Tentative Schedule
Friday, July 16
8:30 – 7:30 Registration
12:30 – 2:30 Familial Prion Disease Meeting *This meeting is only for families affected by a familial prion disease Deana Simpson, RN - Chairman Macomb, Michigan Corporate Director of Clinical Transformation, Detroit Medical Center; Founder and Director, CJD Insight; Member, CJD Foundation Board of Directors
Pierluigi Gambetti, MD Cleveland, Ohio Professor and Director, Division of Neuropathology, Case Western Reserve University School of Medicine and University Hospitals of Cleveland; Director, The National Prion Disease Pathology Surveillance Center; Medical Director, CJD Foundation Thomas Wisniewski, MD New York, New York Professor, Departments of Neurology, Pathology and Psychiatry, New York University School Medicine
3:00 - 5:00 Bereavement Workshop Brian Appleby, MD - Chairman Baltimore, Maryland Co-Director, The Frontotemporal Dementia and Young-Onset Dementias Clinic, The Johns Hopkins Hospital; Assistant Professor, Psychiatry and Behavioral Sciences, Johns Hopkins University Deana Simpson, RN Katrina Hallmark, PsyD San Antonio, Texas Neuropsychologist, Southwest Mental Health Center 6:00 – 7:30 Welcome Reception 1 2 Saturday, July 17
Co-Chairmen: Pierluigi Gambetti, MD Neil Cashman, MD, FRCP(C), FCAHS
7:30 Conference Registration
7:30 – 8:30 Continental Breakfast
8:00 – 8:15 Conference Welcome
Florence Kranitz Akron, Ohio President, The CJD Foundation; Co-Chairman, The CJD International Support Alliance 8:15 – 8:40 Memorial Service
Overviews
8:40 – 9:05 The Future of Prion Disease Research and Treatments John Collinge, MD, FRCP, FRS London, United Kingdom Professor and Head, Department of Neurodegenerative Disease, Institute of Neurology, University College London; Director, UK Medical Research Council's Prion Unit; Director, UK National Prion Clinic, National Hospital for Neurology and Neurosurgery
9:05 – 9:15 Q&A
9:15 – 9:40 CJD World Overview and Difficulties in Making A CJD Diagnosis Robert Will, MD, FRCP(E) Edinburgh, United Kingdom Professor of Neurology, Personal Chair in Clinical Neurology, University of Edinburgh; Consultant Neurologist, Western General Hospital; Former Director and Founder, National CJD Surveillance Unit
9:40 – 9:50 Q&A
9:50 - 10:05 Coffee Break
Diagnosis and Treatment
10:05 – 10:25 The Current State of Prion Disease Diagnostics Jiri Safar, MD Cleveland, Ohio Co-Director, The National Prion Disease Pathology Surveillance Center
10:25 – 10:30 Q&A
10:30 – 10:50 The Future of Prion Disease Diagnostics David Wishart, PhD Alberta, Canada Professor, Departments of Computer Science and Biological Science, University of Alberta; Principal Investigator, Nano Life Sciences, National Institute for Nanotechnology, National Research Council
10:50 - 10:55 Q&A
3
10:55 - 11:15 Human Prion Disease Vaccine Thomas Wisniewski, MD
11:15 - 11:20 Q&A
11:20 - 11:40 Doxycycline Clinical Trial Update Fabrizio Tagliavini, MD Milan, Italy Director, Divisions of Neuropathology and Neurology Fondazione IRCCS Istituto Neurologico Carlo Besta
11:40 - 11:45 Q&A
11:45 - 1:00 Lunch
1:00 - 1:20 The National Prion Monitoring Cohort Study Simon Mead, PhD London, United Kingdom Head, Human Genetics Program, MRC Prion Unit; Lead Clinician, National Prion Clinic
1:20 - 1:25 Q&A Surveillance
1:25 – 1:40 Prion Disease Surveillance in the United States Pierluigi Gambetti, MD
