Co-existence of scrapie prion protein types 1 and 2 in sporadic Creutzfeldt-Jakob disease: its effect on the phenotype and prion-type characteristics.
by: Ignazio Cali, Rudolph Castellani, Amer Alshekhlee, Yvonne Cohen, Janis Blevins, Jue Yuan, Jan P. Langeveld, Piero Parchi, Jiri G. Safar, Wen-Quan Q. Zou, Pierluigi Gambetti Brain : a journal of neurology (4 September 2009)
ABSTRACT
Five phenotypically distinct subtypes have been identified in sporadic Creutzfeldt-Jakob disease (sCJD), based on the methionine/valine polymorphic genotype of codon 129 of the prion protein (PrP) gene and the presence of either one of the two protease K-resistant scrapie prion protein (PrP(Sc)) types identified as 1 and 2. The infrequent co-existence of both PrP(Sc) types in the same case has been known for a long time. Recently, it has been reported, using type-specific antibodies, that the PrP(Sc) type 1 is present in all cases of sCJD carrying PrP(Sc) type 2. The consistent co-occurrence of both PrP(Sc) types complicates the diagnosis and the current classification of sCJD, and has implications for the pathogenesis of naturally occurring prion diseases. In the present study, we investigated the prevalence of PrP(Sc) types 1 and 2 co-occurrence, along with its effects on the disease phenotype and PrP(Sc) strain characteristics, comparatively analysing 34 cases of sCJD, all methionine homozygous at codon 129 of the PrP gene (sCJDMM). To minimize overestimating the prevalence of the sCJDMM cases carrying PrP(Sc) types 1 and 2 (sCJDMM1-2), we used proteinase K concentrations designed to hydrolyse all fragments resulting from an incomplete digestion, while preserving the protease-resistant PrP(Sc) core. Furthermore, we used several antibodies to maximize the detection of both PrP(Sc) types. Our data show that sCJDMM cases associated exclusively with either PrP(Sc) type 1 (sCJDMM1) or PrP(Sc) type 2 (sCJDMM2) do exist; we estimate that they account for approximately 56% and 5% of all the sCJDMM cases, respectively; while in 39% of the cases, both PrP(Sc) types 1 and 2 are present together (sCJDMM1-2) either mixed in the same anatomical region or separate in different regions. Clinically, sCJDMM1-2 had an average disease duration intermediate between the other two sCJDMM subtypes. The histopathology was also intermediate, except for the cerebellum where it resembled that of sCJDMM1. These features, along with the PrP immunostaining pattern, offer a diagnostic clue. We also observed a correlation between the disease duration and the prevalence of PrP(Sc) type 2 and sCJDMM2 phenotypes. The use of different antibodies and of the conformational stability immunoassay indicated that the co-existence of types 1 and 2 in the same anatomical region may confer special conformational characteristics to PrP(Sc) types 1 and 2. All of these findings indicate that sCJDMM1-2 should be considered as a separate entity at this time.
http://www.citeulike.org/user/applebyb/article/5739998
> sCJDMM1-2 should be considered as a separate entity at this time.
Thank you very much !
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html
Tuesday, August 11, 2009
Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants
Brian S. Appleby, MD; Kristin K. Appleby, MD; Barbara J. Crain, MD, PhD; Chiadi U. Onyike, MD, MHS; Mitchell T. Wallin, MD, MPH; Peter V. Rabins, MD, MPH
Background: The classic Creutzfeldt-Jakob disease (CJD), Heidenhain, and Oppenheimer-Brownell variants are sporadic CJD (sCJD) phenotypes frequently described in the literature, but many cases present with neuropsychiatric symptoms, suggesting that there may be additional sCJD phenotypes.
Objective: To characterize clinical, diagnostic, and molecular features of 5 sCJD variants.
Design: Retrospective analysis.
Setting: The Johns Hopkins and Veterans Administration health care systems.
Participants: Eighty-eight patients with definite or probable sCJD.
Main Outcome Measures: Differences in age at onset, illness progression, diagnostic test results, and molecular subtype.
Results: The age at onset differed among sCJD variants (P=.03); the affective variant had the youngest mean age at onset (59.7 years). Survival time (P.001) and the time to clinical presentation (P=.003) differed among groups. Patients with the classic CJD phenotype had the shortest median survival time from symptom onset (66 days) and those who met criteria for the affective sCJD variant had the longest (421 days) and presented to clinicians significantly later (median time from onset to presentation, 92 days; P=.004). Cerebrospinal fluid analyses were positive for 14-3-3 protein in all of the affective variants, regardless of illness duration. Periodic sharp-wave complexes were not detected on any of the electroencephalography tracings in the Oppenheimer-Brownell group; basal ganglia hyperintensity was not detected on brain magnetic resonance imaging in this group either. All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.
Conclusions: The classic CJD phenotype and the Heidenhain, Oppenheimer-Brownell, cognitive, and affective sCJD variants differ by age at disease onset, survival time, and diagnostic test results. Characteristics of these 5 phenotypes are provided to facilitate further clinicopathologic investigation that may lead to more reliable and timely diagnoses of sCJD.
Arch Neurol. 2009;66(2):208-215
snip...
COMMENT
snip...see full text ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html
Sunday, September 6, 2009
MAD COW USA 1997 VIDEO
SEE ANOTHER VIDEO THAT SHOWED IN CANADA, BUT NOT USA, ABOUT ANOTHER USA TSE COVER-UP
MORE BRAINS NOT TESTED PROPERLY, key brain parts missing. ...
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
SEE THIS DAMNING VIDEO AT BOTTOM OF ;
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
TSS
Wednesday, September 9, 2009
Monday, June 15, 2009
CJD FOUNDATION MIAMI FOUNDER CELE SARDO
CJD FOUNDATION MIAMI FOUNDER CELE SARDO
Jun 15, 2009
Greetings CJD Family,
I want to let the old timers, and everyone know, that Cele Sardo, founder of the original CJD Foundation out of Florida, who pioneered support for CJD victims of all types here in the USA first, before the CJD Foundation INC at CWRU took it over, before CJD voice, or CJD watch. Cele passed away this morning about 4 AM. she was my friend, and as twisted as i may seem sometimes, she has always understood my anger. Joe told me that the family will bury Cele in the Kendall area of Miami later this week where Mr. Sardo, Joe's father is buried.Cele lost her husband Joe (Joseph's Father), to sporadic CJD around 1989. Mr. Sardo was 56 when he died from CJD. Cele and and her friend Mayra Lichter did a great job with the CJD Foundation when they had it, and Cele knew too well that the CJD surveillance was lacking here in the USA. Cele Sardo and Mayra Lichter Founded the CJD Foundation originally back in Miami, Florida around 1993, and what an organization of support is was. The Sardo Family has done a _great_ deal for research for CJD. Our thanks go out to them, along with our prayers for the family at this difficult time...
Two Women Against Mad Cow Disease November 1, 2001 Good Housekeeping by Lisa Belkin
http://www.organicconsumers.org/madcow/women110101.cfm
Proper sterilization may ward off deadly CJD transmission Healthcare Purchasing News , May, 2001
http://findarticles.com/p/articles/mi_m0BPC/is_5_25/ai_75644703/
CELE WAS A SOLDIER IN THE BATTLE TO FIND SUPPORT, TO FIND THE CAUSE, AND TO FIND A CURE FOR ALL FORMS OF CJD, OF ALL AGES. ...
with saddest regards,
i will miss my friend. ...terry
Jun 15, 2009
Greetings CJD Family,
I want to let the old timers, and everyone know, that Cele Sardo, founder of the original CJD Foundation out of Florida, who pioneered support for CJD victims of all types here in the USA first, before the CJD Foundation INC at CWRU took it over, before CJD voice, or CJD watch. Cele passed away this morning about 4 AM. she was my friend, and as twisted as i may seem sometimes, she has always understood my anger. Joe told me that the family will bury Cele in the Kendall area of Miami later this week where Mr. Sardo, Joe's father is buried.Cele lost her husband Joe (Joseph's Father), to sporadic CJD around 1989. Mr. Sardo was 56 when he died from CJD. Cele and and her friend Mayra Lichter did a great job with the CJD Foundation when they had it, and Cele knew too well that the CJD surveillance was lacking here in the USA. Cele Sardo and Mayra Lichter Founded the CJD Foundation originally back in Miami, Florida around 1993, and what an organization of support is was. The Sardo Family has done a _great_ deal for research for CJD. Our thanks go out to them, along with our prayers for the family at this difficult time...
Two Women Against Mad Cow Disease November 1, 2001 Good Housekeeping by Lisa Belkin
http://www.organicconsumers.org/madcow/women110101.cfm
Proper sterilization may ward off deadly CJD transmission Healthcare Purchasing News , May, 2001
http://findarticles.com/p/articles/mi_m0BPC/is_5_25/ai_75644703/
CELE WAS A SOLDIER IN THE BATTLE TO FIND SUPPORT, TO FIND THE CAUSE, AND TO FIND A CURE FOR ALL FORMS OF CJD, OF ALL AGES. ...
with saddest regards,
i will miss my friend. ...terry
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Saturday, July, 18, 2009
Greetings,
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. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
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. 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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
2003
Neurology 2003;60:176-181 © 2003 American Academy of Neurology
-------------------------------------------------------------------------------- Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.
http://www.neurology.org/cgi/content/abstract/60/2/176
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
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
Reply to Singletary 26 March 2003
Ryan A. Maddox, MPH
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication).
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.
http://www.neurology.org/cgi/eletters/60/2/176
Posted On December 20, 2003
Mad Cow Scaremongers
Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
http://www.neurology.org/cgi/eletters/60/2/176
http://www.consumerfreedom.com/article_detail.cfm/article/138
Book
The Pathological Protein
Publisher Springer New York DOI 10.1007/b97488 Copyright 2003 ISBN 978-0-387-95508-7 (Print) 978-0-387-21755-0 (Online) DOI 10.1007/0-387-21755-X_14 Pages 223-237 Subject Collection Humanities, Social Sciences and Law SpringerLink
Laying Odds
snip...
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.
snip...
http://www.springerlink.com/content/r2k2622661473336/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=SINGELTARY+pathological+protein+it
2006
FOOD AND DRUG ADMINISTRATION
DEPARTMENT OF HEALTH AND HUMAN SERVICES
This transcripts has not been edited or corrected, but appears as received from the commercial transcribing service. Accordingly, the food and Drug Administration makes no representation as to its accuracy.
Meeting of:
TRANSMISSIBLE
SPONGIFORM ENCEPHALOPATHIES
ADVISORY COMMITTEE
September 18, 2006
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
2008
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
2009
----- Original Message -----
From: Freas, William To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:flounder9@verizon.net Cc: mailto:flounder9@verizon.net
Sent: Monday, June 08, 2009 5:32 PM Subject: Written comments regarding TSEAC
Dear Mr. Singeltary,
Thank you for your written statement regarding the June 12, 2009 TSEAC meeting. Your statement will be copied, given to the committee members, made part of the official meeting record and made available to the public.
Thanks again.
Bill Freas Acting TSEAC Exec. Sec.
From: "Terry S. Singeltary Sr." <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:flounder9@verizon.net> To: <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:william.freas@fda.hhs.gov> Cc: "Dave Cavenaugh" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:cott-dc@earthlink.net>; "DR. LAURA MANUELIDIS" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:laura.manuelidis@yale.edu>; <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:rrohwer@umaryland.edu>;ncashman@prionetcanada.ca> Subject: Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission) Date: Sunday, May 10, 2009 12:55 PM TO: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:william.freas@fda.hhs.gov <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:william.freas@fda.hhs.gov>
May 8, 2009
2009 Meeting Materials, Transmissible Spongiform Encephalopathies Advisory Committee
Updated: 6/4/2009
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm129559.htm
Transmissible Spongiform Encephalopathies Advisory Committee 21st Meeting Final Issue Summary June 12, 2009
Holiday Inn 2 Montgomery Village Avenue Gaithersburg, MD 20879
Topic I:
Modified FDA Risk Assessment for Potential Exposure to the Infectious Agent of Variant Creutzfeldt-Jakob Disease (vCJD) in US-licensed Plasma-Derived Factor VIII (pdFVIII)
ISSUE:
Plasma-derived Factor VIII (pdFVIII) products are used by blood clotting disorder patients with von Willebrand disease and some patients with hemophilia A. The announcement in February 2009 by health authorities in the United Kingdom that a vCJD infection had been recognized in a person with hemophilia treated with a UK manufactured "vCJD-implicated" pdFVIII 11 years earlier has prompted FDA to review the potential vCJD risk for US users of US-licensed pdFVIII products and current risk management strategies for such products.
Results from an updated FDA risk assessment model continue to indicate that the estimated risk of the potential for US-licensed pdFVIII products to transmit the agent of vCJD, the human form of "Mad Cow Disease," is highly uncertain but is most likely to be extremely small.
