USDA FY 2010 AVOIDING HARM FROM INVASIVE SPECIES (USDA Do No Harm 2010 Report)
This is the tenth “USDA Do No Harm Report” to the Invasive Species Advisory Committee and the National Invasive Species Council. It covers the FY 2010 activities for ARS, ARS/NAL, APHIS, NIFA, ERS, USFS and NRCS. The report is dated 14 March 2011.
snip...
Characterization of Nor98 in Canadian sheep.
Identification and characterization of novel scrapie strains, particularly those in sheep considered resistant to classical scrapie, are key components in the US scrapie eradication effort. In association with the USDA Animal Plant Health Inspection Service?s National Veterinary Service Laboratory, ARS scientists in Pullman, WA have previously characterized the Nor98 form of scrapie in US sheep. These scientists have now provided assistance to the Canadian Food Inspection Agency in their characterization of the disorder in Canadian sheep. The disease profiles of all samples were consistent with Nor98 scrapie, a strain that may not be contagious and may be a spontaneous degenerative condition of older sheep. This finding supports the current genetically based control program for scrapie in the US and Canada.
========================snip...
"may not be contagious and may be a spontaneous degenerative condition of older sheep"
what kind of science is this, other than junk science $
this very well MAY NOT be the case...tss
Friday, September 30, 2011
A Review of Archived Canadian Scrapie Cases for Evidence of Bovine Spongiform Encephalopathy
http://scrapie-usa.blogspot.com/2011/09/review-of-archived-canadian-scrapie.html
========================continued...
Prion genotypes in US and Canadian Sheep are similar.
Selection for genetically resistant animals is a foundation of the current scrapie control programs in the US and Canada. In association with the Canadian Food Inspection Agency, ARS researchers in Pullman, WA described the prion genotypes of Canadian sheep diagnosed with scrapie between 1998 and 2008. The susceptible genotypes used in the US scrapie control program were similar to those found in the Canadian study. This finding allows the US and Canada to continue to harmonize their scrapie eradication programs. Prion genotypes of US goats are diverse. The role of prion genetics in sheep scrapie is now well described and selection for genetically resistant animals is a key component of the eradication program.
46
However, the role of prion genetics in goat scrapie is not well understood. More importantly, basic information on the extent of prion gene variation in US goat breeds has been lacking. ARS researchers in Pullman, WA have described the wide variation in gene sequence among several economically important breeds of US goats. This study provides the basis for further examination of the role of prion genotypes in scrapie prevention.
=========================snip...
Monday, June 20, 2011 2011
Annual Conference of the National Institute for Animal Agriculture ATYPICAL NOR-98 LIKE SCRAPIE UPDATE USA
http://nor-98.blogspot.com/2011/06/2011-annual-conference-of-national.html
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html
Thursday, July 14, 2011
Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/histopathological-studies-of-ch1641.html
Thursday, June 2, 2011
USDA scrapie report for April 2011 NEW ATYPICAL NOR-98 SCRAPIE CASES Pennsylvania AND California
http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html
Monday, June 27, 2011
Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease
http://prionopathy.blogspot.com/2011/06/comparison-of-sheep-nor98-with-human.html
BSE: TIME TO TAKE H.B. PARRY SERIOUSLY
If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1988/06/08004001.pdf
Sunday, September 25, 2011
Clinical Heidenhain Variant Of Sporadic Creutzfeldt-Jakob Disease (CJD) With Co-occurrence Of Prion Protein Types 1 and 2
http://creutzfeldt-jakob-disease.blogspot.com/2011/09/clinical-heidenhain-variant-of-sporadic.html
snip...
========================...continued...
Disease progression in Rocky Mountain elk with chronic wasting disease.
Chronic wasting disease (CWD) is the prion disorder of deer and elk. Detailed analyses of the pathways through which the infectious protein moves in the tissues of infected elk are the basis for improved diagnostic testing and control program. In collaboration with Colorado State University, ARS scientists from Pullman, WA, have demonstrated a detailed examination of diseased elk and the pathways through which the agent appears to spread in the brain and eyes. This finding supports the diagnostic testing methods developed by ARS and currently conducted to monitor herds of elk for this fatal disease.
Chronic wasting disease in non-native species.
