, Wisconsin, USA 2Centre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada 3Department of Soil Science and Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, Wisconsin, USA 4Centre for Prions and Protein Folding Diseases, Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, Alberta, Canada
Ingestion of prion-contaminated materials is postulated to be a primary route of prion disease transmission. Binding of prions to soil (micro)particles dramatically enhances peroral disease transmission relative to unbound prions, and it was hypothesized that micrometer– sized particles present in other consumed materials may affect prion disease transmission via the oral route of exposure. Small, insoluble particles are present in many substances, including soil, human foods, pharmaceuticals, and animal feeds. It is known that meat and bone meal (MBM), a feed additive believed responsible for the spread of bovine spongiform encephalopathy (BSE), contains particles smaller than 20 ìm and that the pathogenic prion protein binds to MBM. The potentiation of disease transmission via the oral route by exposure to MBM or three micrometer-sized mineral feed additives was determined. Data showed that when the disease agent was bound to any of the tested materials, the penetrance of disease was increased compared to unbound prions. Our data suggest that in feed or other prion– contaminated substances consumed by animals or, potentially, humans, the addition of MBM or the presence of microparticles could heighten risks of prion disease acquisition.
SNIP...
CONCLUSIONS
Should prions be present in animal feed, their association with MBM or insoluble particles such as those tested (viz. Mte, Kte, and SiO2) could substantially increase the risk of disease acquisition compared to consumption of prions alone. While care needs to be exercised when extrapolating results from laboratory rodent models to ruminants, these data may explain how MBM produced BSE transmission despite the presumably low titers of infectious agent present in cattle feed (Taylor et al., 1995). In addition, inorganic particles in commercial feeds or mineral licks may pose a previously unrecognized risk of enhancing TSE transmission to domestic and wildlife species from agents contaminating these materials or infectivity shed onto feed or licks.
Following consumption, (sub)micrometersized particles can be absorbed by the gut. Goblet cells (Doyle-McCullough et al., 2007), M cells in Peyer’s patches (Florence, 1997), and persorptive mechanisms at the tips of broken intestinal villi (Hillyer & Albrecht, 2001; Volkheimer, 2001) all contribute to intestinal particle uptake. Increased uptake of particlebound prions might explain enhanced oral transmissibility. Alternatively, aluminosilicates may increase residence time of agent in the digestive system (Bringe & Schultz, 1969; Collings et al., 1980; Quisenberry, 1968) and elevate exposure time at sites of conversion. Further investigation into these mechanisms, the effect of digestive processes on bound prions, and alterations of agent physicochemical properties upon binding is warranted.
It is noteworthy that microparticles find widespread use as human food and pharmaceutical additives in Western diets (Lomer et al., 2000, 2004). The average daily consumption dietary microparticles from food, pharmaceuticals, and dentifrices is approximately 40 mg (approximately 1012 particles) per person (Powell et al., 2007). The extent to which microparticles in the human diet influence prion disease acquisition is currently unknown, but these data suggest that microparticle consumption needs to be investigated as a potential risk factor in human TSE acquisition.
SEE FULL TEXT ;
http://www.informaworld.com/smpp/content~content=a931920802~db=all~jumptype=rss
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
Monday, January 17, 2011
MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011
January 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html
Friday, January 7, 2011
MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION
Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.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/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
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.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html
Friday, February 04, 2011
NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico
----- Original Message -----
From: Terry S. Singeltary Sr.
To: President.BenShelly
Cc: sroanhorse ; opvp.nelson ; alaughing; georgehardeen; pressoffice
Sent: Thursday, February 03, 2011 12:15 PM
Subject: NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico
Greetings Honorable People of the Great Navajo Nation, and the Honorable President Ben Shelly,
I send this to you with great concern. ...
http://scrapie-usa.blogspot.com/2011/02/nmlb-and-usda-allow-scrapie-prion.html
Received October 28, 2010. Accepted January 4, 2011. Copyright © 2011, The American Society for Biochemistry and Molecular Biology
Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions
Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, James A. Mastrianni4 and Claudio Soto5,*
http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long
Our findings demonstrate that cervid PrPSc, upon strain adaptation by serial passages in vitro or in cervid transgenic mice, is capable of converting human PrPC to produce PrPSc with unique biochemical properties, likely representing a new human prion strain. The newly generated CWD-huPrPSc material has been inoculated into transgenic mice expressing human PrP to study infectivity and disease phenotype and this data will be published elsewhere. ...end
http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html
Wednesday, March 02, 2011
CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010
http://chronic-wasting-disease.blogspot.com/2011/03/cwd-in-nebraska-is-increasing-with-51.html
Monday, February 28, 2011
South Dakota finds 25 more cases of Chronic Wasting Disease
Latest Chronic Wasting Disease Testing Results
http://chronic-wasting-disease.blogspot.com/2011/02/south-dakota-finds-25-more-cases-of.html
Thursday, February 10, 2011
CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer - Updated 2/07/2011
http://chronic-wasting-disease.blogspot.com/2011/02/cwd-illinois-update-february-2011.html
Thursday, February 10, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-found-in-white.html
Tuesday, February 22, 2011
Chronic wasting disease spreads farther west in Alberta
http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-spreads-farther.html
----- Original Message -----
From: David Colby
To: flounder9@verizon.net
Cc: stanley...
Sent: Tuesday, March 01, 2011 8:25 AM
Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations
Dear Terry Singeltary,
Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.
Warm Regards, David Colby
--
David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html
SEE FULL TEXT AND MORE HERE ;
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html
IF ANY OF YOU WANT TO SEE THE CREDIBILITY OF THE O.I.E., (or the lack of credibility) i urge you to read this, and you will see what an industry laden group they really are. the O.I.E. protects one thing, and one thing only, they protect their own, THE INDUSTRY ;
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
snip...
Greetings,
Thank for your support to the OIE objectives for a safe world.
NOT !
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."