FDA seeks the advice of the Committee on whether additional risk reducing measures are needed (e.g. modifications to current donor deferral policies) to maintain the safety of plasma-derived biologic products and whether FDA should change its communications concerning the risks of vCJD associated with plasma derivatives. ...
snip...
see full text ;
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164322.pdf
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164326.pdf
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164322.pdf
this might be interesting to see what is said here too ;
SNIP...
TSEAC AGENDA, Friday, June 12, 2009 (page 2)
12:30 p.m. Lunch
1:30 p.m. Topic II: Informational Presentations
A. BSE Surveillance and USDA-Regulated Food Controls in the U.S., Janet A. Hughes, DVM, PhD, APHIS, USDA (20')
B. BSE Surveillance and Food/Feed Controls in Europe, Koen van Dyck, DVM, European Commission (20')
C. BSE Surveillance, Animal Feeds and Food Controls in Canada, Dr. Noel Murray, Canadian Food Safety Inspection Agency (20')
D. FDA Enhanced Animal "Feed Ban": Current Status, Burt Pritchett, DVM, CVM, FDA (20')
E. FDA-Regulated Food Controls in the U.S., Amber McCoig, DVM, CFSAN, FDA (20')
F. FDA Proposed BSE "Medical Products" Rule: Current Status, Theresa Finn, Ph. D., OVRR, FDA (20')
SNIP...
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164321.pdf
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm129559.htm
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
Friday, June 12, 2009
vCJD-related abnormal prion protein in a person with haemophilia – an update
http://vcjdtransfusion.blogspot.com/2009/06/vcjd-related-abnormal-prion-protein-in.html
http://vcjdtransfusion.blogspot.com/
Sunday, April 12, 2009
BSE MAD COW TESTING USA 2009 FIGURES
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Saturday, June 13, 2009
BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009
http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html
SPORADIC CJD CASES RISING IN U.S.A 2009 UPDATE
Monday, April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
National Prion Disease Pathology Surveillance Center Cases Examined1
(December 31, 2008)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 42 32 28 4 0 0
1997 115 68 59 9 0 0
1998 93 53 45 7 1 0
1999 115 69 61 8 0 0
2000 151 103 89 14 0 0
2001 210 118 108 9 0 0
2002 258 147 123 22 2 0
2003 273 176 135 41 0 0
2004 335 184 162 21 0 13
2005 346 193 154 38 1 0
2006 380 192 159 32 0 14
2007 370 212 185 26 0 0
2008 383 228 182 23 0 0
TOTAL 30715 17756 1490 254 4 2
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 acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Rev 2/13/09 National
http://www.cjdsurveillance.com/pdf/case-table.pdf
http://www.cjdsurveillance.com/resources-casereport.html
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Greetings,
it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.
are they accumulating ?
did they occur in one year, two years, same state, same city ?
location would be very interesting ?
age group ?
sex ?
how was it determined that nvCJD was ruled out ?
from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS
please see full text here ;
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
don't forget, in people 55 and older, it's 1 in 9,000. the officials seem to forget about that when speaking with the media.
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
http://cjdusa.blogspot.com/
OH, and i might add, confusious is confused again.
IN the states where CJD is only reportable in a certain age group i.e. say only reportable in 55 and younger, how would there ever be an accurate count ???
Connecticut Reportable For under 55 within 12 hours
http://www.ct.gov/dph/lib/dph/infectious_diseases/ctepinews/vol29no1.pdf
In dealing with the news media and public about CJD, it is important to avoid confusion between vCJD and the near half-dozen cases of sporadic CJD that occur in NC each year. Confirmation by brain tissue examination of anyone with suspected CJD/vCJD who is less than 55 years of age is even more important.3
3. “Questions and Answers Regarding Bovine Spongiform Encephalopathy (BSE) and Variant Creutzfeldt-Jakob Disease (vCJD),” Centers for Disease Control and Prevention, 4 January 2007,
www.cdc.gov/ncidod/dvrd/vcjd/qa.htm#surveillance.
http://www.epi.state.nc.us/epi/gcdc/manual/diseasenotes/CREUTZFELDT-JAKOB%20DISEASE_DN.pdf
SO, if CJD is not reportable in some states over age 55, and the rate of CJD in 55 and older is 1 in 9,000, then what is the true count if all states reported it ??? human and animal TSEs and 'friendly fire' i.e. iatrogenic, know no age groups. so why put one on it, and continue to believe in this UKBSEnvCJD only theory $$$
ALL human TSE of ALL ages must be made reportable in every state and Internationally. ...tss
Mad Cow: Linked to thousands of CJD cases?
By STEVE MITCHELL, United Press InternationalPublished: Dec. 30, 2003 at 3:31 PM
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
Rare BSE mutation raises concerns over risks to public health
SIR - Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt-Jakob disease (vCJD) could increase in the human population. Of the atypical BSE cases tested so far, a mutation in the prion protein gene (PRNP) has been detected in just one, a cow in Alabama with BSE; her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATUREVol 45726 February 2009
http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html
see full text ;
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
Monday, June 01, 2009
Biochemical typing of pathological prion protein in aging cattle with BSE
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html
Sunday, June 07, 2009
L-TYPE-BSE, H-TYPE-BSE, C-TYPE-BSE, IBNC-TYPE-BSE, TME, CWD, SCRAPIE, CJD, NORTH AMERICA
http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html
Sunday, May 10, 2009
Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States
http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html
Sunday, May 17, 2009
WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
Saturday, April 04, 2009
An unusually presenting case of sCJD—The VV1 subtype Volume 111, Issue 3, Pages 282-291 (April 2009)
http://creutzfeldt-jakob-disease.blogspot.com/2009/04/unusually-presenting-case-of-scjdthe.html
IT seems we have come full circle from the 'ORIGINAL 10' i.e. the 1st 10 adolescents in the UKBSEnvCJD only theory. and now we find us at the 1st 10 in USA, or is it the first 10, or the tip of the iceburg, many that went undocumented ???
lets look at the full circle, to date ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
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
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
Elsevier Editorial System(tm) for The Lancet Infectious Diseases Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary
Abstract:
TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007. snip...
see full text 31 pages ;
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html
Friday, May 29, 2009
Characterization of a U.S. Sheep Scrapie Isolate with Short Incubation Time
http://scrapie-usa.blogspot.com/2009/05/characterization-of-us-sheep-scrapie.html
Friday, May 29, 2009
Seven Deer Test Positive for Chronic Wasting Disease During 2009 Spring Collections in Hampshire County, West Virginia
http://chronic-wasting-disease.blogspot.com/2009/05/seven-deer-test-positive-for-chronic.html
Tuesday, August 26, 2008
Alzheimer's Transmission of AA-amyloidosis: Similarities with Prion Disorders NEUROPRION 2007 FC4.3
http://betaamyloidcjd.blogspot.com/2008/08/alzheimers-transmission-of-aa.html
Sunday, June 7, 2009
ALZHEIMER'S DISEASE IS TRANSMISSIBLE
http://betaamyloidcjd.blogspot.com/2009/06/alzheimers-disease-is-transmissible.html
Saturday, March 22, 2008
10 Million Baby Boomers to have Alzheimer's in the coming decades 2008 Alzheimer's disease facts and figures
http://betaamyloidcjd.blogspot.com/2008/03/association-between-deposition-of-beta.html
http://betaamyloidcjd.blogspot.com/
see also BMJ year 2000 ;
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... Terry S Singeltary (2 January 2000)
--------------------------------------------------------------------------------
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000
Terry S Singeltary retired Send response to journal: Re: U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
ALL Human and Animal Transmissible Spongiform Encephalopathy, of all phenotypes, of ALL ages, in EVERY State and INTERNATIONALLY, should be made MANDATORY reportable ASAP. to be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Saturday, July, 18, 2009
Greetings,
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. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
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. 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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
2003
Neurology 2003;60:176-181 © 2003 American Academy of Neurology
-------------------------------------------------------------------------------- Views & Reviews
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.
http://www.neurology.org/cgi/content/abstract/60/2/176
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
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
Reply to Singletary 26 March 2003
Ryan A. Maddox, MPH
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication).
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.
http://www.neurology.org/cgi/eletters/60/2/176
Posted On December 20, 2003
Mad Cow Scaremongers
Terry Singletary -- A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.
As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.
Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.
http://www.neurology.org/cgi/eletters/60/2/176
http://www.consumerfreedom.com/article_detail.cfm/article/138
Book
The Pathological Protein
Publisher Springer New York DOI 10.1007/b97488 Copyright 2003 ISBN 978-0-387-95508-7 (Print) 978-0-387-21755-0 (Online) DOI 10.1007/0-387-21755-X_14 Pages 223-237 Subject Collection Humanities, Social Sciences and Law SpringerLink
Laying Odds
snip...
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.
snip...
http://www.springerlink.com/content/r2k2622661473336/
http://books.google.com/books?id=ePbrQNFrHtoC&pg=PA223&lpg=PA223&dq=SINGELTARY+pathological+protein+it
2006
FOOD AND DRUG ADMINISTRATION
DEPARTMENT OF HEALTH AND HUMAN SERVICES
This transcripts has not been edited or corrected, but appears as received from the commercial transcribing service. Accordingly, the food and Drug Administration makes no representation as to its accuracy.
Meeting of:
TRANSMISSIBLE
SPONGIFORM ENCEPHALOPATHIES
ADVISORY COMMITTEE
September 18, 2006
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
2008
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards,
Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
END...TSS
I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
2009
----- Original Message -----
From: Freas, William To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:flounder9@verizon.net Cc: mailto:flounder9@verizon.net
Sent: Monday, June 08, 2009 5:32 PM Subject: Written comments regarding TSEAC
Dear Mr. Singeltary,
Thank you for your written statement regarding the June 12, 2009 TSEAC meeting. Your statement will be copied, given to the committee members, made part of the official meeting record and made available to the public.
Thanks again.
Bill Freas Acting TSEAC Exec. Sec.
From: "Terry S. Singeltary Sr." <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:flounder9@verizon.net> To: <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:william.freas@fda.hhs.gov> Cc: "Dave Cavenaugh" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:cott-dc@earthlink.net>; "DR. LAURA MANUELIDIS" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:laura.manuelidis@yale.edu>; <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:rrohwer@umaryland.edu>;
May 8, 2009
2009 Meeting Materials, Transmissible Spongiform Encephalopathies Advisory Committee
Updated: 6/4/2009
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm129559.htm
Transmissible Spongiform Encephalopathies Advisory Committee 21st Meeting Final Issue Summary June 12, 2009
Holiday Inn 2 Montgomery Village Avenue Gaithersburg, MD 20879
Topic I:
Modified FDA Risk Assessment for Potential Exposure to the Infectious Agent of Variant Creutzfeldt-Jakob Disease (vCJD) in US-licensed Plasma-Derived Factor VIII (pdFVIII)
ISSUE:
Plasma-derived Factor VIII (pdFVIII) products are used by blood clotting disorder patients with von Willebrand disease and some patients with hemophilia A. The announcement in February 2009 by health authorities in the United Kingdom that a vCJD infection had been recognized in a person with hemophilia treated with a UK manufactured "vCJD-implicated" pdFVIII 11 years earlier has prompted FDA to review the potential vCJD risk for US users of US-licensed pdFVIII products and current risk management strategies for such products.
Results from an updated FDA risk assessment model continue to indicate that the estimated risk of the potential for US-licensed pdFVIII products to transmit the agent of vCJD, the human form of "Mad Cow Disease," is highly uncertain but is most likely to be extremely small.
FDA seeks the advice of the Committee on whether additional risk reducing measures are needed (e.g. modifications to current donor deferral policies) to maintain the safety of plasma-derived biologic products and whether FDA should change its communications concerning the risks of vCJD associated with plasma derivatives. ...
snip...
see full text ;
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164322.pdf
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164326.pdf
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164322.pdf
this might be interesting to see what is said here too ;
SNIP...