Chronic wasting disease (CWD) is reported in white tailed deer, black tailed deer, mule deer, Rocky Mountain elk, and Shira?s moose in the US and Canada. The entire host range of this disorder is not known and facilities housing non-native deer or elk species remain at potential risk of infection if those species are susceptible. In this study, ARS researchers in Pullman, WA provided collaborative assistance to the Canadian Food Inspection Agency in a study examining the effect of experimental infection of red deer with CWD. The study demonstrated the susceptibility of this species to disease, the potential for diagnosis early in the disease, and the role of naturally occurring variation in the prion gene on disease susceptibility. The study demonstrated that diagnostic methods developed by ARS are suitable for use in red deer.
Molecular kinship studies in white tailed deer with chronic wasting disease.
Chronic wasting disease (CWD) in white tailed deer can result in very high infection rates with very little evidence of clinical disease in infected animals, even late in disease. The mechanisms by which disease spreads in captive herds are not known. ARS
47
researchers in Pullman, WA collaborated with scientists at the Veterinary Genetics Laboratory wildlife disease unit in Davis, CA to develop a panel of genetic markers that identify the family structure in herds of deer. Using this panel, epidemiologic studies to examine the transmission of the disease among family members in a herd are now possible.
The role of tissue mineral levels in prion disease in Rocky Mountain elk.
Several preliminary studies have suggested an association between the levels of certain dietary minerals in the tissues of elk with chronic wasting disease infection. In collaboration with Colorado State University, the National Park Service, and the USDA Animal Plant Health Inspection Service, ARS researchers in Pullman, WA have shown the increased risk of chronic wasting disease in elk with decreased magnesium and increased manganese levels in brain tissue. This study provides important information on factors affecting disease in the natural host.
Early detection of prion diseases such as sheep scrapie requires concentration of the prion proteins that serve as disease markers from dilute biological samples. Researchers at the Foodborne Contaminants Research Unit in Albany, California, in collaboration with the University of California San Francisco, developed a new method for concentrating prion proteins from animal tissues. We found this method results in a significant increase in prion concentration, allowing more sensitive prion detection. This year we filed a patent application and published a manuscript on this new method, showing how it provides more sensitive and early detection of disease in infected animals.
New strain of mouse for anti-prion antibody production.
Production of antibodies for detection of prion proteins associated with diseases such as sheep scrapie is limited by the resistance of normal mice to making an immune response against their own proteins. Researchers at the Foodborne Contaminants Research Unit in Albany, California, in collaboration with our partners at the University of California San Francisco, have made a new strain of mouse that lacks the prion protein. Unlike normal mice, the new mice are highly sensitive to immunization with prions. This year we filed a patent application and published a manuscript showing the use of these
48
mice in making new antibodies that can bind and detect prions. Such antibodies may be used for more sensitive and early detection of disease in infected animals.
New method for identification of antibodies that detect prion proteins.
Making new monoclonal antibodies for detection of prion proteins in diseases such as sheep scrapie requires selection of the best performing cells from among thousands of candidates. Researchers at the Foodborne Contaminants Research Unit in Albany, California have developed a fast and sensitive method to identify such cells, which are taken from mice that have been immunized to produce antibodies that strongly bind to prion protein. This method was used to identify improved antibodies which are now available for use in detection of disease. Furthermore, the new screening method may be used by other scientists for research to make additional new antibodies for prions.
New antibodies for detection of prion disease.
Sensitive detection of prion proteins for early diagnosis of disease requires antibodies that are capable of strong binding to prions. Researchers at the Foodborne Contaminants Research Unit in Albany, California, in collaboration with our partners at the University of California San Francisco, generated eight new antibodies that detect prion disease in many different animals. We have published a manuscript that describes these anti-prion antibodies and shows their value in improving detection of prions. Improved detection methods will help in herd management and control of the spread of prion diseases. Inoculation of domestic and European bovine spongiform encephalopathy (BSE) isolates into cattle. To date, no side-by-side comparison of domestic BSE has been made with European BSE isolates. Between February 16-18, 2010, ARS researchers at Ames, Iowa, inoculated cattle with domestic and European BSE isolates.
This study is expected to last at least 2 years before all animals will show signs of clinical disease and will provide the first direct comparison of these isolates and provide sufficient material for future studies of BSE. The start of research efforts on 24 milestones characterizing atypical versus classical BSE are dependent on tissues obtained at the completion of this animal study.
49
Production of cattle containing the rare 211K PRNP allele associated with genetic bovine spongiform encephalopathy (BSE).