1:40 – 1:55 Prion Disease Surveillance in Canada Gerard Jansen, MD, FRCP(C) Ottawa, Canada Neuropathologist, Head of Anatomical Pathology, Principal Investigator, CJD Neuropathology, Ottawa Hospital; Medical Specialist, Prion Diagnostics, Public Health Agency of Canada
1:55 - 2:10 Prion Disease Surveillance in the United Kingdom Richard Knight, MD, FRCP(E) Edinburgh, United Kingdom Deputy Director, UK National CJD Surveillance Unit; Professor and Personal Chair, Clinical Neurology, University of Edinburgh; Honorary Consultant, Clinical Neurology, Department of Clinical Neurosciences, Western General Hospital
2:10 – 2:25 Prion Disease Surveillance in China Xiao-Ping Dong, PhD Beijing, China Director, Division of Science and Technology, Chinese Center for Disease Control and Prevention
2:25 - 2:40 Prion Disease Surveillance in France Jean-Philippe Brandel, MD Paris, France Cellulle Nationale de référence des maladies de Creutzfeldt-Jakob Groupe Hospitalier Pitié-Salpêtrière
2:40 – 3:00 Surveillance Q&A Panel
4
3:00 - 3:15 Coffee and Cookie Break
3:15 - 5:00 Moving Round Tables
7:00 – 7:30 Reception
7:30 Banquet
Sunday, July 18 Co-Chairmen: Florence Kranitz Marisa Boarman
7:30 – 9:00 Continental Breakfast
9:00 - 9:15 CJDF Update
Mark Goldfarb Akron, Ohio Chairman, Board of Directors, The CJD Foundation Ruthie George Akron, Ohio Treasurer, Board of Directors, The CJD Foundation
9:15 - 9:30 CJDF Questionnaire Report
=========
http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html
http://cjdquestionnaire.blogspot.com/2009/09/multi-state-study-of-creutzfeldt-jakob.html
http://cjdquestionnaire.blogspot.com/
TSS
================
9:30 - 9:35 Q&A
9:35 - 9:50 The Centers for Disease Control and Prevention Report Ryan Maddox, MPH Atlanta, Georgia Epidemiologist, Prion Disease Office, Office of the Director, Division of Viral and Rickettsial Diseases, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention
9:50 - 9:55 Q&A
9:55 - 10:10 Pentosan Sulphate: A Friendly Delivery System for Therapy in Prion Diseases
2009 CJD Foundation Human Prion Disease Grant Recipient Maurizio Pocchiari, MD Research Director and Head, Clinical, Diagnosis and Therapy of Neurodegenerative Disorders Unit, Department of Cell Biology and Neurosciences, Istituto Superiore di Sanita
10:10 - 10:15 Q&A
10:15 - 10:30 Searching for Custom Dominant Negative PrPs by In Vitro Prion Replication Studies
2009 CJD Foundation Human Prion Disease Grant Recipient Joaquin Castilla, PhD Bizkaia, Spain Principal Investigator, Prion Lab, Proteomic Unit, CIC bioGUNE
10:30 - 10:35 Q&A
5
10:35 - 10:50 Analyses of the Protein Tau to Help Determine Whether the Newly Discovered Protease-Sensitive Prionopathy is the Sporadic Form of Gerstmann-Sträussler-Scheinker Disease (GSS) 2010 Patrick Yobs GSS Memorial Fund Grant Recipient Gianfranco Puoti, MD, PhD Cleveland, Ohio Neurologist and Reserach Associate, The National Prion Disease Pathology Surveillance Center
10:50 - 10:55 Q&A
10:55 - 11:10 Coffee Break
11:10 - 11:25 Etiology of Sporadic CJD: Somatic Mutations of the Human Prion Protein Gene in Brain Cells 2010 CJD Foundation Human Prion Disease Grant Recipient Qingzhong Kong, PhD Cleveland, Ohio Associate Professor, Division of Pathology, Case Western Reserve University; Researcher, The National Prion Disease Pathology Surveillance Center
11:25 - 11:30 Q&A
11:30 - 11:45 Adult Neurogenesis in Prion Diseases: A New Lead for Therapeutics?