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...
please see full text ;
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
*** Thursday, December 23, 2010
Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
Saturday, June 19, 2010
U.S. DENIED UPGRADED BSE STATUS FROM OIE
http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html
Monday, April 12, 2010
Senator Kay Bailey Hutchison says NO to safer food and S. 510 FDA Food Safety Modernization Act of 2009
http://fdafailedus.blogspot.com/2010/04/senator-kay-bailey-hutchison-says-no-to.html
U.S. Department of State
Cases Regarding the Border Closure due to BSE Concerns
Several Canadian claimants have submitted notices of arbitration under the UNCITRAL Arbitration Rules alleging that the United States has violated NAFTA Chapter Eleven by closing the border to the importation of Canadian cattle after the discovery in 2003 of a case of bovine spongiform encephalopathy (BSE or mad cow disease) in a cow in Alberta, Canada. Claimants are Canadian citizens and corporations that own and operate cattle feeding, feedlot and transportation businesses in Canada, which they allege were damaged by the border closure.
Claimants allege that the border closure violates NAFTA Article 1102 (national treatment). The notices of arbitration seek damages of varying amounts, ranging from CAN$38,000 to CAN$95 million. The total amount of damages sought by claimants is approximately US$235 million.
On January 28, 2008, the tribunal issued its Award on Jurisdiction, dismissing the claims against the United States in their entirety. The tribunal’s award, and other documents in the case, appear below.
-01/28/08 Award on Jurisdiction [575 Kb] -10/10/07 Transcript of the Hearing on the Preliminary Issue - Day Two [166 Kb] -10/09/07 Transcript of the Hearing on the Preliminary Issue - Day One [260 Kb] -08/03/07 Procedural Order No. 3 [26 Kb] -07/05/07 Claimants' Rejoinder on the Preliminary Issue [849 Kb] -05/01/07 U.S. Reply on the Preliminary Issue [245 Kb] -03/01/07 Article 1128 Submission of Mexico [47 Kb] -01/30/07 Claimants' Response on the Preliminary Question [2303 Kb] -12/01/06 U.S. Memorial on the Preliminary Issue [167 Kb] -11/07/06 Procedural Order No. 2 [62 Kb] -10/20/06 Procedural Order No. 1 [122 Kb] -06/02/05 Jim McNall Notice of Arbitration [393 Kb] -06/02/05 Leslie Smith Notice of Arbitration [393 Kb] -06/02/05 Michael Sears Notice of Arbitration [393 Kb] -06/02/05 Rex Vandenberg Notice of Arbitration [393 Kb] -06/02/05 Richard Hiebert Notice of Arbitration [392 Kb] -06/02/05 Rod Oosterbroek Notice of Arbitration [392 Kb] -06/02/05 TER Cattle Notice of Arbitration [393 Kb] -05/20/05 Andrew Oosterbroek Notice of Arbitration [392 Kb] -05/20/05 Brad Hopkins Notice of Arbitration [396 Kb] -05/20/05 Brent Byers Notice of Arbitration [395 Kb] -05/20/05 Brent Fisher Notice of Arbitration [393 Kb] -05/20/05 Byron Sedore Notice of Arbitration [394 Kb] -05/20/05 Chris Irwin Notice of Arbitration [394 Kb] -05/20/05 Cornelius Van Hal Notice of Arbitration [392 Kb] -05/20/05 Darren Johnston Notice of Arbitration [394 Kb] -05/20/05 Dave Knapp Notice of Arbitration [394 Kb] -05/20/05 David Hewitt Notice of Arbitration [394 Kb] -05/20/05 Donald Procter Notice of Arbitration [394 Kb] -05/20/05 George Adams Notice of Arbitration [392 Kb] -05/20/05 Glen Thompson Notice of Arbitration [392 Kb] -05/20/05 Graham Alexander Notice of Arbitration [394 Kb] -05/20/05 Helmut Friesen Notice of Arbitration [393 Kb] -05/20/05 James Wiskerke Notice of Arbitration [392 Kb] -05/20/05 Joseph Daunt Notice of Arbitration [394 Kb] -05/20/05 Keith Kerr Notice of Arbitration [394 Kb] -05/20/05 Ken Andreychuk Notice of Arbitration [396 Kb] -05/20/05 Kevin Freiburger Notice of Arbitration [394 Kb] -05/20/05 Larry Brodersen Notice of Arbitration [392 Kb] -05/20/05 Lee Robson Notice of Arbitraiton [450 Kb] -05/20/05 Maria Vanden Elzen Notice of Arbitration [413 Kb] -05/20/05 Murray Johnston Notice of Arbitration [395 Kb] -05/20/05 NFL Holdings Notice of Arbitration [456 Kb] -05/20/05 Paul Gowing Notice of Arbitration [394 Kb] -05/20/05 Paul MacIntyre Notice of Arbitration [394 Kb] -05/20/05 Peter Schwenk Notice of Arbitration [448 Kb] -05/20/05 Peter Vander Heyden Notice of Arbitration [415 Kb] -05/20/05 Robert Emerson Notice of Arbitration [394 Kb] -05/20/05 Robert Laidlaw Notice of Arbitration [393 Kb] -05/20/05 Ron Coulter Notice of Arbitration [393 Kb] -05/20/05 Ross McCall Notice of Arbitration [394 Kb] -05/20/05 Ryan Kasko Notice of Arbitration [393 Kb] -05/11/05 Barry Hillman Notice of Arbitration [392 Kb] -05/11/05 Ben Gardiner Notice of Arbitration [416 Kb] -05/11/05 Bernie Loman Notice of Arbitration [392 Kb] -05/11/05 Blair Bieman Notice of Arbitration [394 Kb] -05/11/05 Blake Holtman Notice of Arbitration [393 Kb] -05/11/05 Bruce Groenenboom Notice of Arbitration [403 Kb] -05/11/05 Butch Martin Notice of Arbitration [441 Kb] -05/11/05 Dale Pallister Notice of Arbitration [394 Kb] -05/11/05 Darwin Ullery Notice of Arbitration [412 Kb] -05/11/05 Dave Gardiner Notice of Arbitration [415 Kb] -05/11/05 Dave Johnston Notice of Arbitration [415 