The 211K PRNP allele identified as being associated with genetic BSE had been identified in only 1 living animal, limiting the ability to actively study the impact of this allele on BSE. ARS researchers at Ames, Iowa, with cooperators at Iowa State University, produced 13 calves to date (about half containing this allele) using superovulation and embryo transfer. Production of these calves initiates a long-term animal study testing the hypothesis that this rare, naturally-occurring allele is a cause of genetic BSE in older cattle. This also enables ARS scientists to expand and preserve a unique scientific resource for the study of BSE as some of these calves are now being used to expand the pool of infectious BSE material from the Alabama 2006 BSE case, which is another resource in limited supply, and will ultimately allow proof of the existence of genetic BSE.
http://www.invasivespecies.gov/global/ISAC/ISAC_Minutes/2011/PDF/USDA_Do_No_Harm_Report_FY10.pdf
Seems they have made their minds up before the science is even proven their theory. plus, even if genetic BSE is proven (my views on genetic TSE are that the genetic gene does NOT cause disease, simply makes one more susceptible), but genetic BSE would also be capable of being transmitted via feed and thus the genetic BSE can be recycled with feed, and transmit genetic BSE the same way as the c-BSE. i don't know which is trying to prove a false assumption the worse, the USDA et al at the ARS, or Gambetti et al at case western, that the USA has some cloaking device that protects us from any form of transmissible mad cow disease. it's all genetic. that's just BSe to me. ...tss
Friday, September 23, 2011
Bovine spongiform encephalopathy associated insertion/deletion polymorphisms of the prion protein gene in the four beef cattle breeds from North China
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/bovine-spongiform-encephalopathy.html
Sunday, September 25, 2011
Clinical Heidenhain Variant Of Sporadic Creutzfeldt-Jakob Disease (CJD) With Co-occurrence Of Prion Protein Types 1 and 2
http://creutzfeldt-jakob-disease.blogspot.com/2011/09/clinical-heidenhain-variant-of-sporadic.html
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
http://prionopathy.blogspot.com/2011/09/variably-protease-sensitive-prionopathy.html
Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html
Saturday, November 6, 2010
TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS
INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation
http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html
Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)
PRION DISEASE UPDATE 2010 (11)
http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. ***It also suggests a similar cause or source for atypical BSE in these countries.***
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Friday, September 30, 2011
BSE: where are we now? Veterinary Record 2011;169:352-353
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/bse-where-are-we-now-veterinary-record.html
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html
Wednesday, August 20, 2008
Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?
http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html
Saturday, February 28, 2009
NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS
"All of the 15 cattle tested showed that the brains had abnormally accumulated PrP"
2009 SEAC 102/2
http://bse-atypical.blogspot.com/2009/02/new-results-on-idiopathic-brainstem.html
Sunday, September 6, 2009
MAD COW USA 1997 (SEE SECRET VIDEO)
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? (see video at bottom)
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html
Saturday, March 5, 2011
MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA
http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html
WHO WILL FOLLOW THE CHILDREN FOR CJD SYMPTOMS ???
Saturday, May 2, 2009
U.S. GOVERNMENT SUES WESTLAND/HALLMARK MEAT OVER USDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/2009/05/us-government-sues-westlandhallmark.html
http://downercattle.blogspot.com/
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/prionet-canada-researchers-in-vancouver.html
Wednesday, March 31, 2010
Atypical BSE in Cattle
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
snip...
http://www.neuroprion.org/en/np-neuroprion.html
Rural and Regional Affairs and Transport References Committee
The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Terry S. Singeltary Sr. has added the following comment:
"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.
The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"
http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
The conclusions state that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Active screening has allowed the identification of 3 new forms of animal TSEs (H-type atypical BSE, L-type atypical BSE, and atypical scrapie), but the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs. There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential. Transmission experiments to human PrP transgenic mice or primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential and indicate that that of the L-type atypical BSE agent appears similar or even higher than that of the classical BSE agent. A single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
Commentary ---------- Following to a request from the European Commission, the Panel on Biological Hazards (BIOHAZ) and the European Centre for Disease Prevention and Control (ECDC) were asked to deliver a scientific opinion on any possible epidemiological or molecular association between transmissible spongiform encephalopathies (TSEs) in animals and humans. The opinion reviews and discusses the existing scientific evidence that links animal and human TSEs currently known.