2010 CJD Foundation Human Prion Disease Grant Recipient #2 Sylvain Lehmann, MD, PhD & Carole Crozet, PhD Montpellier, France Research Group Leader, Department of Molecular and Cellular Pathologies, Institut de Génétique Humaine
11:45 - 11:50 Q&A
11:50 - 12:05 2010 CJD Foundation Human Prion Disease Grant Recipient MEK-inhibitors clear prion-infected cells from PrPSc Elin Allard, PhD Stockholm, Sweden Researcher, Department of Neuroscience, Karolinska Institutet
12:05 - 12:10 Q&A
12:10 - 12:20 Alberta Prion Research Institute (APRI) Kevin Keough, PhD, FCAHS Alberta, Canada Executive Director, The Alberta Prion Research Institute 1 2:20 – 1:30 Lunch Support Organization Reports
1:30 – 1:45 CJD Support Group Network, Australia Suzanne Solvyns Glenhaven NSW, Australia National Coordinator, CJD Support Group Network
6
1:45 – 2:00 Maladie de Creutzfeldt-Jakob par Hormone de Croissance Contaminée (MCJ-HCC), France JB Mathieu Paris, France President, MCJ-HCC
2:00 - 2:15 CJD Foundation, Israel Alice Anane Israel President, CJD Foundation, Israel
2:15 - 2:30 Associazione Italiana Encefalopatie da Prioni (A.I.En.P.), Italy Roberto Borgis Torino, Italy President, A.I.En.P. Raffaella Robello Genova, Italy Vice President, A.I.En.P.
2:30 – 2:45 CJD Support Network, Japan Minae Askawa Japan Counselor, CJD Support Network, Japan
2:45 – 3:00 CJD Support Network, United Kingdom
http://www.cjdfoundation.org/pdfs/2010conference.pdf
CJD 2010 and the CJD Foundation Family Conference
will be held July 16 – 18, 2010 at the
Washington Court Hotel in Washington,
D.C. Advocacy Day on Capitol Hill will
be on Monday, July 19th for interested
families.
P.O. Box 5312, Akron, Ohio 44334
330.665.5590
HelpLine 1.800.659.1991
help@cjdfoundation.org
http://www.cjdfoundation.org/
TSS
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.
see page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
Wednesday, February 24, 2010
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th
ICID International Scientific Exchange Brochure -
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
TSE
http://transmissiblespongiformencephalopathy.blogspot.com/
International Society for Infectious Diseases Web: http://www.isid.org
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas
Irma Linda Andablo CJD Victim, she died at 38 years old on February 6, 2010 in Mesquite Texas.She left 6 Kids and a Husband.The Purpose of this web is to give information in Spanish to the Hispanic community, and to all the community who want's information about this terrible disease.-
Physician Discharge Summary, Parkland Hospital, Dallas Texas
Admit Date: 12/29/2009 Discharge Date: 1/20/2010 Attending Provider: Greenberg, Benjamin Morris; General Neurology Team: General Neurology Team
Linda was a Hispanic female with no past medical history presents with 14 months of incresing/progressive altered mental status, generalized weakness, inability to walk, loss of appetite, inability to speak, tremor and bowel/blader incontinence.She was, in her usual state of health up until February, 2009, when her husbans notes that she began forgetting things like names and short term memories. He also noticed mild/vague personality changes such as increased aggression. In March, she was involved in a hit and run MVA,although she was not injured. The police tracked her down and ticketed her. At that time, her son deployed to Iraq with the Army and her husband assumed her mentation changes were due to stress over these two events. Also in March, she began to have weakness in her legs, making it difficult to walk. Over the next few months, her mentation and personality changes worsened, getting to a point where she could no longer recognized her children. She was eating less and less. She was losing more weight. In the last 2-3 months, she reached the point where she could not walk without an assist, then 1 month ago, she stopped talking, only making grunting/aggressive sounds when anyone came near her. She also became both bowel and bladder incontinent, having to wear diapers. Her '"tremor'" and body jerks worsened and her hands assumed a sort of permanent grip position, leading her family to put tennis balls in her hands to protect her fingers.