Kb] -05/11/05 Dave Matthies, Notice of Arbitration [421 Kb] -05/11/05 David Millsap Notice of Arbitration [394 Kb] -05/11/05 Doug Briggs Notice of Arbitration [394 Kb] -05/11/05 Doug Nieboer Notice of Arbitration [392 Kb] -05/11/05 Doug Shelswel Notice of Arbitration [394 Kb] -05/11/05 Ed Stronks Notice of Arbitration [413 Kb] -05/11/05 Eric Thacker Notice of Arbitration [394 Kb] -05/11/05 Eve t Kraayenbrink Notice of Arbitration [415 Kb] -05/11/05 Firmin Declercq Notice of Arbitration [392 Kb] -05/11/05 Frank Zettler Notice of Arbitration [395 Kb] -05/11/05 G. Lee Hochstein Notice of Arbitration [374 Kb] -05/11/05 George Alton Notice of Arbitration [394 Kb] -05/11/05 George Maxwell Notice of Arbitration [394 Kb] -05/11/05 Glen Armitage Notice of Arbitration [392 Kb] -05/11/05 Grant Nelson Notice of Arbitration [393 Kb] -05/11/05 Harry Duban Notice of Arbitration [393 Kb] -05/11/05 Harry Vandersteen Notice of Arbitration [393 Kb] -05/11/05 Harry Welsch Notice of Arbitration [393 Kb] -05/11/05 Henry Van Hall Notice of Arbitration [392 Kb] -05/11/05 Herb Groenenboom Notice of Arbitration [392 Kb] -05/11/05 Herbert Serfas Notice of Arbitration [403 Kb] -05/11/05 Herman Stroeve Notice of Arbitration [449 Kb] -05/11/05 Ian MacLean Notice of Arbitration [394 Kb] -05/11/05 Jim Steed Notice of Arbitration [394 Kb] -05/11/05 Joe Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Schooten Notice of Arbitration [392 Kb] -05/11/05 John Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Vander Heyden Notice of Arbitration [392 Kb] -05/11/05 Julie Coe Notice of Arbitration [394 Kb] -05/11/05 Keith Scott Notice of Arbitration [392 Kb] -05/11/05 Larry Lehrbass Notice of Arbitration [394 Kb] -05/11/05 Leighton Kolk Notice of Arbitration [392 Kb] -05/11/05 Lloyd Sproule Notice of Arbitration [391 Kb] -05/11/05 Louis Ypma Notice of Arbitration [392 Kb] -05/11/05 Marty Wren Notice of Arbitration [392 Kb] -05/11/05 Mary Conlin Notice of Arbitration [395 Kb] -05/11/05 Murray Brodhagen Notice of Arbitration [394 Kb] -05/11/05 Nick Popovic Notice of Arbitration [394 Kb] -05/11/05 Paul Adams Notice of Arbitration [392 Kb] -05/11/05 Renus Van Hal Notice of Arbitration [392 Kb] -05/11/05 Richard Visser Notice of Arbitration [392 Kb] -05/11/05 Rients Wever Notice of Arbitration [392 Kb] -05/11/05 Robert Cooke Notice of Arbitration [415 Kb] -05/11/05 Robert Vander Heyden Notice of Arbitration [393 Kb] -05/11/05 Ryan Gibson Notice of Arbitration [392 Kb] -05/11/05 Steve McKague Notice of Arbitration [394 Kb] -05/11/05 Stuart Alton Notice of Arbitration [394 Kb] -05/11/05 Ward Takeda Notice of Arbitration [393 Kb] -05/11/05 Wayne Beattie Notice of Arbitration [394 Kb] -05/11/05 Wilfred Haines Notice of Arbitration [415 Kb] -03/16/05 Cor Van Raay Notice of Arbitration [396 Kb] -03/16/05 Joe Groenenboom Notice of Arbitration [392 Kb] -03/16/05 John Vander Heyden Notice of Arbitration [393 Kb] -03/16/05 Larry Nolan Notice of Arbitration [393 Kb] -03/16/05 Theodorus de Boer Notice of Arbitration [392 Kb]
http://www.state.gov/s/l/c14683.htm
TEST, TEST, TEST !!! why is that so difficult to do $$$ USDA did not do it correctly during the june 2004 enhanced BSE cover-up program, so why did they shut the testing numbers down so low they could not find anymore cases ??? could it be they are afraid of what they would find. ....
this is just how i view this ongoing nightmare since the death of my mother to the heidenhain variant of creutzfeldt jakob disease confirmed on 12/14/97.
i just made a promise to her i would not let this issue be swept under the rug like asbestos and tobacco was $$$
TSS
Wednesday, March 9, 2011
27 U.S. Senators want to force feed Japan Highly Potential North America Mad Cow Beef TSE PRION CJD
March 8, 2011
President Barack Obama The White House
1600 Pennsylvania Avenue, W Washington, DC 20500
Dear President Obama:
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/27-us-senators-want-to-force-feed-japan.html
----- Original Message -----
From: noreply@whitehouse.gov
To: flounder9@verizon.net
Sent: Wednesday, March 09, 2011 6:37 PM
Subject: Message Notification
Dear Friend,
Thank you for your message. On behalf of President Obama, we appreciate hearing from you. The President has promised the most transparent administration in history, and we are committed to listening to and responding to you.
In order to better handle the millions of electronic messages we are receiving and respond more quickly, we have implemented a new contact form on our website:
http://www.whitehouse.gov/contact/
Please note that this web form has replaced comments@whitehouse.gov. That email address is no longer monitored, so we encourage you to resubmit your message through the link above. Thank you for using the web form and helping us improve communications with you.
Sincerely,
The Presidential Correspondence Team
Thank You! Thank you for contacting the White House.
=================================
President Obama is committed to creating the most open and accessible Administration in history. That begins with taking comments and questions from you, the American people, through our website.