The opinion first considers the definition of zoonoses and the principles for the identification of zoonotic diseases, which can be based on evidence gathered from both epidemiological and laboratory studies. The opinion describes the challenges involved in identifying TSEs as zoonoses, due to the specific characteristics of TSE infections/diseases, such as the nature of TSE agents, the occurrence of animal and human TSEs, and the type of monitoring applied, the long incubation period of TSEs etc. The example of the process that led to establishing a link between bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) is reviewed. The epidemiological and laboratory criteria that can be used to investigate such a link are described in detail, since those criteria might be useful for the identification of links between other animal and human TSEs.
The opinion discusses the strain diversity of the TSE agents described in sheep, goats, cattle, cervids, and humans, based on the current knowledge, which highlights that multiple TSE agents exist in each species. The factors influencing the capacity of TSE agents to cross the species transmission barrier are then considered in detail, including the variability in host and donor PrP gene and protein, the TSE strain type involved and its interaction with the host PrP, and the route of infection.
The opinion critically assesses the tools and methodologies currently available to study and evaluate the possible association between animal and human TSEs. The use of epidemiology is discussed for TSEs in both animals and humans, and the possibility to compare the 2 sources of information is presented as a possible method to study the possible links.
Both in vivo and in vitro laboratory methods are considered and discussed, including neuropathology, transmission experiments involving different animal models (wild type and transgenic mice, primates and other species), biochemical methods, cell-free conversion assays, protein misfolding cyclic amplification (PMCA), and cell culture assays. Characteristics, advantages, and disadvantages of the different methods are reviewed, including the opportunity to collate data from different types of experiments for the study of potential associations between animal and human TSEs.
The opinion then reviews the scientific evidence currently available for the different animal and human TSEs, including classical BSE, atypical BSE (H-type and L-type), classical scrapie, atypical scrapie, chronic wasting disease (CWD), transmissible mink encephalopathy (TME), and human TSEs. In particular, the following aspects are systematically discussed for each TSE agent: epidemiology, pathogenesis, and in vivo and in vitro transmission experiments.
The opinion concludes that, at present, the only TSE agent demonstrated to be zoonotic is the classical BSE agent. With regard to human TSEs, detected cases of sporadic CJD are randomly distributed in time and geographical location. These observations have been interpreted as a supportive argument that sporadic CJD is not environmentally acquired. However, the epidemiological evidence in relation to sporadic CJD cannot be regarded as definitive, and the possibility that a small proportion of cases are zoonotic cannot be excluded.
It also concludes that a series of uncertainties in relation to the epidemiological patterns of animal and human TSEs indicate that even a rough comparison of the present epidemiological patterns of human and animal TSEs other than classical BSE is unlikely to be informative. Because of these uncertainties, it is an imperative to continue to carry out systematic surveillance of human TSE diseases, and to continue and improve the surveillance of animal TSE diseases.
The opinion highlights that the active screening has allowed the identification of 3 new forms of animal TSEs (L-type atypical BSE, H-type atypical BSE, and atypical scrapie), but that the information obtained has major limitations due to the unknown sensitivity of the current monitoring system for these TSEs.
There is no epidemiological evidence to suggest that classical scrapie is zoonotic. The epidemiological data are too limited to conclude whether the atypical scrapie agent has a zoonotic potential.
Transmission experiments to human PrP transgenic mice suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE and classical BSE in sheep agents) might have zoonotic potential, whereas for other agents there is no evidence provided of a zoonotic potential (H-type atypical BSE and CWD), or no published studies are available (classical and atypical scrapie). In addition, transmission experiments to primates suggest that some TSE agents other than the classical BSE agent in cattle (namely L-type atypical BSE, classical BSE in sheep, TME, CWD agents) might have zoonotic potential. In particular, primates are highly permissive to L-type atypical BSE, even by the oral route.
The opinion emphasizes that laboratory transmission experiments indicate that the L-type atypical BSE agent has a significant zoonotic potential, which appears similar or even higher than that of the classical BSE agent. While transmission data for evaluating the zoonotic potential of classical scrapie in primates and human PrP transgenic mice are extremely limited or not yet available, a single study reported efficient transmission of a natural sheep classical scrapie isolate to primates.