The husband says that they have lived in Nebraska for the past 21 years. They had seen a doctor there during the summer time who prescribed her Seroquel and Lexapro, Thinking these were sx of a mood disorder. However, the medications did not help and she continued to deteriorate clinically. Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. The husband says that he does not know any fellow workers with a similar illness. He also says that she did not have any preceeding illness or travel.
http://www.recordandoalinda.com/index.php?option=com_content&view=article&id=19:cjd-english-info&catid=9:cjd-ingles&Itemid=8
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
http://creutzfeldt-jakob-disease.blogspot.com/2010/03/irma-linda-andablo-cjd-victim-she-died.html
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
http://cjdtexas.blogspot.com/2010/03/cjd-texas-38-year-old-female-worked.html
YOU can be assured they are squirming behind closed doors, and that they are doing there best to squirm right out of this one. they will come up with something, international travel long ago, or some strange PRNP mutation that they might say like sporadic ffi ??? or a case of atypical case of inherited Creutzfeldt-Jakob disease (CJD) ??? they will make up something. but it will be anything but BSE related here in the USA, in my opinion. sporadic FFI, or sporadic GSS, or sporadic inherited CJD is an oxymoron. it's either familial or not. or even this new novel human disease known as Protease-Sensitive Prionopathy (PSPr), they might come up with that. if they cannot do this, it will be an occupational TSE infection, whether they want to admit it or not. and they don't admit those to often, they cover them up. just like that Spanish Doctor that handled cjd infected tissue. but we never heard nothing about that one either ;
Investigator succumbs to CJD THE head of Pathological Anatomy at Principe de Asturias hospital in Alcala de Henares, Dr Antonio Ruiz Villaescusa, has died from Creutzfeldt-Jakob's disease. It is believed that Dr Ruiz, a specialist in CJD, contracted the disease after exposure to tissue from infected patients.
http://www.euroweeklynews.com/news_spanish_press.html
http://74.125.47.132/search?q=cache:MfWnPKrMDEwJ:www.euroweeklynews.com/news_spanish_press.html+Principe+de+Asturias+in+Alcala+de+Henares+cjd&cd=5&hl=en&ct=clnk&gl=us
please read Senate 'Down Under' link at bottom of the following url ;
http://transmissiblespongiformencephalopathy.blogspot.com/
Wednesday, March 31, 2010
Atypical BSE in Cattle / position: Post Doctoral Fellow
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.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
please see full text ;
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html
Sunday, March 28, 2010
Nor-98 atypical Scrapie, atypical BSE, spontaneous TSE, trade policy, sound science ?
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-atypical-bse.html
*****URGENT NOTE HERE ABOUT OIE AND THEIR JUNK SCIENCE ABOUT ATYPICAL BSE*****
Wednesday, March 31, 2010
Atypical BSE in Cattle
http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.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
Wednesday, March 3, 2010
NOR-98 ATYPICAL SCRAPIE USA 4 CASES DETECTED JANUARY 2010
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-usa-4-cases.html
Canada - Case of BSE (Mad cow disease) in 6 year old cow 17th domestic case
http://bseusa.blogspot.com/2010/03/canada-case-of-bse-mad-cow-disease-in-6.html
Thursday, March 11, 2010
CANADA TYPICAL AND ATYPICAL SCRAPIE REPORT TO MARCH 2010
http://nor-98.blogspot.com/2010/03/canada-typical-and-atypical-scrapie.html
Tuesday, February 09, 2010
Chronic Wasting Disease: Surveillance Update: February 2010
http://chronic-wasting-disease.blogspot.com/2010/02/chronic-wasting-disease-surveillance.html
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Friday, February 05, 2010
New Variant Creutzfelt Jakob Disease case reports United States 2010 A Review
http://vcjd.blogspot.com/2010/02/new-variant-creutzfelt-jakob-disease.html
Prion data suggest BSE link to sporadic CJD Declan Butler
Predicting the number of cases of Creutzfeldt-Jakob disease (CJD) in people as a result of transmission of bovine spongiform encephalopathy (BSE) has just got more difficult.Whereas it was thought that BSE only caused a new form of the disease called variant CJD (vCJD), a study in mice from a team led by John Collinge at University College London suggests that it may also cause a disease indistinguishable from the commonest form of classical, or 'sporadic', CJD (E.
http://www.nature.com/nature/journal/v420/n6915/full/420450a.html
Mouse model sheds new light on human prion disease
snip...
Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD.
snip...
http://www.mrc.ac.uk/txt/index/public-interest/public-news-4/public-news_archive/public-news-archive_nov_dec_02/public-bse_and_sporadic_cjd.htm
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
http://www.nature.com/emboj/journal/v21/n23/full/7594869a.html
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.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
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Sunday, March 07, 2010 5:41 PM
Subject: Re: [BSE-L] FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
see full text, and be sure to read the BSE Inquiry documents toward the bottom ;
http://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html
Wednesday, March 3, 2010
NOR-98 ATYPICAL SCRAPIE USA 4 CASES DETECTED JANUARY 2010
http://nor-98.blogspot.com/2010/03/nor-98-atypical-scrapie-usa-4-cases.html
Tuesday, August 04, 2009
Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
snip...