Our office receives thousands of messages from Americans each day. We do our best to reply to as many as we can, but please be aware that you may find more information and answers to your questions online. To follow news and learn more about President Obama's plans for winning the future, you can sign up for updates from the White House, read the White House Blog, or listen to White House podcasts.
For an easy-to-navigate source of information on Federal government services, please visit: www.USA.gov.
Thank you again for your message.
The Office of Presidential Correspondence
http://www.whitehouse.gov/thank-you
Sunday, March 6, 2011
U.K. and U.S.A. vCJD, CJD, TSE screen (a) the blood supply and (b) blood donors Commons Hansard Written Answers and FDA March 2011
vCJD screen (a) the UK blood supply and (b) blood donors for vCJD. [43356] Commons Hansard Written Answers March 1-3 2011
3 Mar 2011 : Column 535W—continued
vCJD Simon Kirby: To ask the Secretary of State for Health if he will take steps to screen (a) the UK blood supply and (b) blood donors for vCJD. [43356]
Anne Milton: No such screening can yet take place as at present as there are no validated blood screening tests for variant Creutzfeldt-Jakob disease available. The Department, together with the United Kingdom Blood Services, continues to monitor scientific research and development in this area.
Simon Kirby: To ask the Secretary of State for Health (1) if he will assess the merits of removing the warning Risk of Adverse Reaction Infection Including 3 Mar 2011 : Column 559W vCJD from blood bags; and if he will make a statement; [43357]
(2) for what reasons his Department places the warning Risk of Adverse Reaction Infection Including vCJD on blood bags. [43358]
Anne Milton: To comply with the requirements of Good Manufacturing Practice the United Kingdom Blood Services place warnings on blood bags as a final alert to clinical staff that blood components, being of human origin, always carry a potential risk of transmission of infection. Transfusions can also cause other unpredictable side effects, such as allergic reactions. Though fortunately any such events are rare, there is no intention to remove warnings from blood bags.
Variant Creutzfeldt-Jakob disease (vCJD) is mentioned specifically on blood pack labels because it is a relatively new and rare infection. There have been three cases where blood has been the presumed route of vCJD transmission, all from donations in 1999 or before, from donations where the donor later went on to develop clinical vCJD to a recipient who themselves later went on to develop clinical vCJD.
Simon Kirby: To ask the Secretary of State for Health if he will ensure the provision of advice to people who are about to receive blood or blood components on the risk of infection of vCJD. [43359]
Anne Milton: Guidance from the Department places responsibility on Hospital Transfusion Committees to ensure that patients who are likely to receive a blood transfusion are given timely information, informing them of the indication for transfusion, the risks and benefits of transfusion, and any available alternatives to transfusion.
NHS Blood and Transplant (NHSBT) provides a patient information leaflet for hospital staff to give to patients who may receive a transfusion. It indicates that patients should be told that transfusions should only be given if the benefits outweigh the risks, and they should be informed of alternatives to transfusion if these are appropriate and available. The infective risks of blood transfusion are clearly stated. The section on variant Creutzfeldt-Jakob disease (vCJD) specifically states:
"Although the risk of getting variant CJD is probably low from a single transfusion, the risk of any infection will increase with additional blood transfusions. Each year approximately 2 million units of blood are transfused in England, and there have just been a handful of cases where patients are known to have become infected with vCJD from a blood transfusion."
The leaflet is publicly available on the NHSBT website at:
http://hospital.blood.co.uk/library/pdf/INF_PCS_HL_001_05_will_i_need_leaflet_ENGLISH.pdf
http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110303/text/110303w0002.htm#11030356000121
1 Mar 2011 : Column 368W—continued
CJD Frank Dobson: To ask the Secretary of State for Health what estimate he has made of the cost to the public purse of measures taken by the (a) blood service and (b) NHS, excluding the blood service, to reduce the risk of transmission of Creutzfeldt-Jakob disease by blood or blood products since 1998. [41549]
Anne Milton: Since 1998 a number of measures have been introduced by the United Kingdom blood services to reduce the risk of transfusion transmitted variant Creutzfeldt-Jakob disease (vGJD). These measures include the introduction of leucodepletion (the removal of white blood cells), the importation of fresh frozen plasma for children and the deferral from donation of transfusion recipients. In addition, the use of plasma from UK donors for fractionation purposes has ceased.
For national health service blood and transplant the highest costs associated with these measures are the estimated loss of income from the sale of plasma from UK blood donors (£325 million) and the introduction of leucodepletion (£182 million). Further measures bring the estimated total cost to £540 million since 1998, with an estimated current annual cost of approximately £40 million.
There is no separate assessment of such costs for the NHS outside the blood service. However, synthetic (recombinant) clotting factor for the treatment of bleeding disorders, such as haemophilia, has been provided to all patients for whom it is suitable since 2005, and to those under the age of 16 since 1998, at a current annual cost of approximately £200 million.
Commons Hansard Written Answers Text for 1 March 2011
http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110301/text/110301w0003.htm#1103022000031
Wednesday, February 2, 2011
Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay
http://transmissiblespongiformencephalopathy.blogspot.com/2011/02/detection-of-prion-infection-in-variant.html
vCJD, CJD, TSE screen (a) the USA blood supply and (b) blood donors for vCJD, CJD, TSE 2011
Posted: 3/2/2011
October 28, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244061.htm
October 29, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244062.htm
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
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
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
May 8, 2009
Greetings again Dr. Freas, TSEAC et al,
I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability from my neck injury, I will not be attending this meeting either, however I hope for my submission to be read and submitted. ...
IN reply to ;
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
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: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
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:
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html
Thursday, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products
http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.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
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
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Wednesday, December 29, 2010
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.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, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products
http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.html
Wednesday, March 2, 2011 Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011
October 28, 2010
http://tseac.blogspot.com/2011/03/transmissible-spongiform.html
Tuesday, September 28, 2010
Variant CJD: where has it gone, or has it?