TSEAC AGENDA, Friday, June 12, 2009 (page 2)
12:30 p.m. Lunch
1:30 p.m. Topic II: Informational Presentations
A. BSE Surveillance and USDA-Regulated Food Controls in the U.S., Janet A. Hughes, DVM, PhD, APHIS, USDA (20')
B. BSE Surveillance and Food/Feed Controls in Europe, Koen van Dyck, DVM, European Commission (20')
C. BSE Surveillance, Animal Feeds and Food Controls in Canada, Dr. Noel Murray, Canadian Food Safety Inspection Agency (20')
D. FDA Enhanced Animal "Feed Ban": Current Status, Burt Pritchett, DVM, CVM, FDA (20')
E. FDA-Regulated Food Controls in the U.S., Amber McCoig, DVM, CFSAN, FDA (20')
F. FDA Proposed BSE "Medical Products" Rule: Current Status, Theresa Finn, Ph. D., OVRR, FDA (20')
SNIP...
http://www.fda.gov/downloads/AdvisoryCommittees/Calendar/UCM164321.pdf
http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm129559.htm
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html
Friday, June 12, 2009
vCJD-related abnormal prion protein in a person with haemophilia – an update
http://vcjdtransfusion.blogspot.com/2009/06/vcjd-related-abnormal-prion-protein-in.html
http://vcjdtransfusion.blogspot.com/
Sunday, April 12, 2009
BSE MAD COW TESTING USA 2009 FIGURES
Month Number of Tests
Feb 2009 -- 1,891
Jan 2009 -- 4,620
http://www.aphis.usda.gov/newsroom/hot_issues/bse/surveillance/ongoing_surv_results.shtml
http://madcowtesting.blogspot.com/2009/04/bse-mad-cow-testing-usa-2009-figures.html
Saturday, June 13, 2009
BSE FEED VIOLATIONS USA UPDATE From 01/01/2009 To 06/10/2009
http://madcowfeed.blogspot.com/2009/06/bse-feed-violations-usa-update-from.html
SPORADIC CJD CASES RISING IN U.S.A 2009 UPDATE
Monday, April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
National Prion Disease Pathology Surveillance Center Cases Examined1
(December 31, 2008)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 42 32 28 4 0 0
1997 115 68 59 9 0 0
1998 93 53 45 7 1 0
1999 115 69 61 8 0 0
2000 151 103 89 14 0 0
2001 210 118 108 9 0 0
2002 258 147 123 22 2 0
2003 273 176 135 41 0 0
2004 335 184 162 21 0 13
2005 346 193 154 38 1 0
2006 380 192 159 32 0 14
2007 370 212 185 26 0 0
2008 383 228 182 23 0 0
TOTAL 30715 17756 1490 254 4 2
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 acquired in Saudi Arabia; 5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; 6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Rev 2/13/09 National
http://www.cjdsurveillance.com/pdf/case-table.pdf
http://www.cjdsurveillance.com/resources-casereport.html
http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45
*5 Includes 20 cases in which the diagnosis is pending, and 17 inconclusive cases; *6 Includes 25 cases with type determination pending in which the diagnosis of vCJD has been excluded.
Greetings,
it would be interesting to know what year these atypical cases occurred, as opposed to lumping them in with the totals only.
are they accumulating ?
did they occur in one year, two years, same state, same city ?
location would be very interesting ?
age group ?
sex ?
how was it determined that nvCJD was ruled out ?
from 1997, the year i started dealing with this nightmare, there were 28 cases (per this report), up until 2007 where the total was 185 cases (per this report), and to date 2008 is at 182. a staggering increase in my opinion, for something that just happens spontaneously as some would have us believe. i don't believe it, not in 85%+ of all sporadic CJD cases. actually, i do not believe yet that anyone has proven that any of the sporadic CJD cases have been proven to be a spontaneous misfolding of a protein. there are many potential routes and sources for the sporadic CJD's. ...TSS
please see full text here ;
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
don't forget, in people 55 and older, it's 1 in 9,000. the officials seem to forget about that when speaking with the media.
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
http://cjdusa.blogspot.com/
OH, and i might add, confusious is confused again.
IN the states where CJD is only reportable in a certain age group i.e. say only reportable in 55 and younger, how would there ever be an accurate count ???
Connecticut Reportable For under 55 within 12 hours
http://www.ct.gov/dph/lib/dph/infectious_diseases/ctepinews/vol29no1.pdf
In dealing with the news media and public about CJD, it is important to avoid confusion between vCJD and the near half-dozen cases of sporadic CJD that occur in NC each year. Confirmation by brain tissue examination of anyone with suspected CJD/vCJD who is less than 55 years of age is even more important.3
3. “Questions and Answers Regarding Bovine Spongiform Encephalopathy (BSE) and Variant Creutzfeldt-Jakob Disease (vCJD),” Centers for Disease Control and Prevention, 4 January 2007,
www.cdc.gov/ncidod/dvrd/vcjd/qa.htm#surveillance.
http://www.epi.state.nc.us/epi/gcdc/manual/diseasenotes/CREUTZFELDT-JAKOB%20DISEASE_DN.pdf
SO, if CJD is not reportable in some states over age 55, and the rate of CJD in 55 and older is 1 in 9,000, then what is the true count if all states reported it ??? human and animal TSEs and 'friendly fire' i.e. iatrogenic, know no age groups. so why put one on it, and continue to believe in this UKBSEnvCJD only theory $$$
ALL human TSE of ALL ages must be made reportable in every state and Internationally. ...tss
Mad Cow: Linked to thousands of CJD cases?
By STEVE MITCHELL, United Press InternationalPublished: Dec. 30, 2003 at 3:31 PM
http://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/UPI-47861072816318/
Rare BSE mutation raises concerns over risks to public health
SIR - Atypical forms (known as H- and L-type) of bovine spongiform encephalopathy (BSE) have recently appeared in several European countries as well as in Japan, Canada and the United States. This raises the unwelcome possibility that variant Creutzfeldt-Jakob disease (vCJD) could increase in the human population. Of the atypical BSE cases tested so far, a mutation in the prion protein gene (PRNP) has been detected in just one, a cow in Alabama with BSE; her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000138/!x-usc:mailto:maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA
NATUREVol 45726 February 2009
http://www.nature.com/nature/journal/v457/n7233/full/4571079b.html
see full text ;
Monday, May 11, 2009
Rare BSE mutation raises concerns over risks to public health
http://bse-atypical.blogspot.com/2009/05/rare-bse-mutation-raises-concerns-over.html
Monday, June 01, 2009
Biochemical typing of pathological prion protein in aging cattle with BSE
http://bse-atypical.blogspot.com/2009/06/biochemical-typing-of-pathological.html
Sunday, June 07, 2009
L-TYPE-BSE, H-TYPE-BSE, C-TYPE-BSE, IBNC-TYPE-BSE, TME, CWD, SCRAPIE, CJD, NORTH AMERICA
http://bse-atypical.blogspot.com/2009/06/l-type-bse-h-type-bse-c-type-bse-ibnc.html
Sunday, May 10, 2009
Identification and characterization of bovine spongiform encephalopathy cases diagnosed and not diagnosed in the United States
http://bse-atypical.blogspot.com/2009/05/identification-and-characterization-of.html
Sunday, May 17, 2009
WHO WILL WATCH THE CHILDREN ? SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
http://downercattle.blogspot.com/2009/05/who-will-watch-children.html
Saturday, April 04, 2009
An unusually presenting case of sCJD—The VV1 subtype Volume 111, Issue 3, Pages 282-291 (April 2009)
http://creutzfeldt-jakob-disease.blogspot.com/2009/04/unusually-presenting-case-of-scjdthe.html
IT seems we have come full circle from the 'ORIGINAL 10' i.e. the 1st 10 adolescents in the UKBSEnvCJD only theory. and now we find us at the 1st 10 in USA, or is it the first 10, or the tip of the iceburg, many that went undocumented ???
lets look at the full circle, to date ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
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
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
Elsevier Editorial System(tm) for The Lancet Infectious Diseases Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary
Abstract:
TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007. snip...
see full text 31 pages ;
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.
http://www.cjdfoundation.org/fact.html
Attending Dr.: Date / Time Admitted : 12/14/97 1228
UTMB University of Texas Medical Branch Galveston, Texas 77555-0543 (409) 772-1238 Fax (409) 772-5683 Pathology Report
FINAL AUTOPSY DIAGNOSIS Autopsy' Office (409)772-2858
FINAL AUTOPSY DIAGNOSIS
I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.
http://creutzfeldt-jakob-disease.blogspot.com/2008/07/heidenhain-variant-creutzfeldt-jakob.html
Friday, May 29, 2009
Characterization of a U.S. Sheep Scrapie Isolate with Short Incubation Time
http://scrapie-usa.blogspot.com/2009/05/characterization-of-us-sheep-scrapie.html
Friday, May 29, 2009
Seven Deer Test Positive for Chronic Wasting Disease During 2009 Spring Collections in Hampshire County, West Virginia
http://chronic-wasting-disease.blogspot.com/2009/05/seven-deer-test-positive-for-chronic.html
Tuesday, August 26, 2008
Alzheimer's Transmission of AA-amyloidosis: Similarities with Prion Disorders NEUROPRION 2007 FC4.3
http://betaamyloidcjd.blogspot.com/2008/08/alzheimers-transmission-of-aa.html
Sunday, June 7, 2009
ALZHEIMER'S DISEASE IS TRANSMISSIBLE
http://betaamyloidcjd.blogspot.com/2009/06/alzheimers-disease-is-transmissible.html
Saturday, March 22, 2008
10 Million Baby Boomers to have Alzheimer's in the coming decades 2008 Alzheimer's disease facts and figures
http://betaamyloidcjd.blogspot.com/2008/03/association-between-deposition-of-beta.html
http://betaamyloidcjd.blogspot.com/
see also BMJ year 2000 ;
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... Terry S Singeltary (2 January 2000)
--------------------------------------------------------------------------------
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000
Terry S Singeltary retired Send response to journal: Re: U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
http://www.bmj.com/cgi/eletters/320/7226/8/b#6117
ALL Human and Animal Transmissible Spongiform Encephalopathy, of all phenotypes, of ALL ages, in EVERY State and INTERNATIONALLY, should be made MANDATORY reportable ASAP. to be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Monday, April 27, 2009
The first Japanese patient with variant Creutzfeldt-Jakob disease (vCJD) Case Report
Case Report The first Japanese patient with variant Creutzfeldt-Jakob disease (vCJD)
Akiyo Shinde, 1 Takenobu Kunieda, 1 Yoshimi Kinoshita, 1 Reika Wate, 1 Satoshi Nakano, 1 Hidefumi Ito, 1 Masahito Yamada, 2 Tetsuyuki Kitamoto, 3 Yosikazu Nakamura, 4 Sadayuki Matsumoto 5 and Hirofumi Kusaka 1 1 Department of Neurology, Kansai Medical University, Moriguchi, 2 Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa, 3 Division of CJD Science and Technology, Department of Prion Research, Center for Translational and Advanced Animal Research on Human Diseases, Tohoku University Graduate School of Medicine, Sendai, 4 Department of Public Health – Inquiry, Jichi Medical University, Shimotsuke, and 5 Department of Neurology, Kitano Hospital, Osaka, Japan Correspondence to Akiyo Shinde, md, Department of Neurology, Kansai Medical University, Fumizono-cho 10-15, Moriguchi 570-8506, Japan. Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:shindea@takii.kmu.ac.jp This case was presented in a preliminary form in the annual meeting of Japanese Neuropathological Association in Tokyo, 2008.
Copyright © 2009 Japanese Society of Neuropathology KEYWORDS latent period • periodic synchronous discharge • pulvinar sign • spongiform encephalopathy • variant Creutzfeldt–Jakob disease
ABSTRACT
Eleven years after a brief visit to some European countries, a 48-year-old Japanese man developed writing difficulty, irritability and general fatigue. Then he complained of dysesthetic pains in his legs, for which benzodiazepines were prescribed. However, at the time pulvinar sign was retrospectively confirmed on brain MRI. Eighteen months after the onset, his gait became ataxic with rapid deterioration of mental status over the following several months. Thirty-one months after the onset, he became akinetic and mute with periodic synchronous discharges on EEG, and died at the age of 51. The total clinical course was approximately 43 months. Pathological examination revealed the characteristic alterations of spongiform encephalopathy, severe in the thalamus, moderate but widely spread in the cerebral cortices, and moderate in the cerebellum. Abundant amyloid plaques were easily identified in the cerebral cortex and the cerebellum on HE staining. Immunohistochemistry for abnormal prion protein (PrPsc) confirmed amyloid plaques in several forms, such as florid, uni- and multi-centric plaques as well as perineuronal and periaxonal deposits in the basal ganglia and synaptic patterns in the thalami. A Western blotting study identified type 2B protease-resistant PrP. This is the first Japanese patient who was definitely diagnosed as variant Creutzfeldt-Jakob disease (vCJD). The pathological findings were similar to those of previous reports of vCJD in the UK. However, the changes were much more severe both in degree and distribution, probably due to a longer duration of the illness than those in the UK.
--------------------------------------------------------------------------------
Received 5 November 2008; revised and accepted 7 January 2009.
DIGITAL OBJECT IDENTIFIER (DOI) 10.1111/j.1440-1789.2009.01006.x About DOI
http://www3.interscience.wiley.com/journal/122241574/abstract?CRETRY=1&SRETRY=0
http://www.ncbi.nlm.nih.gov/pubmed/19389077?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
----- Original Message -----
From: "TERRY SINGELTARY" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:flounder9@VERIZON.NET>
To: <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:BSE-L@LISTS.AEGEE.ORG>
Sent: Tuesday, March 10, 2009 9:03 PM
Subject: [BSE-L] JAPAN-Local governments to carry on BSE testing despite subsidy cuts
-------------------- mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:BSE-L@LISTS.AEGEE.ORG --------------------
11/03/2009 00:54:58
Japan-BSE Testing.