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay,
Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D.
Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG
HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
snip...
http://chronic-wasting-disease.blogspot.com/2009/08/susceptibilities-of-nonhuman-primates.html
Thursday, December 10, 2009
Chronic Wasting Disease (CWD) Susceptibility of Several North American Rodents That Are Sympatric with Cervid CWD Epidemics
http://chronic-wasting-disease.blogspot.com/2009/12/chronic-wasting-disease-cwd.html
CHRONIC WASTING DISEASE (CWD)
http://chronic-wasting-disease.blogspot.com/
What about CJD in the USA ?
USA sporadic CJD cases rising ;
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
CJD USA RISING, with UNKNOWN PHENOTYPE ;
5 Includes 41 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 46 cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
JOURNAL OF NEUROLOGY
MARCH 26, 2003
Send Post-Publication Peer Review to journal:
Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
flounder@wt.net
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
http://www.neurology.org/cgi/eletters/60/2/176#535
Newsdesk The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Xavier Bosch
"My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem." 49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)-the relative of mad cow disease seen among deer and elk in the USA. Although his feverish.
http://linkinghub.elsevier.com/retrieve/pii/S1473309903007151
http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00715-1/fulltext
http://www.mdconsult.com/das/article/body/180784492-2/jorg=journal&source=&sp=13979213&sid=0/N/368742/1.html?issn=14733099
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. FREE FULL TEXT
http://jama.ama-assn.org/cgi/content/extract/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=singeltary&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755
"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.
Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...
http://www.spiegel.de/spiegel/print/d-18578755.html
http://wissen.spiegel.de/wissen/image/show.html?did=18578755&aref=image024/E0108/SCSP200100901440145.pdf&thumb=false
http://service.spiegel.de/digas/servlet/find/DID=18578755
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html
UPDATE 2010
hmmm, this is getting interesting now...
> Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,
see also ;
> All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html
(American Journal of Pathology. 2009;175:2566-2573.) © 2009 American Society for Investigative Pathology DOI: 10.2353/ajpath.2009.090623
Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types
Wiebke M. Wemheuer*, Sylvie L. Benestad, Arne Wrede*, Ulf Schulze-Sturm*, Wilhelm E. Wemheuer, Uwe Hahmann*, Joanna Gawinecka, Ekkehard Schütz, Inga Zerr, Bertram Brenig, Bjørn Bratberg, Olivier Andréoletti¶ and Walter J. Schulz-Schaeffer* From the Prion and Dementia Research Unit,* Department of Neuropathology, and the National Transmissible Spongiform Encephalopathies Reference Center, Department of Neurology, University Medical Center Goettingen, Goettingen, Germany; the Department of Pathology, National Veterinary Institute, Oslo, Norway; the Institute of Veterinary Medicine, Faculty for Agricultural Sciences, University of Goettingen, Goettingen, Germany; and Animal Health,¶ Interactions Hôte Agent Pathogène, Ecole Nationale Vétérinaire de Toulouse, Toulouse, France
Transmissible spongiform encephalopathies such as scrapie in sheep, Creutzfeldt-Jakob disease (CJD) in humans, and bovine sporadic encephalopathy in cattle are characterized by the accumulation of a misfolded protein: the pathological prion protein. Ever since bovine sporadic encephalopathy was discovered as the likely cause of the new variant of CJD in humans, parallels between human and animal transmissible spongiform encephalopathies must be viewed under the aspect of a disease risk for humans. In our study we have compared prion characteristics of different forms of sheep scrapie with those of different phenotypes of sporadic CJD. The disease characteristics of sporadic CJD depend considerably on the prion type 1 or 2. Our results show that there are obvious parallels between sporadic CJD type 1 and the so-called atypical/Nor98 scrapie. These parelleles apply to the deposition form of pathological prion protein in the brain, detected by the paraffin-embedded-tissue blot and the prion aggregate stability with regard to denaturation by the chaotropic salt guanidine hydrochloride. The same applies to sporadic CJD type 2 and classical scrapie. The observed parallels between types of sporadic CJD and types of sheep scrapie demonstrate that distinct groups of prion disease exist in different species. This should be taken into consideration when discussing interspecies transmission.