Pract Neurol 2010; 10: 250-251
http://vcjdtransfusion.blogspot.com/2010/09/variant-cjd-where-has-it-gone-or-has-it.html
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html
Saturday, July 17, 2010
Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.
2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE
http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.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
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.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
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
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
USA Blood products, collected from a donor who was at risk for vCJD, were distributed
Enforcement Report for October 20, 2010
October 20, 2010
PRODUCT
1) Cryoprecipitated AHF. Recall # B-2523-10;
2) Plasma. Recall # B-2524-10;
3) Red Blood Cells. Recall # B-2525-10;
4) Fresh Frozen Plasma. Recall # B-2526-10
CODE
1) Unit: W038508310277;
2) Units: 3127765, W038508310277, 3129157, 4121927;
3) Units: W038508310277, 3129157, 3127765, 4025397, 4121927, 4018030;
4) Units: 4025397, 4018030
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on July 22, 2010 and July 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
13 units
DISTRIBUTION
GA, MD, SC, Austria, Israel, South Korea, Switzerland
___________________________________
PRODUCT
1) Fresh Frozen Plasma. Recall # B-2531-10;
2) Recovered Plasma. Recall # B-2532-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2533-10
CODE
1) Unit: W115910041730;
2) Units: W115910080008, W115910081199;
3) Units: W115910080008, W115910041730, W115910081199
RECALLING FIRM/MANUFACTURER
Central California Blood Center, Fresno, CA, by e-mail on July 19, 2010 and July 23, 2010 and by facsimile on July 23, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
6 units
DISTRIBUTION
Austria, CA
END OF ENFORCEMENT REPORT FOR OCTOBER 20, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm230357.htm
Enforcement Report for October 13, 2010
October 13, 2010
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2275-10;
2) Recovered Plasma. Recall # B-2276-10;
3) Cryoprecipitated AHF, Pooled. Recall # B-2277-10
CODE
1), 2) and 3) Unit: 6400811
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by fax on April 7, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
FL, TX
___________________________________
PRODUCT
Fresh Frozen Plasma. Recall # B-2283-10
CODE
Units: W001606004574; W001606003405
RECALLING FIRM/MANUFACTURER
Department of the Air Force 88th Medical Group SGQC WPAFB, Wright Patterson, AFB, OH, by letter dated April 17, 2008. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who may have warranted deferral for residency in an area at risk for variant Creutzfeldt-Jakob Disease, were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NJ
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2322-10
2) Fresh Frozen Plasma. Recall # B-2323-10
CODE
1) and 2) Unit: W280310400336
RECALLING FIRM/MANUFACTURER
Upstate New York Transplant Services, Inc., Buffalo, NY, by telephone and fax on June 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NY
___________________________________
PRODUCT
Red Blood Cells. Recall # B-2324-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
NY
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2325-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Switzerland
___________________________________
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm229271.htm
TSS
----- Original Message -----
From: Terry S. Singeltary Sr.
To: BLOODCJD@YAHOOGROUPS.COM
Sent: Thursday, October 07, 2010 12:58 PM
Subject: [BLOODCJD] USA Blood products, collected from a donor who was at risk for vCJD, were distributed END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan
___________________________________
PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY
___________________________________
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm
PRODUCT
1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;
2) Recovered Plasma. Recall # B-2156-10
CODE
1) Unit: W036309907231;
2) Unit: W036309616077
RECALLING FIRM/MANUFACTURER
BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX, Switzerland
___________________________________
PRODUCT
Red Blood Cells Leukocytes Reduced. Recall # B-2157-10
CODE
Unit: 6371718
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
TX
___________________________________
PRODUCT
Source Plasma. Recall # B-2212-10
CODE
Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599
RECALLING FIRM/MANUFACTURER
BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
10 units
DISTRIBUTION
CA
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;
2) Recovered Plasma. Recall # B-2214
CODE
1) and 2) Unit: 6325245
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
FL, TX
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm
PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm
PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC
___________________________________
PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN
___________________________________
PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan
___________________________________
PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY
___________________________________
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm
PRODUCT
1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;
2) Recovered Plasma. Recall # B-2156-10
CODE
1) Unit: W036309907231;
2) Unit: W036309616077
RECALLING FIRM/MANUFACTURER
BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX, Switzerland
___________________________________
PRODUCT
Red Blood Cells Leukocytes Reduced. Recall # B-2157-10
CODE
Unit: 6371718
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
TX
___________________________________
PRODUCT
Source Plasma. Recall # B-2212-10
CODE
Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599
RECALLING FIRM/MANUFACTURER
BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
10 units
DISTRIBUTION
CA
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;
2) Recovered Plasma. Recall # B-2214
CODE
1) and 2) Unit: 6325245
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
FL, TX
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm
PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm
PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC
___________________________________
PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN
___________________________________
PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm
i have not checked out 2011 recalls of USA blood that has NOT been screened for vCJD. let's just check out the latest and see what's going on ;
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0812-11; 2) Recovered Plasma. Recall # B-0813-11 CODE 1) and 2) Unit: 0679506 RECALLING FIRM/MANUFACTURER Blood Centers of the Pacific, San Francisco, CA, by telephone and letter on May 22, 2002. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION CA, Switzerland
___________________________________
PRODUCT Source Plasma. Recall # B-0840-11 CODE Units 381070540, 381070350, 381069984, 381069808, 381068965, 381068783, 381068313, 381068151, 381067718, 381067473, 381067140, 381066944, 381066586, 381066289, 381065935, 381064526, 381065364, 381064386, 381064220, 381063426, 381063033, 381062874, 381062488, 381061767, 381061614, 381061260, 381060375, 381060162, 381059688, 381059534, 381059093, 381058859, 381058451, 381058224, 381057903, 381057624, 381057317, 381057103, 381056525, 381055667, 381054442, 381054328, 381053845, 381053686, 381053078, 381052342, 381051924, 381051688, 381048523 and 381048512 RECALLING FIRM/MANUFACTURER Recalling Firm: Talecris Plasma Resources, Research Triangle Park, NC, by facsimile on May 14, 2010. Manufacturer: Talecris Plasma Resources, Peoria, IL. Firm initiated recall is complete. REASON Blood products, collected from a donor who was previously deferred due to a history of Dura Mater Graft, were distributed. VOLUME OF PRODUCT IN COMMERCE 50 units DISTRIBUTION NC
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PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0848-11; 2) Red Blood Cells Leukocytes Reduced Washed. Recall # B-0849-11; 3) Recovered Plasma. Recall # B-0850-11 CODE 1) Units: 3618494; 2528285; 2) Unit: 3679207; 3) Units: 3679207; 3618494; 2528285 RECALLING FIRM/MANUFACTURER Central California Blood Center, Fresno, CA, by letter dated September 7, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 6 units DISTRIBUTION CA
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END OF ENFORCEMENT REPORT FOR MARCH 2, 2011
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm245369.htm
Greetings,
I am sure there are many more in the previous weeks of 2011. I just don't have time now to search them by week. it's pretty much been a weekly event for years and years and years.