JAPAN-Local governments to carry on BSE testing despite subsidy cuts
Every local government across the country with meat inspection facilities will continue to test all beef cows for mad cow disease during the next fiscal year, a Mainichi survey has found.
The finding comes despite the central government's abolition of about 200 million yen in annual subsidies to local governments for bovine spongiform encephalopathy (BSE) tests. Japan is the only country where all beef cows are tested for the disease.
In August 2005, the Health, Labor and Welfare Ministry deemed that there is no need for BSE tests on cows 20 months old or younger, on the grounds that no cow born before January 2002 has been found infected with BSE and that there is little chance of finding BSE in such young cows even if they have been infected.
Nevertheless, the ministry had extended subsidies to local governments conducting BSE tests on all beef cows until July last year.
Officials in charge at all 77 prefectural and municipal governments that have beef inspection facilities said they will continue BSE tests on all beef cows in fiscal 2009.
Among the reasons given was the need to "maintain the brand image of their locally produced beef" and "prevent confusion in the marketing process."
However, 30 government bodies said that there was no discussion on whether to continue testing. The survey also suggested that governments tend to abide by the policy of their peers and requests from local residents.
"It would take a lot of nerve to stop it while other prefectures are continuing it," said an official at the Akita Prefectural Government.
"We'd like to stop it but we can't gain support from local residents," a Miyagi Prefectural Government representative said. An official at the Yokohama Municipal Government said that the national government needs to take the initiative in convincing the public of the safety of beef.
The Toyohashi Municipal Government in Aichi Prefecture called on the national government to organize a nationwide BSE testing system. "Since beef is marketed in widespread areas, there is no point in conducting inspections on them unless they are coordinated.."
The government has also applied with the World Organization for Animal Health to raise its evaluation of Japan's BSE countermeasures from the lowest level of "a country whose BSE risk is unknown" to the middle level of "a country having a controlled BSE risk.."
Japan filed the application after it was decided to abolish a practice called "pithing" at all meat treatment centers across the country by the end of this fiscal year. In pithing, a wire is inserted into the cow's head to destroy the brains and spinal marrow and to prevent them from thrashing around. The practice is feared to raise the risk of BSE infections.
The government expects its application to be approved at a general meeting of the organization to be held in May this year.
http://www.farminguk.com/news/Japan-BSE-Testing.12958.asp
I applaud Japans effort to continue to try and eradicate BSE (TSE) i.e. mad cow from their herds. A far cry as to what the USDA has done here in the USA. they did just the opposite. the truth hurts sometimes when reality sets in $$$
WITHOUT a doubt, IF the USA, Canada, and Mexico can have a terribly flawed favorable rating, even though they are BSE GBR risk factor III, and even at that it was on flawed data, with all this, why not Japan being as controlled as the USA and North America ??? it's all about money is it not $$$ that's what Prusiner et al told the hearing committee in California ;
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN
''they don't wanna know, the dont' care''
http://maddeer.org/video/embedded/prusinerclip.html
----- Original Message -----
From: TERRY SINGELTARY
To: mailto:BSE-L@LISTS.AEGEE.ORG
Cc:
Sent: Friday, March 06, 2009 4:27 PM
Subject: Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
Journal of Veterinary Medical Science
Vol. 71 (2009) , No. 2 February pp.133-138
Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
Katsuaki SUGIURA1), Toyoko KUSAMA1), Tomotaro YOSHIDA1), Naoki SHINODA1) and Takashi ONODERA2)
1) Food and Agricultural Materials Inspection Center 2) Department of Molecular Immunology, University of Tokyo
(Received 10-Mar-2008) (Accepted 3-Sep-2008)
ABSTRACT. All cattle imported from the United Kingdom to Japan since 1980 and slaughtered before 2002 were traced (n=33), and the number of cattle that were possibly infected with BSE and entered the animal feed chain was calculated. Because there was no effective system to avoid recycling of the BSE agent via animal feed until the early 1990s, of the 33 cattle imported from the UK into Japan, most probably 7 or 8 were infected and entered the animal feed chain, 2 of which entered the animal feed chain in each of 1992 and 1993. In terms of infectivity, 400-550 cattle oral ID50 of the BSE agent entered the feed chain in each of these years. The amount of infectivity that entered the feed chain in 1989, 1991 and 1995 was smaller but still substantial, suggesting that the BSE agent might have entered the Japanese feed chain in any of these years.
KEY WORDS: bovine spongiform encephalopathy (BSE), import risk analysis, Japan, live cattle, simulation
snip...
http://www.jstage.jst.go.jp/article/jvms/71/2/133/_pdf
REFERENCES
http://www.jstage.jst.go.jp/article/jvms/71/2/71_133/_cit
Greetings BSE-L members !
Because there was no effective system to avoid recycling of the BSE agent via animal feed until the early 1990s, of the 33 cattle imported from the UK into Japan, most probably 7 or 8 were infected and entered the animal feed chain, 2 of which entered the animal feed chain in each of 1992 and 1993. In terms of infectivity, 400-550 cattle oral ID50 of the BSE agent entered the feed chain in each of these years. The amount of infectivity that entered the feed chain in 1989, 1991 and 1995 was smaller but still substantial, suggesting that the BSE agent might have entered the Japanese feed chain in any of these years.<<< usa =" 496" canada =" 198" href="http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf">http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf
HERE is another look at all the imports for both the USA and Canada of UK live cattle and greaves exports ;
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK EXPORTS OF MBM TO WORLD
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
OTHERS
SNIP...
*** SEE FULL TEXT ;
Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
http://bseusa.blogspot.com/2009/03/risk-of-introduction-of-bse-into-japan.html
SEE FULL TEXT HERE ;
Tuesday, March 10, 2009
JAPAN-Local governments to carry on BSE testing despite subsidy cuts
http://madcowtesting.blogspot.com/2009/03/japan-local-governments-to-carry-on-bse.html
USA
Monday, April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
TSS
Akiyo Shinde, 1 Takenobu Kunieda, 1 Yoshimi Kinoshita, 1 Reika Wate, 1 Satoshi Nakano, 1 Hidefumi Ito, 1 Masahito Yamada, 2 Tetsuyuki Kitamoto, 3 Yosikazu Nakamura, 4 Sadayuki Matsumoto 5 and Hirofumi Kusaka 1 1 Department of Neurology, Kansai Medical University, Moriguchi, 2 Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Kanazawa, 3 Division of CJD Science and Technology, Department of Prion Research, Center for Translational and Advanced Animal Research on Human Diseases, Tohoku University Graduate School of Medicine, Sendai, 4 Department of Public Health – Inquiry, Jichi Medical University, Shimotsuke, and 5 Department of Neurology, Kitano Hospital, Osaka, Japan Correspondence to Akiyo Shinde, md, Department of Neurology, Kansai Medical University, Fumizono-cho 10-15, Moriguchi 570-8506, Japan. Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:shindea@takii.kmu.ac.jp This case was presented in a preliminary form in the annual meeting of Japanese Neuropathological Association in Tokyo, 2008.
Copyright © 2009 Japanese Society of Neuropathology KEYWORDS latent period • periodic synchronous discharge • pulvinar sign • spongiform encephalopathy • variant Creutzfeldt–Jakob disease
ABSTRACT
Eleven years after a brief visit to some European countries, a 48-year-old Japanese man developed writing difficulty, irritability and general fatigue. Then he complained of dysesthetic pains in his legs, for which benzodiazepines were prescribed. However, at the time pulvinar sign was retrospectively confirmed on brain MRI. Eighteen months after the onset, his gait became ataxic with rapid deterioration of mental status over the following several months. Thirty-one months after the onset, he became akinetic and mute with periodic synchronous discharges on EEG, and died at the age of 51. The total clinical course was approximately 43 months. Pathological examination revealed the characteristic alterations of spongiform encephalopathy, severe in the thalamus, moderate but widely spread in the cerebral cortices, and moderate in the cerebellum. Abundant amyloid plaques were easily identified in the cerebral cortex and the cerebellum on HE staining. Immunohistochemistry for abnormal prion protein (PrPsc) confirmed amyloid plaques in several forms, such as florid, uni- and multi-centric plaques as well as perineuronal and periaxonal deposits in the basal ganglia and synaptic patterns in the thalami. A Western blotting study identified type 2B protease-resistant PrP. This is the first Japanese patient who was definitely diagnosed as variant Creutzfeldt-Jakob disease (vCJD). The pathological findings were similar to those of previous reports of vCJD in the UK. However, the changes were much more severe both in degree and distribution, probably due to a longer duration of the illness than those in the UK.
--------------------------------------------------------------------------------
Received 5 November 2008; revised and accepted 7 January 2009.
DIGITAL OBJECT IDENTIFIER (DOI) 10.1111/j.1440-1789.2009.01006.x About DOI
http://www3.interscience.wiley.com/journal/122241574/abstract?CRETRY=1&SRETRY=0
http://www.ncbi.nlm.nih.gov/pubmed/19389077?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
----- Original Message -----
From: "TERRY SINGELTARY" <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:flounder9@VERIZON.NET>
To: <mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:BSE-L@LISTS.AEGEE.ORG>
Sent: Tuesday, March 10, 2009 9:03 PM
Subject: [BSE-L] JAPAN-Local governments to carry on BSE testing despite subsidy cuts
-------------------- mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000276/!x-usc:mailto:BSE-L@LISTS.AEGEE.ORG --------------------
11/03/2009 00:54:58
Japan-BSE Testing.
JAPAN-Local governments to carry on BSE testing despite subsidy cuts
Every local government across the country with meat inspection facilities will continue to test all beef cows for mad cow disease during the next fiscal year, a Mainichi survey has found.
The finding comes despite the central government's abolition of about 200 million yen in annual subsidies to local governments for bovine spongiform encephalopathy (BSE) tests. Japan is the only country where all beef cows are tested for the disease.
In August 2005, the Health, Labor and Welfare Ministry deemed that there is no need for BSE tests on cows 20 months old or younger, on the grounds that no cow born before January 2002 has been found infected with BSE and that there is little chance of finding BSE in such young cows even if they have been infected.
Nevertheless, the ministry had extended subsidies to local governments conducting BSE tests on all beef cows until July last year.
Officials in charge at all 77 prefectural and municipal governments that have beef inspection facilities said they will continue BSE tests on all beef cows in fiscal 2009.
Among the reasons given was the need to "maintain the brand image of their locally produced beef" and "prevent confusion in the marketing process."
However, 30 government bodies said that there was no discussion on whether to continue testing. The survey also suggested that governments tend to abide by the policy of their peers and requests from local residents.
"It would take a lot of nerve to stop it while other prefectures are continuing it," said an official at the Akita Prefectural Government.
"We'd like to stop it but we can't gain support from local residents," a Miyagi Prefectural Government representative said. An official at the Yokohama Municipal Government said that the national government needs to take the initiative in convincing the public of the safety of beef.
The Toyohashi Municipal Government in Aichi Prefecture called on the national government to organize a nationwide BSE testing system. "Since beef is marketed in widespread areas, there is no point in conducting inspections on them unless they are coordinated.."
The government has also applied with the World Organization for Animal Health to raise its evaluation of Japan's BSE countermeasures from the lowest level of "a country whose BSE risk is unknown" to the middle level of "a country having a controlled BSE risk.."
Japan filed the application after it was decided to abolish a practice called "pithing" at all meat treatment centers across the country by the end of this fiscal year. In pithing, a wire is inserted into the cow's head to destroy the brains and spinal marrow and to prevent them from thrashing around. The practice is feared to raise the risk of BSE infections.