http://ajp.amjpathol.org/cgi/content/abstract/175/6/2566
P.5.21
Parallels between different forms of sheep scrapie and types of Creutzfeldt-Jakob disease (CJD)
Wiebke M. Wemheuer1, Sylvie L. Benestad2, Arne Wrede1, Wilhelm E. Wemheuer3, Tatjana Pfander1, Bjørn Bratberg2, Bertram Brenig3,Walter J. Schulz-Schaeffer1 1University Medical Center Goettingen, Germany; 2Institute of Veterinary Medicine Oslo, Norway; 3Institute of Veterinary Medicine Goettingen, Germany
Background: Scrapie in sheep and goats is often regarded as the archetype of prion diseases. In 1998, a new form of scrapie - atypical/Nor98 scrapie - was described that differed from classical scrapie in terms of epidemiology, Western blot profile, the distribution of pathological prion protein (PrPSc) in the body and its stability against proteinase K. In a similar way, distinct disease types exist in sporadic Creutzfeldt-Jakob disease (CJD). They differ with regard to their clinical outcome, Western blot profile and PrPSc deposition pattern in the central nervous system (CNS).
Objectives: The comparison of PrPSc deposits in sheep scrapie and human sporadic CJD.
Methods: Tissues of the CNS of sheep with classical scrapie, sheep with atypical/Nor98 scrapie and 20 patients with sporadic CJD were examined using the sensitive Paraffin Embedded Tissue (PET) blot method. The results were compared with those obtained by immunohistochemistry. With the objective of gaining information on the protein conformation, the PrPSc of classical and atypical/Nor98 sheep scrapie and sporadic CJD was tested for its stability against denaturation with guanidine hydrochloride (GdnHCl) using a Membrane Adsorption Assay.
Results: The PrPSc of atypical/Nor98 scrapie cases and of CJD prion type 1 patients exhibits a mainly reticular/synaptic deposition pattern in the brain and is relatively sensitive to denaturation with GdnHCl. In contrast classical scrapie cases and CJD prion type 2 patients have a more complex PrPSc deposition pattern in common that consists of larger PrPSc aggregates and the PrPSc itself is comparatively stable against denaturation.
Discussion: The similarity between CJD types and scrapie types indicates that at least two comparable forms of the misfolded prion protein exist beyond species barriers and can elicit prion diseases. It seems therefore reasonable to classify classical and atypical/Nor98 scrapie - in analogy to the existing CJD types - as different scrapie types.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.html
EVIDENCE OF SCRAPIE IN SHEEP AS A RESULT OF FOOD BORNE EXPOSURE
This is provided by the statistically significant increase in the incidence of sheep scrape from 1985, as determined from analyses of the submissions made to VI Centres, and from individual case and flock incident studies. ........
http://web.archive.org/web/20010305222246/www.bseinquiry.gov.uk/files/yb/1994/02/07002001.pdf
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie A] The Problem
Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries.
The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep.
It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible.
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
http://www.nature.com/nature/journal/v236/n5341/abs/236073a0.html
Epidemiology of Scrapie in the United States 1977
http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
NEW URL ;
http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
Tuesday, April 28, 2009
Nor98-like Scrapie in the United States of America
http://nor-98.blogspot.com/2009/04/nor98-like-scrapie-in-united-states-of.html
Scrapie USA
http://scrapie-usa.blogspot.com/
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406
Sunday, August 10, 2008
A New Prionopathy OR more of the same old BSe and sporadic CJD
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
CHAPTER 14
Laying Odds
Are prion diseases more prevalent than we thought?
Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?
Revisiting Sporadic CJD
It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.