I still have not gotten an answer about these type recalls ;
"REASON Blood products, collected from donors in which donor suitability was not adequately determined, were distributed."
DOES this include vCJD ?
i personally think they are missing the bigger picture by not including all human TSE prion disease, especially since we know GSS will transmit by blood, and now that we know that some sporadic CJD cases are caused by atypical BSE. just does not make sense to me. i still say it's a band aid approach to something that needs a tourniquet. ...TSS
Saturday, January 20, 2007
Fourth case of transfusion-associated vCJD infection in the United Kingdom
http://vcjdtransfusion.blogspot.com/2007_01_01_archive.html
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.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
P02.35
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass.
Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE.
By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice.
The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
O.11.3
Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
O.2.4
Detection of prions in blood leucocytes
Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK
Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.
O.2.6
Human urine and PrP
Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy
Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *
O.4.6
All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion
Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK
Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.
Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.
Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.
Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.
Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)
O.8.1
Variant CJD and plasma products
Robert G. Will National CJD Surveillance Unit, Edinburgh, UK
Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.
O.8.2
Blood safety: from screening tests to prion removal
Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK
Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.
O.9.3
Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.
Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA
Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.
Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.
Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.
Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.
Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.
P.10.7
Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2
Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK
Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.
Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.
Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.
Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.
Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.
P.5.1
Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection
Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany
Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).
Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.
Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 - 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.
Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
http://vcjdtransfusion.blogspot.com/2007_01_01_archive.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified 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
In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
TSS
3 Mar 2011 : Column 535W—continued
vCJD Simon Kirby: To ask the Secretary of State for Health if he will take steps to screen (a) the UK blood supply and (b) blood donors for vCJD. [43356]
Anne Milton: No such screening can yet take place as at present as there are no validated blood screening tests for variant Creutzfeldt-Jakob disease available. The Department, together with the United Kingdom Blood Services, continues to monitor scientific research and development in this area.
Simon Kirby: To ask the Secretary of State for Health (1) if he will assess the merits of removing the warning Risk of Adverse Reaction Infection Including 3 Mar 2011 : Column 559W vCJD from blood bags; and if he will make a statement; [43357]
(2) for what reasons his Department places the warning Risk of Adverse Reaction Infection Including vCJD on blood bags. [43358]
Anne Milton: To comply with the requirements of Good Manufacturing Practice the United Kingdom Blood Services place warnings on blood bags as a final alert to clinical staff that blood components, being of human origin, always carry a potential risk of transmission of infection. Transfusions can also cause other unpredictable side effects, such as allergic reactions. Though fortunately any such events are rare, there is no intention to remove warnings from blood bags.
Variant Creutzfeldt-Jakob disease (vCJD) is mentioned specifically on blood pack labels because it is a relatively new and rare infection. There have been three cases where blood has been the presumed route of vCJD transmission, all from donations in 1999 or before, from donations where the donor later went on to develop clinical vCJD to a recipient who themselves later went on to develop clinical vCJD.
Simon Kirby: To ask the Secretary of State for Health if he will ensure the provision of advice to people who are about to receive blood or blood components on the risk of infection of vCJD. [43359]
Anne Milton: Guidance from the Department places responsibility on Hospital Transfusion Committees to ensure that patients who are likely to receive a blood transfusion are given timely information, informing them of the indication for transfusion, the risks and benefits of transfusion, and any available alternatives to transfusion.
NHS Blood and Transplant (NHSBT) provides a patient information leaflet for hospital staff to give to patients who may receive a transfusion. It indicates that patients should be told that transfusions should only be given if the benefits outweigh the risks, and they should be informed of alternatives to transfusion if these are appropriate and available. The infective risks of blood transfusion are clearly stated. The section on variant Creutzfeldt-Jakob disease (vCJD) specifically states:
"Although the risk of getting variant CJD is probably low from a single transfusion, the risk of any infection will increase with additional blood transfusions. Each year approximately 2 million units of blood are transfused in England, and there have just been a handful of cases where patients are known to have become infected with vCJD from a blood transfusion."
The leaflet is publicly available on the NHSBT website at:
http://hospital.blood.co.uk/library/pdf/INF_PCS_HL_001_05_will_i_need_leaflet_ENGLISH.pdf
http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110303/text/110303w0002.htm#11030356000121
1 Mar 2011 : Column 368W—continued
CJD Frank Dobson: To ask the Secretary of State for Health what estimate he has made of the cost to the public purse of measures taken by the (a) blood service and (b) NHS, excluding the blood service, to reduce the risk of transmission of Creutzfeldt-Jakob disease by blood or blood products since 1998. [41549]
Anne Milton: Since 1998 a number of measures have been introduced by the United Kingdom blood services to reduce the risk of transfusion transmitted variant Creutzfeldt-Jakob disease (vGJD). These measures include the introduction of leucodepletion (the removal of white blood cells), the importation of fresh frozen plasma for children and the deferral from donation of transfusion recipients. In addition, the use of plasma from UK donors for fractionation purposes has ceased.