The government expects its application to be approved at a general meeting of the organization to be held in May this year.
http://www.farminguk.com/news/Japan-BSE-Testing.12958.asp
I applaud Japans effort to continue to try and eradicate BSE (TSE) i.e. mad cow from their herds. A far cry as to what the USDA has done here in the USA. they did just the opposite. the truth hurts sometimes when reality sets in $$$
WITHOUT a doubt, IF the USA, Canada, and Mexico can have a terribly flawed favorable rating, even though they are BSE GBR risk factor III, and even at that it was on flawed data, with all this, why not Japan being as controlled as the USA and North America ??? it's all about money is it not $$$ that's what Prusiner et al told the hearing committee in California ;
DAMNING TESTIMONY FROM STANLEY PRUSINER THE NOBEL PEACE PRIZE WINNER ON PRIONS SPEAKING ABOUT ANN VENEMAN
''they don't wanna know, the dont' care''
http://maddeer.org/video/embedded/prusinerclip.html
----- Original Message -----
From: TERRY SINGELTARY
To: mailto:BSE-L@LISTS.AEGEE.ORG
Cc:
Sent: Friday, March 06, 2009 4:27 PM
Subject: Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
Journal of Veterinary Medical Science
Vol. 71 (2009) , No. 2 February pp.133-138
Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
Katsuaki SUGIURA1), Toyoko KUSAMA1), Tomotaro YOSHIDA1), Naoki SHINODA1) and Takashi ONODERA2)
1) Food and Agricultural Materials Inspection Center 2) Department of Molecular Immunology, University of Tokyo
(Received 10-Mar-2008) (Accepted 3-Sep-2008)
ABSTRACT. All cattle imported from the United Kingdom to Japan since 1980 and slaughtered before 2002 were traced (n=33), and the number of cattle that were possibly infected with BSE and entered the animal feed chain was calculated. Because there was no effective system to avoid recycling of the BSE agent via animal feed until the early 1990s, of the 33 cattle imported from the UK into Japan, most probably 7 or 8 were infected and entered the animal feed chain, 2 of which entered the animal feed chain in each of 1992 and 1993. In terms of infectivity, 400-550 cattle oral ID50 of the BSE agent entered the feed chain in each of these years. The amount of infectivity that entered the feed chain in 1989, 1991 and 1995 was smaller but still substantial, suggesting that the BSE agent might have entered the Japanese feed chain in any of these years.
KEY WORDS: bovine spongiform encephalopathy (BSE), import risk analysis, Japan, live cattle, simulation
snip...
http://www.jstage.jst.go.jp/article/jvms/71/2/133/_pdf
REFERENCES
http://www.jstage.jst.go.jp/article/jvms/71/2/71_133/_cit
Greetings BSE-L members !
Because there was no effective system to avoid recycling of the BSE agent via animal feed until the early 1990s, of the 33 cattle imported from the UK into Japan, most probably 7 or 8 were infected and entered the animal feed chain, 2 of which entered the animal feed chain in each of 1992 and 1993. In terms of infectivity, 400-550 cattle oral ID50 of the BSE agent entered the feed chain in each of these years. The amount of infectivity that entered the feed chain in 1989, 1991 and 1995 was smaller but still substantial, suggesting that the BSE agent might have entered the Japanese feed chain in any of these years.<<< usa =" 496" canada =" 198" href="http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf">http://www.inspection.gc.ca/english/sci/ahra/bseris/bserise.pdf
HERE is another look at all the imports for both the USA and Canada of UK live cattle and greaves exports ;
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK EXPORTS OF MBM TO WORLD
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
OTHERS
SNIP...
*** SEE FULL TEXT ;
Risk of Introduction of BSE into Japan by the Historical Importation of Live Cattle from the United Kingdom
http://bseusa.blogspot.com/2009/03/risk-of-introduction-of-bse-into-japan.html
SEE FULL TEXT HERE ;
Tuesday, March 10, 2009
JAPAN-Local governments to carry on BSE testing despite subsidy cuts
http://madcowtesting.blogspot.com/2009/03/japan-local-governments-to-carry-on-bse.html
USA
Monday, April 20, 2009
National Prion Disease Pathology Surveillance Center Cases Examined1 (December 31, 2008)
http://prionunitusaupdate2008.blogspot.com/2009/04/national-prion-disease-pathology.html
TSS
Tuesday, April 21, 2009
Doctor Antonio Ruiz Villaespesa, pathologist and CJD researcher deceased because of Creutzfeldt-Jakob Disease SPAIN
CESM lamenta la muerte del anatomopatólogo Ruiz Villaespesa, relacionada con el ejercicio de su profesión
La Confederación Estatal de Sindicatos Médicos (CESM) lamenta profundamente la muerte del doctor Antonio Ruiz Villaespesa, fallecido según todos los indicios por la enfermedad de Creutzfeldt-Jakob, y pide que desde todas las instancias concernidas se extremen las medidas de protección adecuadas para que casos así nunca vuelvan a producirse.
Hay que recordar que este jefe del servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias (Alcalá de Henares), era además neuropatólogo y llevaba acumuladas más de 500 necropsias relativas a esta subespecialidad, de lo que se deduce que pudo entrar en más de una ocasión en contacto con polvo óseo procedente de cráneos humanos afectados por la Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob).
Es sabido, por otra parte, que esta enfermedad no sólo se transmite por comer carne o entrar en contacto directo con los tejidos de de animales contaminados. Hay otra modalidad de transmisión, la iatrogénica o CJD, que se produce a partir de procesos quirúrgicos, como trasplante de córnea de donantes infectados o la trepanación craneal para realizar necropsias. En estos casos, a los que estuvo expuesto en más de una ocasión el compañero fallecido, se produce un polvo óseo a través del cual pueden difundirse priones (partículas más pequeñas que los virus) que una vez inhalados son capaces de desencadenar el síndrome referido.
Dado que estamos ante un tipo de enfermedad profesional así reconocido, CESM no duda de que el doctor Ruiz Villaespesa contaba con todos los recursos necesarios para protegerse de la transmisión, aunque como organización que tiene entre sus fines velar por las condiciones en que se lleva a cabo el trabajo de los médicos, sí considera conveniente hacer una llamada de atención para que existan todas las garantías al respecto.
En cuanto al compañero fallecido sólo nos resta extender nuestro pesar a su familia y rendirle tributo a él personalmente por haber muerto a causa de su entrega a la ciencia. Sin duda él sabía el riesgo a que se exponía, y lo afrontó en beneficio de su profesión y de los pacientes a los que se debía. Que descanse en paz.
Noticias relacionadas:
En España habrá unos 20 afectados por el mal de las "vacas locas", pero Villaescusa no está entre ellos, según Badiola/30-03-2009
Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob /30-03-2009
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505932&categoria=34
Confederación Estatal de Sindicatos Médicos (CESM) lamenta profundamente la muerte del doctor Antonio Ruiz Villaespesa, fallecido a causa de la enfermedad de Creutzfeldt-Jakob, y pide que desde todas las instancias concernidas se extremen las medidas de protección adecuadas para que casos así nunca vuelvan a producirse. Hay que recordar que este jefe del servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias (Alcalá de Henares), era además neuropatólogo y llevaba acumuladas más de 500 autopsias clínicas, de lo que se deduce que pudo entrar en más de una ocasión en contacto con polvo óseo procedente de cráneos humanos afectados por la Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob). Es sabido, por otra parte, que esta enfermedad no sólo se transmite por comer carne o entrar en contacto directo con los tejidos de de animales contaminados. Hay otra modalidad de transmisión, la iatrogénica o CJD, que se produce a partir de procesos quirúrgicos, como trasplante de córnea de donantes infectados o la trepanación craneal para realizar necropsias. En estos casos, a los que estuvo expuesto en más de una ocasión el compañero fallecido, se produce un polvo óseo a través del cual pueden difundirse priones (partículas más pequeñas que los virus) que una vez inhalados son capaces de desencadenar el síndrome referido. Dado que estamos ante un tipo de enfermedad profesional así reconocido, CESM no duda de que el doctor Ruiz Villaespesa contaba con todos los recursos necesarios para protegerse de la transmisión, aunque como organización que tiene entre sus fines velar por las condiciones en que se lleva a cabo el trabajo de los médicos, sí considera conveniente hacer una llamada de atención para que existan todas las garantías al respecto. En cuanto al compañero fallecido sólo nos resta extender nuestro pesar a su familia y rendirle tributo a él personalmente por haber muerto a causa de su entrega a la ciencia. Sin duda él sabía el riesgo a que se exponía, y lo afrontó en beneficio de su profesión y de los pacientes a los que se debía. Que descanse en paz. Noticias relacionadas: Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob /30-03-2009 lunes, 30 de marzo de 2009. Publicado por: CESM
http://www.simeg.org/noticiasanteriores/noticias2009/documents/CESM30-03-09.pdf
In English
State confederation of Medical Unions (CESM) is sorry deeply death of doctor Antonio Ruiz Villaespesa, deceased because of the disease of Creutzfeldt-Jakob, and asks that from all the concerned instances the suitable measures of protection are carried far so that cases thus never return a to take place. It is necessary to remember that this head of the service of Pathological Anatomy of the University Hospital Prince of Asturias (Alcala de Henares), he was in addition neuropatólogo and it took accumulated more than 500 clinical autopsies, than it is deduced that it could enter more than an occasion in contact with bony dust coming from human skulls affected by Human Transmissible Spongiform Encephalopathy (Creutzfeldt-Jakob). It is known, on the other hand, that this disease not only is transmitted to eat meat or to enter direct bonding with weaves of of contaminated animal. There is another modality of transmission, iatrogenic or the CJD, that takes place from surgical processes, as transplant of cornea of infected donors or cranial trepanation to realise post-mortem examinations. In these cases, to which it was exposed in more than an occasion the passed away companion, takes place a bony dust through what they can spread priones (particles smaller than the virus) that once inhaled is able to trigger the referred syndrome. Since we are before a type of professional disease thus recognized, CESM nondoubt that doctor Ruiz Villaespesa counted on all the resources necessary to protect themselves of the transmission, although like organization whom it has between his aims velar by the conditions in which the work of the doctors is carried out, yes considers advisable to make a call of attention so that all the exist guarantees on the matter. As far as the passed away companion to only it remains us to extend our grief to his family and to render tribute to him to him personally by to have died because of his delivery to science. Without a doubt he knew the risk to that he was exposed, confronted and it to the benefit of its profession and of the patients to whom it had. That it rests peacefully. The related news: The head of Pathological Anatomy of the Hospital of Alcala de Henares by possible Creutzfeldt-Jakob /30-03-2009 passes away Monday, 30 of March of 2009. Published by: CESM
En España habrá unos 20 afectados por el mal de las "vacas locas", pero Villaespesa no está entre ellos, según Badiola
Cree que este experto fue "víctima de su propia profesión", aunque de ser así el contagio se habría producido hace más de 15 años
MADRID, 30 Mar. (EUROPA PRESS) - El director del Centro Nacional de Referencia de las Encefalopatías Espongiformes Transmisibles, Juan José Badiola, afirmó hoy que en España está previsto que se diagnostiquen en los próximos años entre 15 y 20 casos por la variante en humanos de la encefalopatía espongiforme de Creutzfeldt-Jakob (EETH), conocido como el mal de las ´vacas locas´, aunque no cree que entre ellos esté el jefe del Servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias, Antonio Ruiz Villaespesa, que falleció este viernes por causas que todavía se desconocen.
Badiola quiso distinguir así entre la variante humana de esta enfermedad, relacionada con la ingesta de carne con tejido nervioso infectado y de la que ya se han detectado cinco casos en España desde 2005 y más de 160 en Reino Unido, y otros tipos como el esporádico o iatrogénico, en cuyo caso la muerte de este experto estaría causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo.
Según el diagnóstico principal y falta de los resultados que determinen el origen de la enfermedad, el Gobierno de la Comunidad de Madrid afirma que la muerte de Ruiz Villaespesa estaría asociada a cualquiera de estas dos últimas variantes.
"Parece que este experto murió víctima de su propia profesión", explicó Badiola, quien matizó que de ser así el contagio se habría producido hace más de 15 años, ya que es éste el tiempo que tarda en incubarse la enfermedad hasta que aparece los primeros síntomas.
Además, de confirmarse esta hipótesis, Badiola aseguró que "hace 20 años no existían los mismos protocolos de seguridad que ahora" por lo que considera normal que se pudiera haber producido algún contagio, "sobre todo en un hombre que realizó tantas autopsias en su vida como él".
Desde el año 2001 se han registrado en España 702 casos de EETH, de los cuales 87 se han notificado en la Comunidad de Madrid, y sólo cinco son la variante humana de esta enfermedad, conocida desde hace más de un siglo pero cuyos estudios se intensificaron tras la aparición de una nueva variante en los años 90 en Inglaterra.
Sin embargo, y dado el periodo de incubación de la variante humana de la enfermedad, Badiola aseguró que se seguirán detectando algunos casos más, aunque todos ellos se tratarán de contagios precedentes a la entrada en vigor de la red de vigilancia establecido en toda Europa a raíz de los primeros casos en Reino Unido.
lunes, 30 de marzo de 2009.
Publicado por: CESM
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505936&categoria=34
Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob
El jefe del Servicio de Anatomía Patológica del Hospital General de Alcalá de Henares, Antonio Ruiz Villaespesa, falleció el sábado en dicho centro sanitario diagnosticado de posible enfermedad de Creutzfeldt-Jakob, según informó el sábado el Gobierno regional madrileño y recogen EUROPA PRESS y demás medios. Según el diagnóstico principal, se trata de un caso calificado de probable Creutzfeldt-Jakob, bien esporádico o iatrogénico. Dada la profesión del fallecido, habrá que establecer si la enfermedad ha sido causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo. En estos momentos se están realizando las pruebas necesarias para proceder al diagnóstico definitivo del tipo de EETH, lo que se confirmará con un estudio posmorten o necropsia.