The opinion concludes that human PrP transgenic mice and primates are currently the most relevant models for investigating the human transmission barrier, but the extent to which such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. It is unpredictable whether a TSE agent will transmit to a new host, and if the transmission principally occurs, what the transmission rate will be.
Based on the results obtained with in vitro conversion assays, the opinion concludes that there is probably no absolute molecular barrier to transmission of TSE agents between mammalian species. Results also suggest that these assays may be developed as a tool for quantifying the transmission barriers between species for different TSE agent strains; however, there is no means at the moment to transpose in vitro results into the likelihood of in vivo interspecies transmission.
-- Communicated by: Terry S Singeltary Sr
[ProMED-mail thanks Terry S Singeltary Sr for drawing attention to this comprehensive document which provides a current evaluation of experimental work designed to explore the zoonotic potential of the various recently recognised TSEs of domestic and other animals.
It is concluded that at present the only TSE agent demonstrated to be zoonotic is the classical BSE agent. Nor can it be entirely excluded at the present time that a small proportion of cases of sporadic CJD may be environmentally acquired. - Mod.CP]
******
http://www.promedmail.org/pls/apex/f?p=2400:1202:888892554804923::NO::F2400_P1202_CHECK_DISPLAY,F2400_P1202_PUB_MAIL_ID:X,88784
Saturday, January 2, 2010
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html
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.
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf
my comments to PLosone here ;
http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd
Sunday, September 25, 2011
Mad Cow Scaremongers
Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
TSS
Friday, September 30, 2011
Wednesday, December 22, 2010
Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?
A Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle.
Dr. Earl Van Assen pleaded guilty to two counts of contravening the Health of Animals Act.
The United States Department of Agriculture placed severe restrictions on importing Canadian cattle following the “mad cow” scare early last decade. Restrictions have since been relaxed, but Canadian veterinarians are still required to certify that cattle bound for export to the U.S. were born after March 1999.
“Some people might feel this is not a big deal,” Crown attorney Christina Cheater told Judge John Guy. “The wrongful certification of cattle... has the potential to cause serious disruption to the export of cattle to the U.S.”
Court heard Van Assen submitted certification documents in February 2009 for 42 cows claiming he inspected the animals and found them suitable for export. Following a subsequent investigation, Van Assen admitted he accepted the word of the farmer exporting the cattle and did not inspect all the animals himself.
Veterinarians are expected to establish a cow’s age in one of three ways: through birth records, a visual inspection or an examination of its teeth.
“Unfortunately, Dr. Van Assen didn’t do any of these things,” Cheater said.
There is no indication any of the exported cattle was diseased, Cheater said.
“But the problem is the USDA is going to look at this very seriously because we are unable to protect our border,” she said.
Defence lawyer Greg Brodsky said Van Assen is guilty of carelessness, not deceit.
“He did make random checks,” Brodsky said. “This wasn’t him trying to fool anybody.”
http://www.winnipegsun.com/news/manitoba/2010/12/21/16639166.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Monday, August 30, 2010
Bovine Spongiform Encephalopathy (BSE) CANADA Import Policy for Bovine Animals and Their Products (TAHD-DSAT-IE-2005-9-2) Import Policy updates August
http://madcowtesting.blogspot.com/2010/08/bovine-spongiform-encephalopathy-bse.html
Thursday, August 19, 2010
SCRAPIE CANADA UPDATE Current as of 2010-07-31 The following table lists sheep flocks and/or goat herds confirmed to be infected with scrapie in Canada in 2010.
Current as of: 2010-07-31
http://nor-98.blogspot.com/2010/08/scrapie-canada-update-current-as-of.html
Friday, September 24, 2010 BSE
Surveillance Continues to Benefit Canadian Cattle Producers September 24, 2010 - Notice to Industry
http://madcowtesting.blogspot.com/2010/09/bse-surveillance-continues-to-benefit.html
Saturday, October 2, 2010
BSE surveillance front and centre: CFIA and USA
http://madcowtesting.blogspot.com/2010/10/bse-surveillance-front-and-centre-cfia.html
Cases Regarding the Border Closure due to BSE Concerns
Several Canadian claimants have submitted notices of arbitration under the UNCITRAL Arbitration Rules alleging that the United States has violated NAFTA Chapter Eleven by closing the border to the importation of Canadian cattle after the discovery in 2003 of a case of bovine spongiform encephalopathy (BSE or mad cow disease) in a cow in Alberta, Canada. Claimants are Canadian citizens and corporations that own and operate cattle feeding, feedlot and transportation businesses in Canada, which they allege were damaged by the border closure.