For national health service blood and transplant the highest costs associated with these measures are the estimated loss of income from the sale of plasma from UK blood donors (£325 million) and the introduction of leucodepletion (£182 million). Further measures bring the estimated total cost to £540 million since 1998, with an estimated current annual cost of approximately £40 million.
There is no separate assessment of such costs for the NHS outside the blood service. However, synthetic (recombinant) clotting factor for the treatment of bleeding disorders, such as haemophilia, has been provided to all patients for whom it is suitable since 2005, and to those under the age of 16 since 1998, at a current annual cost of approximately £200 million.
Commons Hansard Written Answers Text for 1 March 2011
http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110301/text/110301w0003.htm#1103022000031
Wednesday, February 2, 2011
Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay
http://transmissiblespongiformencephalopathy.blogspot.com/2011/02/detection-of-prion-infection-in-variant.html
vCJD, CJD, TSE screen (a) the USA blood supply and (b) blood donors for vCJD, CJD, TSE 2011
Posted: 3/2/2011
October 28, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244061.htm
October 29, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244062.htm
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
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
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
May 8, 2009
Greetings again Dr. Freas, TSEAC et al,
I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability from my neck injury, I will not be attending this meeting either, however I hope for my submission to be read and submitted. ...
IN reply to ;
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
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: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
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:
http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)
THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html
Thursday, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products
http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.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
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
http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html
Wednesday, December 29, 2010
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31
http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011
Prions
David W. Colby1,* and Stanley B. Prusiner1,2
http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.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, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products
http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.html
Wednesday, March 2, 2011 Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011
October 28, 2010
http://tseac.blogspot.com/2011/03/transmissible-spongiform.html
Tuesday, September 28, 2010
Variant CJD: where has it gone, or has it?
Pract Neurol 2010; 10: 250-251
http://vcjdtransfusion.blogspot.com/2010/09/variant-cjd-where-has-it-gone-or-has-it.html
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html
Saturday, July 17, 2010
Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.
2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE
http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.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
Friday, February 18, 2011
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"
http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html
i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.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
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
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
USA Blood products, collected from a donor who was at risk for vCJD, were distributed
Enforcement Report for October 20, 2010
October 20, 2010
PRODUCT
1) Cryoprecipitated AHF. Recall # B-2523-10;
2) Plasma. Recall # B-2524-10;
3) Red Blood Cells. Recall # B-2525-10;
4) Fresh Frozen Plasma. Recall # B-2526-10
CODE
1) Unit: W038508310277;
2) Units: 3127765, W038508310277, 3129157, 4121927;
3) Units: W038508310277, 3129157, 3127765, 4025397, 4121927, 4018030;
4) Units: 4025397, 4018030
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on July 22, 2010 and July 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
13 units
DISTRIBUTION
GA, MD, SC, Austria, Israel, South Korea, Switzerland
___________________________________
PRODUCT
1) Fresh Frozen Plasma. Recall # B-2531-10;
2) Recovered Plasma. Recall # B-2532-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2533-10
CODE
1) Unit: W115910041730;
2) Units: W115910080008, W115910081199;
3) Units: W115910080008, W115910041730, W115910081199
RECALLING FIRM/MANUFACTURER
Central California Blood Center, Fresno, CA, by e-mail on July 19, 2010 and July 23, 2010 and by facsimile on July 23, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
6 units
DISTRIBUTION
Austria, CA
END OF ENFORCEMENT REPORT FOR OCTOBER 20, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm230357.htm
Enforcement Report for October 13, 2010
October 13, 2010
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2275-10;
2) Recovered Plasma. Recall # B-2276-10;
3) Cryoprecipitated AHF, Pooled. Recall # B-2277-10
CODE
1), 2) and 3) Unit: 6400811
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by fax on April 7, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units
DISTRIBUTION
FL, TX
___________________________________
PRODUCT
Fresh Frozen Plasma. Recall # B-2283-10
CODE
Units: W001606004574; W001606003405
RECALLING FIRM/MANUFACTURER
Department of the Air Force 88th Medical Group SGQC WPAFB, Wright Patterson, AFB, OH, by letter dated April 17, 2008. Firm initiated recall is complete.
REASON
Blood products, collected from a donor who may have warranted deferral for residency in an area at risk for variant Creutzfeldt-Jakob Disease, were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NJ
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2322-10
2) Fresh Frozen Plasma. Recall # B-2323-10
CODE
1) and 2) Unit: W280310400336
RECALLING FIRM/MANUFACTURER
Upstate New York Transplant Services, Inc., Buffalo, NY, by telephone and fax on June 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
NY
___________________________________
PRODUCT
Red Blood Cells. Recall # B-2324-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
NY
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2325-10
CODE
Unit: W121610120511
RECALLING FIRM/MANUFACTURER
The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Switzerland
___________________________________
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm229271.htm
TSS
----- Original Message -----
From: Terry S. Singeltary Sr.