Este doctor, de prestigio nacional e internacional en los campos de la anamopatología y la neuropatología, dedicó gran parte de su vida profesional al estudio de la Encefalopatía Espongiforme Transmisible Humana (EETH).
Su actividad profesional se desarrolló desde los años 70, primero en el hospital de La Paz, y posteriormente, en el Príncipe de Asturias, habiendo dedicado toda su vida a la sanidad pública y al diagnóstico de enfermedades.
Más información: EL PAIS, EL MUNDO
lunes, 30 de marzo de 2009.
Publicado por: CESM
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505930&categoria=34
Se estudian las causas del contagio Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob
MADRID, 29 Mar (EUROPA PRESS) El jefe del Servicio de Anatomía Patológica del Hospital General de Alcalá de Henares, Antonio Ruiz Villaescusa, falleció el sábado en dicho centro sanitario diagnosticado de posible enfermedad de Creutzfeldt-Jakob, según informó ayer el Gobierno regional madrileño.
Este doctor, de prestigio nacional e internacional en los campos de la anamopatología y la neuropatología, dedicó gran parte de su vida profesional al estudio de la Encefalopatía Espongiforme Transmisible Humana (EETH).
Su actividad profesional se desarrolló desde los años 70, primero en el hospital de La Paz, y posteriormente, en el Príncipe de Asturias, habiendo dedicado toda su vida a la sanidad pública y al diagnóstico de enfermedades.
Según el diagnóstico principal, se trata de un caso calificado de probable Creutzfeldt-Jakob, bien esporádico o iatrogénico. Dada la profesión del fallecido, habrá que establecer si la enfermedad ha sido causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo.
En estos momentos se están realizando las pruebas necesarias para proceder al diagnóstico definitivo del tipo de EETH, lo que se confirmará con un estudio posmorten o necropsia.
En principio, el caso no está relacionado con la ingesta de carne contaminada por priones (una partícula transmisible), que se asocia con la variante humana de Creutzfeldt-Jakob (vECJ), ya que se ha demostrado que hay "considerables diferencias" en la manifestación clínica y la duración de la enfermedad desde su diagnóstico hasta la defunción del paciente.
Desde el año 2001 se han registrado en España 702 casos de EETH, de los cuales 87 se han notificado en la Comunidad de Madrid.
La Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob) es una enfermedad conocida desde hace más de un siglo, pero los estudios sobre la misma se intensificaron tras la aparición de una nueva variante en los años 90 en Inglaterra.
El Jefe de Servicio de Anatomía Patológica de la Fundación Alcorcón, el doctor Rábano, se encargará de realizar la autopsia, cuyos resultados finales se conocerán aproximadamente en un mes.
La Consejería de Sanidad de la Comunidad de Madrid ya ha puesto en conocimiento de la Dirección General de Salud Pública del Ministerio de Sanidad dicho fallecimiento.
http://www.europapress.es/madrid/noticia-fallece-jefe-anatomia-patologica-hospital-alcala-henares-posible-creutzfeldt-jakob-20090329140143.html
stats for Spain as follows as of March 10, 2009. nvCJD holds at 5 documented to date, and 3 probable cases of sporadic CJD to date. does not mean that a case of nvCJD could not transmit, and or has not transmitted via 'friendly fire' i.e. the medical and or surgical and or occupational arena, and or what that pathology might look like via 2nd, 3rd, 4th passaged. will it continue to look like nvCJD or will it look like sporadic CJD and or any of the subtypes there of ? this case in question as ProMED said, has a great deal of information lacking to date. hopefully, a short report will be forth coming from the Instituto de Salud Carlos III. until then, i thought some of you might be interested in the recent stats. page 12 of 23 has a good chart. on the sporadic cjd cases, in terms of 3 to date, that was for 2009 'probable'. the reference to the nvCJD was a total of 5.....terry
(Situación a 10 de marzo de 2009) ;
REGISTRO NACIONAL DE ENCEFALOPATÍAS ESPONGIFORMES TRANSMISIBLES HUMANAS C.N.E y Servicios de Vigilancia Epidemiológica de CCAA (Situación a 10 de marzo de 2009)
http://www.isciii.es/htdocs/pdf/DatosRegistroCreutzfeldJacob2.pdf
ALSO, please note ;
SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)
SEAC
Agenda
102nd Meeting on Wednesday 4 March 2009
Room 808, Nobel House, 17 Smith Square, Defra, London SW1P 3JR
10.05 Approval of draft minutes from SEAC 101
snip...
ITEM 3 - CURRENT ISSUES 8. SEAC was informed about the following issues: . A mother and son in Spain had died of variant Creutzfeldt-Jakob Disease (vCJD). This is the first recorded instance of more than one case of vCJD within one family. As both the mother and son lived in a region of Spain with a history of BSE, had frequently shared meals of cattle brain, and as no other risk factor has been identified, it seems most likely that both infections were acquired from dietary exposure. Furthermore, the similar times of onset of disease of the cases did not suggest transmission had occurred from one to the other.
snip...
Thursday, February 26, 2009
SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)
see full text ;
http://www.seac.gov.uk/papers/102-1.pdf
http://seac992007.blogspot.com/2009/02/seac-102nd-meeting-on-wednesday-4-march.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
La Confederación Estatal de Sindicatos Médicos (CESM) lamenta profundamente la muerte del doctor Antonio Ruiz Villaespesa, fallecido según todos los indicios por la enfermedad de Creutzfeldt-Jakob, y pide que desde todas las instancias concernidas se extremen las medidas de protección adecuadas para que casos así nunca vuelvan a producirse.
Hay que recordar que este jefe del servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias (Alcalá de Henares), era además neuropatólogo y llevaba acumuladas más de 500 necropsias relativas a esta subespecialidad, de lo que se deduce que pudo entrar en más de una ocasión en contacto con polvo óseo procedente de cráneos humanos afectados por la Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob).
Es sabido, por otra parte, que esta enfermedad no sólo se transmite por comer carne o entrar en contacto directo con los tejidos de de animales contaminados. Hay otra modalidad de transmisión, la iatrogénica o CJD, que se produce a partir de procesos quirúrgicos, como trasplante de córnea de donantes infectados o la trepanación craneal para realizar necropsias. En estos casos, a los que estuvo expuesto en más de una ocasión el compañero fallecido, se produce un polvo óseo a través del cual pueden difundirse priones (partículas más pequeñas que los virus) que una vez inhalados son capaces de desencadenar el síndrome referido.
Dado que estamos ante un tipo de enfermedad profesional así reconocido, CESM no duda de que el doctor Ruiz Villaespesa contaba con todos los recursos necesarios para protegerse de la transmisión, aunque como organización que tiene entre sus fines velar por las condiciones en que se lleva a cabo el trabajo de los médicos, sí considera conveniente hacer una llamada de atención para que existan todas las garantías al respecto.
En cuanto al compañero fallecido sólo nos resta extender nuestro pesar a su familia y rendirle tributo a él personalmente por haber muerto a causa de su entrega a la ciencia. Sin duda él sabía el riesgo a que se exponía, y lo afrontó en beneficio de su profesión y de los pacientes a los que se debía. Que descanse en paz.
Noticias relacionadas:
En España habrá unos 20 afectados por el mal de las "vacas locas", pero Villaescusa no está entre ellos, según Badiola/30-03-2009
Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob /30-03-2009
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505932&categoria=34
Confederación Estatal de Sindicatos Médicos (CESM) lamenta profundamente la muerte del doctor Antonio Ruiz Villaespesa, fallecido a causa de la enfermedad de Creutzfeldt-Jakob, y pide que desde todas las instancias concernidas se extremen las medidas de protección adecuadas para que casos así nunca vuelvan a producirse. Hay que recordar que este jefe del servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias (Alcalá de Henares), era además neuropatólogo y llevaba acumuladas más de 500 autopsias clínicas, de lo que se deduce que pudo entrar en más de una ocasión en contacto con polvo óseo procedente de cráneos humanos afectados por la Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob). Es sabido, por otra parte, que esta enfermedad no sólo se transmite por comer carne o entrar en contacto directo con los tejidos de de animales contaminados. Hay otra modalidad de transmisión, la iatrogénica o CJD, que se produce a partir de procesos quirúrgicos, como trasplante de córnea de donantes infectados o la trepanación craneal para realizar necropsias. En estos casos, a los que estuvo expuesto en más de una ocasión el compañero fallecido, se produce un polvo óseo a través del cual pueden difundirse priones (partículas más pequeñas que los virus) que una vez inhalados son capaces de desencadenar el síndrome referido. Dado que estamos ante un tipo de enfermedad profesional así reconocido, CESM no duda de que el doctor Ruiz Villaespesa contaba con todos los recursos necesarios para protegerse de la transmisión, aunque como organización que tiene entre sus fines velar por las condiciones en que se lleva a cabo el trabajo de los médicos, sí considera conveniente hacer una llamada de atención para que existan todas las garantías al respecto. En cuanto al compañero fallecido sólo nos resta extender nuestro pesar a su familia y rendirle tributo a él personalmente por haber muerto a causa de su entrega a la ciencia. Sin duda él sabía el riesgo a que se exponía, y lo afrontó en beneficio de su profesión y de los pacientes a los que se debía. Que descanse en paz. Noticias relacionadas: Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob /30-03-2009 lunes, 30 de marzo de 2009. Publicado por: CESM
http://www.simeg.org/noticiasanteriores/noticias2009/documents/CESM30-03-09.pdf
In English
State confederation of Medical Unions (CESM) is sorry deeply death of doctor Antonio Ruiz Villaespesa, deceased because of the disease of Creutzfeldt-Jakob, and asks that from all the concerned instances the suitable measures of protection are carried far so that cases thus never return a to take place. It is necessary to remember that this head of the service of Pathological Anatomy of the University Hospital Prince of Asturias (Alcala de Henares), he was in addition neuropatólogo and it took accumulated more than 500 clinical autopsies, than it is deduced that it could enter more than an occasion in contact with bony dust coming from human skulls affected by Human Transmissible Spongiform Encephalopathy (Creutzfeldt-Jakob). It is known, on the other hand, that this disease not only is transmitted to eat meat or to enter direct bonding with weaves of of contaminated animal. There is another modality of transmission, iatrogenic or the CJD, that takes place from surgical processes, as transplant of cornea of infected donors or cranial trepanation to realise post-mortem examinations. In these cases, to which it was exposed in more than an occasion the passed away companion, takes place a bony dust through what they can spread priones (particles smaller than the virus) that once inhaled is able to trigger the referred syndrome. Since we are before a type of professional disease thus recognized, CESM nondoubt that doctor Ruiz Villaespesa counted on all the resources necessary to protect themselves of the transmission, although like organization whom it has between his aims velar by the conditions in which the work of the doctors is carried out, yes considers advisable to make a call of attention so that all the exist guarantees on the matter. As far as the passed away companion to only it remains us to extend our grief to his family and to render tribute to him to him personally by to have died because of his delivery to science. Without a doubt he knew the risk to that he was exposed, confronted and it to the benefit of its profession and of the patients to whom it had. That it rests peacefully. The related news: The head of Pathological Anatomy of the Hospital of Alcala de Henares by possible Creutzfeldt-Jakob /30-03-2009 passes away Monday, 30 of March of 2009. Published by: CESM
En España habrá unos 20 afectados por el mal de las "vacas locas", pero Villaespesa no está entre ellos, según Badiola
Cree que este experto fue "víctima de su propia profesión", aunque de ser así el contagio se habría producido hace más de 15 años
MADRID, 30 Mar. (EUROPA PRESS) - El director del Centro Nacional de Referencia de las Encefalopatías Espongiformes Transmisibles, Juan José Badiola, afirmó hoy que en España está previsto que se diagnostiquen en los próximos años entre 15 y 20 casos por la variante en humanos de la encefalopatía espongiforme de Creutzfeldt-Jakob (EETH), conocido como el mal de las ´vacas locas´, aunque no cree que entre ellos esté el jefe del Servicio de Anatomía Patológica del Hospital Universitario Príncipe de Asturias, Antonio Ruiz Villaespesa, que falleció este viernes por causas que todavía se desconocen.
Badiola quiso distinguir así entre la variante humana de esta enfermedad, relacionada con la ingesta de carne con tejido nervioso infectado y de la que ya se han detectado cinco casos en España desde 2005 y más de 160 en Reino Unido, y otros tipos como el esporádico o iatrogénico, en cuyo caso la muerte de este experto estaría causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo.
Según el diagnóstico principal y falta de los resultados que determinen el origen de la enfermedad, el Gobierno de la Comunidad de Madrid afirma que la muerte de Ruiz Villaespesa estaría asociada a cualquiera de estas dos últimas variantes.
"Parece que este experto murió víctima de su propia profesión", explicó Badiola, quien matizó que de ser así el contagio se habría producido hace más de 15 años, ya que es éste el tiempo que tarda en incubarse la enfermedad hasta que aparece los primeros síntomas.