Singeltary has similar inclinations. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
http://www.thepathologicalprotein.com/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=the+pathological+protein+laying+odds+It%E2%80%99s+not+hard+to+get+Terry+Singeltary+going&source=bl&ots=um0PFAZSZD&sig=JWaGR7M7-1WeAr2qAXq8D6J_jak&hl=en&ei=MhtjS8jMJM2ztgeFoa2iBg&sa=X&oi=book_result&ct=result&resnum=1&ved=0CAcQ6AEwAA#v=onepage&q=&f=false
http://www.springerlink.com/content/r2k2622661473336/fulltext.pdf?page=1
http://www.thepathologicalprotein.com/
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD
only theory JUNE 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html
http://cjdquestionnaire.blogspot.com/
Friday, January 29, 2010
14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
http://bse-atypical.blogspot.com/2010/01/14th-international-congress-on.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Monday, July 27, 2009
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
WHY DID THIS VIDEO NOT SHOW ON EVERY NEWS CHANNEL IN THE U.S.A. $$$
IT IS A DAMNING VIDEO !!!
I WATCHED THIS RECENTLY, and had never seen it. i was so mad, i was spitting nails out faster than a framing gun.
WHY DID THE CANADIAN MEDIA ONLY PRESENT THIS TO THE U.S.A. PUBLIC (thank you very much though), and why has the U.S.A. MEDIA FAILED US ???
SNIP...
SEE DAMNING VIDEO AT BOTTOM OF BLOG HERE ;
Monday, July 27, 2009
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
NOW, AFTER SEEING THAT VIDEO, (first watch the video) lets go back in mad cow time here in the USA, shall we.
THERE must be an independent review of this cover-up, and the infamous ENHANCED BSE SURVEILLANCE AND TESTING OF 2004, that was nothing but a cover-up, and blundered at that, and plus a REDO of the testing of no less than 1 million head of cattle tested each year, for five years, with scientist from the EU overseeing the testing protocols, surveillance, and confirmation of all cases.
this video states the 'USA had to _admit_ a home grown case of mad cow in TEXAS." fact was, they did not finally admit anything, IT TOOK AN ACT OF CONGRESS, THE HONORABLE PHYLISS FONG AND THE O.I.G., TO MAKE THEM RETEST AND CONFIRM! that my friend is fact. and only after Prof. Aguzzi, Dr. Jean-Philippe Deslys, Dr. Collinge et al slammed them over the testing of that animal. and then we had the mad cow in Texas that they just refused to test, and was sent to a pet food rendering plant. NO TEST AT ALL. you must realize, when other officials, doctors, and such from other country's confront issues about things in the USA, they must walk on ice when doing so. read inbetween the lines here ;
i wrote all these scientist and doctors and the OIG about that damn texas cow, gave them the evidence i had from TAHC. so did others, but finally fong et al did something.
Tuesday, July 28, 2009
MAD COW COVER-UP USA MASKED AS SPORADIC CJD
http://madcowtesting.blogspot.com/2009/07/mad-cow-cover-up-usa-masked-as-sporadic.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
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
http://madcowtesting.blogspot.com/2009/07/us-emergency-bovine-spongiform.html
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
...snip
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
Wed, 29 Nov 2000 14:14:18 -0500
a private email from the late Dr. Gibbs, a true pioneer in the research of human/animal TSEs and one that never wavered on helping the families and victims of this horrible disease, and one that helped me many times in trying to seek out the truth;
Subject: Re: Hello Dr. Gibbs...........
Date: Wed, 29 Nov 2000 14:14:18 -0500
From: "Clarence J. Gibbs, Jr., Ph.D."
To: "Terry S. Singeltary Sr." References: <3a254430.9fb97284@wt.net>
Hi Terry:
326 E Stret N.E., Washington, D. C. 20002.
Better shrimp and oysters than cards!!!!
Have a happy holiday and thanks for all the information you bring to the screen.
Joe Gibbs ==========
please see full text ;
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
Monday, October 12, 2009
SEAC Science and Technology Committee's investigation of research funding priorities on behalf of the Advisory Committee on Dangerous Pathogens TSE
• Are some commoner types of neurodegenerative disease (including Alzheimer's disease and Parkinson's disease) also transmissible? Some recent scientific research has suggested this possibility
http://www.seac.gov.uk/pdf/hol-response091008.pdf
http://bse-atypical.blogspot.com/2009/10/seac-science-and-technology-committees.html
Monday, January 4, 2010
Rising Tide: The Impact of Dementia in Canada Huge wave of dementia cases coming, warns report
http://betaamyloidcjd.blogspot.com/2010/01/rising-tide-impact-of-dementia-in.html
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
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