To: BLOODCJD@YAHOOGROUPS.COM
Sent: Thursday, October 07, 2010 12:58 PM
Subject: [BLOODCJD] USA Blood products, collected from a donor who was at risk for vCJD, were distributed END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan
___________________________________
PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY
___________________________________
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm
PRODUCT
1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;
2) Recovered Plasma. Recall # B-2156-10
CODE
1) Unit: W036309907231;
2) Unit: W036309616077
RECALLING FIRM/MANUFACTURER
BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX, Switzerland
___________________________________
PRODUCT
Red Blood Cells Leukocytes Reduced. Recall # B-2157-10
CODE
Unit: 6371718
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
TX
___________________________________
PRODUCT
Source Plasma. Recall # B-2212-10
CODE
Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599
RECALLING FIRM/MANUFACTURER
BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
10 units
DISTRIBUTION
CA
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;
2) Recovered Plasma. Recall # B-2214
CODE
1) and 2) Unit: 6325245
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
FL, TX
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm
PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm
PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC
___________________________________
PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN
___________________________________
PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm
PRODUCT
1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;
2) Red Blood Cells. Recall # B-2449-10;
3) Cryoprecipitated AHF. Recall # B-2450-10;
4) Plasma. Recall # B-2451-10
CODE
1) Units: W038509802210, W038509800965;
2) Units: W038509802210, W038509800965, W038508801111, W038508330725;
3) Unit: W03850830725;
4) Units: W038509801111, W038508330725
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
9 units
DISTRIBUTION
Korea, SC, GA
___________________________________
PRODUCT
Recovered Plasma. Recall # B-2306-10
CODE
Unit: W137508110097
RECALLING FIRM/MANUFACTURER
Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
___________________________________
PRODUCT
Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10
CODE
Units: W041609075327D (part a and b), 3922801 (part a and b)
RECALLING FIRM/MANUFACTURER
Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
4 units
DISTRIBUTION
MS
___________________________________
PRODUCT
1) Recovered Plasma. Recall # B-2363-10;
2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;
3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10
CODE
1) and 3) Units: 2613522, 2578779;
2) Unit: 2578779
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
5 units
DISTRIBUTION
TX
___________________________________
END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm
PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan
___________________________________
PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY
___________________________________
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm
PRODUCT
1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;
2) Recovered Plasma. Recall # B-2156-10
CODE
1) Unit: W036309907231;
2) Unit: W036309616077
RECALLING FIRM/MANUFACTURER
BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
TX, Switzerland
___________________________________
PRODUCT
Red Blood Cells Leukocytes Reduced. Recall # B-2157-10
CODE
Unit: 6371718
RECALLING FIRM/MANUFACTURER
South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.
REASON
Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
TX
___________________________________
PRODUCT
Source Plasma. Recall # B-2212-10
CODE
Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599
RECALLING FIRM/MANUFACTURER
BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
10 units
DISTRIBUTION
CA
___________________________________
PRODUCT
1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;
2) Recovered Plasma. Recall # B-2214
CODE
1) and 2) Unit: 6325245
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
FL, TX
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm
PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm
PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC
___________________________________
PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN
___________________________________
PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN
___________________________________
END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm
i have not checked out 2011 recalls of USA blood that has NOT been screened for vCJD. let's just check out the latest and see what's going on ;
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0812-11; 2) Recovered Plasma. Recall # B-0813-11 CODE 1) and 2) Unit: 0679506 RECALLING FIRM/MANUFACTURER Blood Centers of the Pacific, San Francisco, CA, by telephone and letter on May 22, 2002. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION CA, Switzerland
___________________________________
PRODUCT Source Plasma. Recall # B-0840-11 CODE Units 381070540, 381070350, 381069984, 381069808, 381068965, 381068783, 381068313, 381068151, 381067718, 381067473, 381067140, 381066944, 381066586, 381066289, 381065935, 381064526, 381065364, 381064386, 381064220, 381063426, 381063033, 381062874, 381062488, 381061767, 381061614, 381061260, 381060375, 381060162, 381059688, 381059534, 381059093, 381058859, 381058451, 381058224, 381057903, 381057624, 381057317, 381057103, 381056525, 381055667, 381054442, 381054328, 381053845, 381053686, 381053078, 381052342, 381051924, 381051688, 381048523 and 381048512 RECALLING FIRM/MANUFACTURER Recalling Firm: Talecris Plasma Resources, Research Triangle Park, NC, by facsimile on May 14, 2010. Manufacturer: Talecris Plasma Resources, Peoria, IL. Firm initiated recall is complete. REASON Blood products, collected from a donor who was previously deferred due to a history of Dura Mater Graft, were distributed. VOLUME OF PRODUCT IN COMMERCE 50 units DISTRIBUTION NC
___________________________________
PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0848-11; 2) Red Blood Cells Leukocytes Reduced Washed. Recall # B-0849-11; 3) Recovered Plasma. Recall # B-0850-11 CODE 1) Units: 3618494; 2528285; 2) Unit: 3679207; 3) Units: 3679207; 3618494; 2528285 RECALLING FIRM/MANUFACTURER Central California Blood Center, Fresno, CA, by letter dated September 7, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 6 units DISTRIBUTION CA
___________________________________
END OF ENFORCEMENT REPORT FOR MARCH 2, 2011
#
http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm245369.htm
Greetings,
I am sure there are many more in the previous weeks of 2011. I just don't have time now to search them by week. it's pretty much been a weekly event for years and years and years.
I still have not gotten an answer about these type recalls ;
"REASON Blood products, collected from donors in which donor suitability was not adequately determined, were distributed."
DOES this include vCJD ?
i personally think they are missing the bigger picture by not including all human TSE prion disease, especially since we know GSS will transmit by blood, and now that we know that some sporadic CJD cases are caused by atypical BSE. just does not make sense to me. i still say it's a band aid approach to something that needs a tourniquet. ...TSS
Saturday, January 20, 2007
Fourth case of transfusion-associated vCJD infection in the United Kingdom
http://vcjdtransfusion.blogspot.com/2007_01_01_archive.html
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.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
P02.35
Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass.
Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE.
By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice.
The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
O.11.3
Infectivity in skeletal muscle of BASE-infected cattle
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
O.2.4
Detection of prions in blood leucocytes
Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK
Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.
O.2.6
Human urine and PrP
Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy
Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *
O.4.6
All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion
Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK
Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.
Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.
Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.
Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.
Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)
O.8.1
Variant CJD and plasma products
Robert G. Will National CJD Surveillance Unit, Edinburgh, UK
Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.
O.8.2
Blood safety: from screening tests to prion removal
Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK
Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.
O.9.3
Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.
Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA
Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.
Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.
Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.
Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.
Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.
P.10.7
Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2
Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK
Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.
Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.
Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.
Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.
Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.
P.5.1
Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection
Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany
Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).
Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.
Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 - 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.
Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
http://vcjdtransfusion.blogspot.com/2007_01_01_archive.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified 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
In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
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