Además, de confirmarse esta hipótesis, Badiola aseguró que "hace 20 años no existían los mismos protocolos de seguridad que ahora" por lo que considera normal que se pudiera haber producido algún contagio, "sobre todo en un hombre que realizó tantas autopsias en su vida como él".
Desde el año 2001 se han registrado en España 702 casos de EETH, de los cuales 87 se han notificado en la Comunidad de Madrid, y sólo cinco son la variante humana de esta enfermedad, conocida desde hace más de un siglo pero cuyos estudios se intensificaron tras la aparición de una nueva variante en los años 90 en Inglaterra.
Sin embargo, y dado el periodo de incubación de la variante humana de la enfermedad, Badiola aseguró que se seguirán detectando algunos casos más, aunque todos ellos se tratarán de contagios precedentes a la entrada en vigor de la red de vigilancia establecido en toda Europa a raíz de los primeros casos en Reino Unido.
lunes, 30 de marzo de 2009.
Publicado por: CESM
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505936&categoria=34
Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob
El jefe del Servicio de Anatomía Patológica del Hospital General de Alcalá de Henares, Antonio Ruiz Villaespesa, falleció el sábado en dicho centro sanitario diagnosticado de posible enfermedad de Creutzfeldt-Jakob, según informó el sábado el Gobierno regional madrileño y recogen EUROPA PRESS y demás medios. Según el diagnóstico principal, se trata de un caso calificado de probable Creutzfeldt-Jakob, bien esporádico o iatrogénico. Dada la profesión del fallecido, habrá que establecer si la enfermedad ha sido causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo. En estos momentos se están realizando las pruebas necesarias para proceder al diagnóstico definitivo del tipo de EETH, lo que se confirmará con un estudio posmorten o necropsia.
Este doctor, de prestigio nacional e internacional en los campos de la anamopatología y la neuropatología, dedicó gran parte de su vida profesional al estudio de la Encefalopatía Espongiforme Transmisible Humana (EETH).
Su actividad profesional se desarrolló desde los años 70, primero en el hospital de La Paz, y posteriormente, en el Príncipe de Asturias, habiendo dedicado toda su vida a la sanidad pública y al diagnóstico de enfermedades.
Más información: EL PAIS, EL MUNDO
lunes, 30 de marzo de 2009.
Publicado por: CESM
http://www.cesm.org/nueva/index.asp?pag=detallenoticia.asp&formid=505930&categoria=34
Se estudian las causas del contagio Fallece el jefe de Anatomía Patológica del Hospital de Alcalá de Henares por posible Creutzfeldt-Jakob
MADRID, 29 Mar (EUROPA PRESS) El jefe del Servicio de Anatomía Patológica del Hospital General de Alcalá de Henares, Antonio Ruiz Villaescusa, falleció el sábado en dicho centro sanitario diagnosticado de posible enfermedad de Creutzfeldt-Jakob, según informó ayer el Gobierno regional madrileño.
Este doctor, de prestigio nacional e internacional en los campos de la anamopatología y la neuropatología, dedicó gran parte de su vida profesional al estudio de la Encefalopatía Espongiforme Transmisible Humana (EETH).
Su actividad profesional se desarrolló desde los años 70, primero en el hospital de La Paz, y posteriormente, en el Príncipe de Asturias, habiendo dedicado toda su vida a la sanidad pública y al diagnóstico de enfermedades.
Según el diagnóstico principal, se trata de un caso calificado de probable Creutzfeldt-Jakob, bien esporádico o iatrogénico. Dada la profesión del fallecido, habrá que establecer si la enfermedad ha sido causada por la exposición a tejidos de pacientes humanos infectados en el transcurso de su trabajo.
En estos momentos se están realizando las pruebas necesarias para proceder al diagnóstico definitivo del tipo de EETH, lo que se confirmará con un estudio posmorten o necropsia.
En principio, el caso no está relacionado con la ingesta de carne contaminada por priones (una partícula transmisible), que se asocia con la variante humana de Creutzfeldt-Jakob (vECJ), ya que se ha demostrado que hay "considerables diferencias" en la manifestación clínica y la duración de la enfermedad desde su diagnóstico hasta la defunción del paciente.
Desde el año 2001 se han registrado en España 702 casos de EETH, de los cuales 87 se han notificado en la Comunidad de Madrid.
La Encefalopatía Espongiforme Transmisible Humana (Creutzfeldt-Jakob) es una enfermedad conocida desde hace más de un siglo, pero los estudios sobre la misma se intensificaron tras la aparición de una nueva variante en los años 90 en Inglaterra.
El Jefe de Servicio de Anatomía Patológica de la Fundación Alcorcón, el doctor Rábano, se encargará de realizar la autopsia, cuyos resultados finales se conocerán aproximadamente en un mes.
La Consejería de Sanidad de la Comunidad de Madrid ya ha puesto en conocimiento de la Dirección General de Salud Pública del Ministerio de Sanidad dicho fallecimiento.
http://www.europapress.es/madrid/noticia-fallece-jefe-anatomia-patologica-hospital-alcala-henares-posible-creutzfeldt-jakob-20090329140143.html
stats for Spain as follows as of March 10, 2009. nvCJD holds at 5 documented to date, and 3 probable cases of sporadic CJD to date. does not mean that a case of nvCJD could not transmit, and or has not transmitted via 'friendly fire' i.e. the medical and or surgical and or occupational arena, and or what that pathology might look like via 2nd, 3rd, 4th passaged. will it continue to look like nvCJD or will it look like sporadic CJD and or any of the subtypes there of ? this case in question as ProMED said, has a great deal of information lacking to date. hopefully, a short report will be forth coming from the Instituto de Salud Carlos III. until then, i thought some of you might be interested in the recent stats. page 12 of 23 has a good chart. on the sporadic cjd cases, in terms of 3 to date, that was for 2009 'probable'. the reference to the nvCJD was a total of 5.....terry
(Situación a 10 de marzo de 2009) ;
REGISTRO NACIONAL DE ENCEFALOPATÍAS ESPONGIFORMES TRANSMISIBLES HUMANAS C.N.E y Servicios de Vigilancia Epidemiológica de CCAA (Situación a 10 de marzo de 2009)
http://www.isciii.es/htdocs/pdf/DatosRegistroCreutzfeldJacob2.pdf
ALSO, please note ;
SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)
SEAC
Agenda
102nd Meeting on Wednesday 4 March 2009
Room 808, Nobel House, 17 Smith Square, Defra, London SW1P 3JR
10.05 Approval of draft minutes from SEAC 101
snip...
ITEM 3 - CURRENT ISSUES 8. SEAC was informed about the following issues: . A mother and son in Spain had died of variant Creutzfeldt-Jakob Disease (vCJD). This is the first recorded instance of more than one case of vCJD within one family. As both the mother and son lived in a region of Spain with a history of BSE, had frequently shared meals of cattle brain, and as no other risk factor has been identified, it seems most likely that both infections were acquired from dietary exposure. Furthermore, the similar times of onset of disease of the cases did not suggest transmission had occurred from one to the other.
snip...
Thursday, February 26, 2009
SEAC 102nd Meeting on Wednesday 4 March 2009 (SEE DH risk assessment on sourcing and pooling plasma)
see full text ;
http://www.seac.gov.uk/papers/102-1.pdf
http://seac992007.blogspot.com/2009/02/seac-102nd-meeting-on-wednesday-4-march.html
Tuesday, August 12, 2008
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html
kind regards, terry
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
Tuesday, March 31, 2009
Variant Creutzfeldt-Jakob disease in France and the United Kingdom: Evidence for the same agent strain
Research Article
Variant Creutzfeldt-Jakob disease in France and the United Kingdom: Evidence for the same agent strain
Jean-Philippe Brandel, MD 1 2 3 *, Craig A. Heath, MD 4, Mark W. Head, PhD 5, Etienne Levavasseur, PhD 2, Richard Knight, MD 5, Jean-Louis Laplanche, PharmD, PhD 6, Jan PM. Langeveld, PhD 7, James W. Ironside, MD 5, Jean-Jacques Hauw, MD 2 8, Jan Mackenzie 5, Annick Alpérovitch, MD 1, Robert G. Will, MD 5, Stéphane Haïk, MD, PhD 2 3 8 1Institut National de la Santé et de la Recherche Médicale, Equipe Avenir Human Prion Diseases, Paris, F-75013, France 2Institut National de la Santé et de la Recherche Médicale, U 708, Paris, F-75013, France 3Assistance Publique-Hôpitaux de Paris, Hôpital de la Salpêtrière, Cellule Nationale de Référence des Maladies de Creutzfeldt-Jakob, Paris, F-75013, France 4Department of Neurology, Ninewells Hospital, Dundee, DD1 9S7, UK 5National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh, EH42XU, UK 6Assistance Publique-Hôpitaux de Paris, Hôpital Lariboisière, Service de Biochimie et de Biologie Moléculaire, Paris, F-75010, France 7Central Veterinary Institute of Wageningen UR (CVI), NL-8200 AB, Lelystad, The Netherlands 8Assistance Publique-Hôpitaux de Paris, Hôpital de la Salpêtrière, Laboratoire Raymond Escourolle, Paris, F-75013, France
email: Jean-Philippe Brandel (mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000061/!x-usc:mailto:jean-philippe.brandel@psl.aphp.fr)
*Correspondence to Jean-Philippe Brandel, Cellule Nationale de Référence des Maladies de Creutzfeldt-Jakob, Groupe Hospitalier Pitié-Salpêtrière, 47-83 Boulevard de l'Hôpital, 75651 Paris Cedex 13 France
Potential conflict of interest: Nothing to report.
Funded by: Department of Health and the Scottish Government; Grant Number: R40500 la Région Ile de France; Grant Number: F-07-691/R Neuroprion Network of Excellence; Grant Number: FOOD-CT-2004-506579 DG SANCO; Grant Number: 2003201
Abstract
Objective
Variant Creutzfeldt-Jakob disease (vCJD) was first reported in the United Kingdom in 1996. Since then, the majority of cases have been observed in the United Kingdom where there was a major epidemic of bovine spongiform encephalopathy. France was the second country affected. To address the hypothesis of the involvement of a common strain of agent, we have compared clinical, neuropathological, and biochemical data on vCJD patients from both countries.
Methods
In France and the United Kingdom, epidemiological and clinical data were obtained from analysis of medical records and direct interview of the family of the patients using the same standardized questionnaire in both countries. When brain material was available, we performed with similar methods a comparative study of brain lesions and PrPres glycoform ratios in both vCJD populations.
Results
Clinical data, genetic background, neuropathological finding, and biochemical findings in the 185 patients observed in France (n = 23) and the United Kingdom (n = 162) were similar except for age at death. Currently, blood transfusion is a risk factor identified only in the United Kingdom.
Interpretation
The close similarity between the cases of vCJD in France and the United Kingdom supports the hypothesis that a common strain of infectious agent is involved in both countries. The 5-year delay in the peak that we observed in France compared with the United Kingdom fits well with the increase in the importation of beef products to France from the United Kingdom between 1985 and 1995. Ann Neurol 2009;65:249-256
--------------------------------------------------------------------------------
Received: 20 May 2008; Revised: 9 September 2008; Accepted: 17 October 2008 Digital Object Identifier (DOI)
10.1002/ana.21583 About DOI
http://www3.interscience.wiley.com/journal/122261459/abstract?CRETRY=1&SRETRY=0
one strain, two very close geographical locations, so what about the other TSE strains atypical BSEs, which are more virulent than the typical c-BSE, what about the other TSE in other species ???
do they transmit to man ??? or not $$$
how long will this UKBSEnvCJD only charade continue ???
Saturday, January 24, 2009
Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Wednesday, February 04, 2009
Creutzfeldt-Jacob disease presenting as severe depression: a case report
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/creutzfeldt-jacob-disease-presenting-as.html
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
Wednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay
http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html
PLEASE NOTE, THEY ARE NOT RECALLING ALL THIS CWD POSITIVE ELK MEAT FROM COMMERCE FOR THE ELKS WELL BEING. think again ???
RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
___________________________________
PRODUCT
a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;
CODE
Elk Meats with production dates of December 29, 30, and 31
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.
Manufacturer: Noah's Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.
REASON
Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE
Unknown
DISTRIBUTION
NV, CA, TX, CO, NY, UT, FL, OK
___________________________________
http://www.fda.gov/bbs/topics/ENFORCE/2009/ENF01099.html
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
snip...
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
http://www.jbc.org/
snip...
Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.
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http://www.emboj.org/current.shtml
snip
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
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: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html
Wednesday, March 18, 2009 Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
SCRAPIE USA
INFECTED AND SOURCE FLOCKS
There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip
POSITIVE SCRAPIE CASES
As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip
CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)
snip...
However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.
ANIMALS SAMPLED FOR SCRAPIE TESTING
As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).
TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...
PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
http://scrapie-usa.blogspot.com/
CHAPTER 3 Animal Disease Eradication Programs and Control and Certification Programs
snip...
In FY 2007, two field cases, one validation study case, and two RSSS cases were consistent with a variant of the disease known as Nor98 scrapie.1 These five cases originated from flocks in California, Minnesota, Colorado, Wyoming, and Indiana, respectively.
snip...
http://www.aphis.usda.gov/publications/animal_health/content/printable_version/AHR_Web_PDF_07/D_Chapter_3.pdf
NOR-98 Scrapie FY 2008 to date 1
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
Monday, September 1, 2008
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1]
September 1, 2008
http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
http://www.pnas.org/cgi/content/abstract/0502296102v1
NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007
http://nor-98.blogspot.com/2008/04/seac-spongiform-encephalopathy-advisory.html
Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html
http://nor-98.blogspot.com/
CONFIDENTIAL PAPER No: SEAC 78/9 Amendment 2 2 In March 2002, a SEAC Sub-Group considered the risks associated with certain genotypes entering the food chain if BSE were ever isolated from sheep. In contrast to the SSC opinion, SEAC concluded that: • In line with previous SEAC advice, only animals carrying the ARR allele should enter the food chain • On a precautionary basis, the 12 month cut off previously advised by SEAC remained appropriate for ARR heterozygotes. However, in view of existing SRM regulations there was no justification for any age cut off in ARR homozygotes • In line with SEAC advice in 2001, only milk from ARR homozygous sheep could be considered as highly unlikely to contain the infectious agent. Further experimental work was required before potential risks from small ruminant milk from goats and semi-resistant or susceptible sheep could be excluded. There is therefore a disparity of opinion between the SSC and SEAC on this issue. Whilst recognising the uncertainties relating to the science in this area, it is important that contingency planning is based on the most up to date scientific developments and assessments of risk that are available. SEAC will be presented with an update on the ongoing BSE in sheep studies, funded by Defra (Annex 31). This covering paper also provides a history of previous SEAC advice on this issue. BACKGROUND...snip...end
http://www.seac.gov.uk/papers/78-9-closed.pdf
12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY
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A The Present Position with respect to Scrapie 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 is 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 emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize 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 scrapie problem urgent if the sheep industry is not to suffer grievously.
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76/10.12/4.6
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.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.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=6997404&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
Wednesday, January 28, 2009
TAFS1 Position Paper on BSE in small ruminants (January 2009)
http://scrapie-usa.blogspot.com/2009/01/tafs1-position-paper-on-bse-in-small.html
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.
We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.
snip...
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
YOU BET THERE IS, AND HAS BEEN, AND WE BEEN FEEDING THE MOST HIGH RISK I.E. DEAD STOCK DOWNER COWS TO OUR CHILDREN FOR DECADES, who will follow these children for human TSE from mad cow disease here in the USA in the years, decades to come, and how many will they expose from the 'pass it forward' friendly fire modes ???
http://downercattle.blogspot.com/2008/12/evaluation-of-fsis-management-controls.html
http://downercattle.blogspot.com/
Saturday, March 14, 2009 Agriculture Secretary Tom Vilsack Announces Final Rule for Handling of Non-Ambulatory Cattle
Release No. 0060.09 Contact: Amanda Eamich (202) 720-9113
http://downercattle.blogspot.com/2009/03/agriculture-secretary-tom-vilsack.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html
Thursday, July 10, 2008 A New Prionopathy update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
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
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
TSS
Variant Creutzfeldt-Jakob disease in France and the United Kingdom: Evidence for the same agent strain
Jean-Philippe Brandel, MD 1 2 3 *, Craig A. Heath, MD 4, Mark W. Head, PhD 5, Etienne Levavasseur, PhD 2, Richard Knight, MD 5, Jean-Louis Laplanche, PharmD, PhD 6, Jan PM. Langeveld, PhD 7, James W. Ironside, MD 5, Jean-Jacques Hauw, MD 2 8, Jan Mackenzie 5, Annick Alpérovitch, MD 1, Robert G. Will, MD 5, Stéphane Haïk, MD, PhD 2 3 8 1Institut National de la Santé et de la Recherche Médicale, Equipe Avenir Human Prion Diseases, Paris, F-75013, France 2Institut National de la Santé et de la Recherche Médicale, U 708, Paris, F-75013, France 3Assistance Publique-Hôpitaux de Paris, Hôpital de la Salpêtrière, Cellule Nationale de Référence des Maladies de Creutzfeldt-Jakob, Paris, F-75013, France 4Department of Neurology, Ninewells Hospital, Dundee, DD1 9S7, UK 5National Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Edinburgh, EH42XU, UK 6Assistance Publique-Hôpitaux de Paris, Hôpital Lariboisière, Service de Biochimie et de Biologie Moléculaire, Paris, F-75010, France 7Central Veterinary Institute of Wageningen UR (CVI), NL-8200 AB, Lelystad, The Netherlands 8Assistance Publique-Hôpitaux de Paris, Hôpital de la Salpêtrière, Laboratoire Raymond Escourolle, Paris, F-75013, France
email: Jean-Philippe Brandel (mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000061/!x-usc:mailto:jean-philippe.brandel@psl.aphp.fr)
*Correspondence to Jean-Philippe Brandel, Cellule Nationale de Référence des Maladies de Creutzfeldt-Jakob, Groupe Hospitalier Pitié-Salpêtrière, 47-83 Boulevard de l'Hôpital, 75651 Paris Cedex 13 France
Potential conflict of interest: Nothing to report.
Funded by: Department of Health and the Scottish Government; Grant Number: R40500 la Région Ile de France; Grant Number: F-07-691/R Neuroprion Network of Excellence; Grant Number: FOOD-CT-2004-506579 DG SANCO; Grant Number: 2003201
Abstract
Objective
Variant Creutzfeldt-Jakob disease (vCJD) was first reported in the United Kingdom in 1996. Since then, the majority of cases have been observed in the United Kingdom where there was a major epidemic of bovine spongiform encephalopathy. France was the second country affected. To address the hypothesis of the involvement of a common strain of agent, we have compared clinical, neuropathological, and biochemical data on vCJD patients from both countries.
Methods
In France and the United Kingdom, epidemiological and clinical data were obtained from analysis of medical records and direct interview of the family of the patients using the same standardized questionnaire in both countries. When brain material was available, we performed with similar methods a comparative study of brain lesions and PrPres glycoform ratios in both vCJD populations.
Results
Clinical data, genetic background, neuropathological finding, and biochemical findings in the 185 patients observed in France (n = 23) and the United Kingdom (n = 162) were similar except for age at death. Currently, blood transfusion is a risk factor identified only in the United Kingdom.
Interpretation
The close similarity between the cases of vCJD in France and the United Kingdom supports the hypothesis that a common strain of infectious agent is involved in both countries. The 5-year delay in the peak that we observed in France compared with the United Kingdom fits well with the increase in the importation of beef products to France from the United Kingdom between 1985 and 1995. Ann Neurol 2009;65:249-256
--------------------------------------------------------------------------------
Received: 20 May 2008; Revised: 9 September 2008; Accepted: 17 October 2008 Digital Object Identifier (DOI)
10.1002/ana.21583 About DOI
http://www3.interscience.wiley.com/journal/122261459/abstract?CRETRY=1&SRETRY=0
one strain, two very close geographical locations, so what about the other TSE strains atypical BSEs, which are more virulent than the typical c-BSE, what about the other TSE in other species ???
do they transmit to man ??? or not $$$
how long will this UKBSEnvCJD only charade continue ???
Saturday, January 24, 2009
Bovine Spongiform Encephalopathy h-BSE ATYPICAL USA 2008 Annual Report Research Project: Study of Atypical Bse
Location: Virus and Prion Diseases of Livestock
2008 Annual Report
http://bse-atypical.blogspot.com/2009/01/bovine-spongiform-encephalopathy-h-bse.html
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
see full text ;
http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html
Wednesday, February 04, 2009
Creutzfeldt-Jacob disease presenting as severe depression: a case report
http://creutzfeldt-jakob-disease.blogspot.com/2009/02/creutzfeldt-jacob-disease-presenting-as.html
Thursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html
Wednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay
http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html
PLEASE NOTE, THEY ARE NOT RECALLING ALL THIS CWD POSITIVE ELK MEAT FROM COMMERCE FOR THE ELKS WELL BEING. think again ???
RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
___________________________________
PRODUCT
a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;
CODE
Elk Meats with production dates of December 29, 30, and 31
RECALLING FIRM/MANUFACTURER
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.
Manufacturer: Noah's Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.
REASON
Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE
Unknown
DISTRIBUTION
NV, CA, TX, CO, NY, UT, FL, OK
___________________________________
http://www.fda.gov/bbs/topics/ENFORCE/2009/ENF01099.html
Monday, February 09, 2009
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD
snip...
Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST
our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.
http://www.jbc.org/
snip...
Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.
snip...
http://www.emboj.org/current.shtml
snip
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
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: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html
Wednesday, March 18, 2009 Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf
SCRAPIE USA
INFECTED AND SOURCE FLOCKS
There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip
POSITIVE SCRAPIE CASES
As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip
CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)
snip...
However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.
ANIMALS SAMPLED FOR SCRAPIE TESTING
As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).
TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...
PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
http://scrapie-usa.blogspot.com/
CHAPTER 3 Animal Disease Eradication Programs and Control and Certification Programs
snip...
In FY 2007, two field cases, one validation study case, and two RSSS cases were consistent with a variant of the disease known as Nor98 scrapie.1 These five cases originated from flocks in California, Minnesota, Colorado, Wyoming, and Indiana, respectively.
snip...
http://www.aphis.usda.gov/publications/animal_health/content/printable_version/AHR_Web_PDF_07/D_Chapter_3.pdf
NOR-98 Scrapie FY 2008 to date 1
http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps
Monday, September 1, 2008
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1]
September 1, 2008
http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)
http://www.pnas.org/cgi/content/abstract/0502296102v1
NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007
http://nor-98.blogspot.com/2008/04/seac-spongiform-encephalopathy-advisory.html
Tuesday, June 3, 2008 SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA
http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html
http://nor-98.blogspot.com/
CONFIDENTIAL PAPER No: SEAC 78/9 Amendment 2 2 In March 2002, a SEAC Sub-Group considered the risks associated with certain genotypes entering the food chain if BSE were ever isolated from sheep. In contrast to the SSC opinion, SEAC concluded that: • In line with previous SEAC advice, only animals carrying the ARR allele should enter the food chain • On a precautionary basis, the 12 month cut off previously advised by SEAC remained appropriate for ARR heterozygotes. However, in view of existing SRM regulations there was no justification for any age cut off in ARR homozygotes • In line with SEAC advice in 2001, only milk from ARR homozygous sheep could be considered as highly unlikely to contain the infectious agent. Further experimental work was required before potential risks from small ruminant milk from goats and semi-resistant or susceptible sheep could be excluded. There is therefore a disparity of opinion between the SSC and SEAC on this issue. Whilst recognising the uncertainties relating to the science in this area, it is important that contingency planning is based on the most up to date scientific developments and assessments of risk that are available. SEAC will be presented with an update on the ongoing BSE in sheep studies, funded by Defra (Annex 31). This covering paper also provides a history of previous SEAC advice on this issue. BACKGROUND...snip...end
http://www.seac.gov.uk/papers/78-9-closed.pdf
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 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 is 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 emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize 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 scrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.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.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=6997404&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus
Wednesday, January 28, 2009
TAFS1 Position Paper on BSE in small ruminants (January 2009)
http://scrapie-usa.blogspot.com/2009/01/tafs1-position-paper-on-bse-in-small.html
SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.
We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.
snip...
PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986
http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
YOU BET THERE IS, AND HAS BEEN, AND WE BEEN FEEDING THE MOST HIGH RISK I.E. DEAD STOCK DOWNER COWS TO OUR CHILDREN FOR DECADES, who will follow these children for human TSE from mad cow disease here in the USA in the years, decades to come, and how many will they expose from the 'pass it forward' friendly fire modes ???
http://downercattle.blogspot.com/2008/12/evaluation-of-fsis-management-controls.html
http://downercattle.blogspot.com/
Saturday, March 14, 2009 Agriculture Secretary Tom Vilsack Announces Final Rule for Handling of Non-Ambulatory Cattle
Release No. 0060.09 Contact: Amanda Eamich (202) 720-9113
http://downercattle.blogspot.com/2009/03/agriculture-secretary-tom-vilsack.html
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
snip...
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
snip...
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html
Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/novel-human-disease-with-abnormal-prion.html
Thursday, July 10, 2008 A New Prionopathy update July 10, 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/07/new-prionopathy-update-july-10-2008.html
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
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
TSS
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