Claimants allege that the border closure violates NAFTA Article 1102 (national treatment). The notices of arbitration seek damages of varying amounts, ranging from CAN$38,000 to CAN$95 million. The total amount of damages sought by claimants is approximately US$235 million.
On January 28, 2008, the tribunal issued its Award on Jurisdiction, dismissing the claims against the United States in their entirety. The tribunal’s award, and other documents in the case, appear below.
-01/28/08 Award on Jurisdiction [575 Kb] -10/10/07 Transcript of the Hearing on the Preliminary Issue - Day Two [166 Kb] -10/09/07 Transcript of the Hearing on the Preliminary Issue - Day One [260 Kb] -08/03/07 Procedural Order No. 3 [26 Kb] -07/05/07 Claimants' Rejoinder on the Preliminary Issue [849 Kb] -05/01/07 U.S. Reply on the Preliminary Issue [245 Kb] -03/01/07 Article 1128 Submission of Mexico [47 Kb] -01/30/07 Claimants' Response on the Preliminary Question [2303 Kb] -12/01/06 U.S. Memorial on the Preliminary Issue [167 Kb] -11/07/06 Procedural Order No. 2 [62 Kb] -10/20/06 Procedural Order No. 1 [122 Kb] -06/02/05 Jim McNall Notice of Arbitration [393 Kb] -06/02/05 Leslie Smith Notice of Arbitration [393 Kb] -06/02/05 Michael Sears Notice of Arbitration [393 Kb] -06/02/05 Rex Vandenberg Notice of Arbitration [393 Kb] -06/02/05 Richard Hiebert Notice of Arbitration [392 Kb] -06/02/05 Rod Oosterbroek Notice of Arbitration [392 Kb] -06/02/05 TER Cattle Notice of Arbitration [393 Kb] -05/20/05 Andrew Oosterbroek Notice of Arbitration [392 Kb] -05/20/05 Brad Hopkins Notice of Arbitration [396 Kb] -05/20/05 Brent Byers Notice of Arbitration [395 Kb] -05/20/05 Brent Fisher Notice of Arbitration [393 Kb] -05/20/05 Byron Sedore Notice of Arbitration [394 Kb] -05/20/05 Chris Irwin Notice of Arbitration [394 Kb] -05/20/05 Cornelius Van Hal Notice of Arbitration [392 Kb] -05/20/05 Darren Johnston Notice of Arbitration [394 Kb] -05/20/05 Dave Knapp Notice of Arbitration [394 Kb] -05/20/05 David Hewitt Notice of Arbitration [394 Kb] -05/20/05 Donald Procter Notice of Arbitration [394 Kb] -05/20/05 George Adams Notice of Arbitration [392 Kb] -05/20/05 Glen Thompson Notice of Arbitration [392 Kb] -05/20/05 Graham Alexander Notice of Arbitration [394 Kb] -05/20/05 Helmut Friesen Notice of Arbitration [393 Kb] -05/20/05 James Wiskerke Notice of Arbitration [392 Kb] -05/20/05 Joseph Daunt Notice of Arbitration [394 Kb] -05/20/05 Keith Kerr Notice of Arbitration [394 Kb] -05/20/05 Ken Andreychuk Notice of Arbitration [396 Kb] -05/20/05 Kevin Freiburger Notice of Arbitration [394 Kb] -05/20/05 Larry Brodersen Notice of Arbitration [392 Kb] -05/20/05 Lee Robson Notice of Arbitraiton [450 Kb] -05/20/05 Maria Vanden Elzen Notice of Arbitration [413 Kb] -05/20/05 Murray Johnston Notice of Arbitration [395 Kb] -05/20/05 NFL Holdings Notice of Arbitration [456 Kb] -05/20/05 Paul Gowing Notice of Arbitration [394 Kb] -05/20/05 Paul MacIntyre Notice of Arbitration [394 Kb] -05/20/05 Peter Schwenk Notice of Arbitration [448 Kb] -05/20/05 Peter Vander Heyden Notice of Arbitration [415 Kb] -05/20/05 Robert Emerson Notice of Arbitration [394 Kb] -05/20/05 Robert Laidlaw Notice of Arbitration [393 Kb] -05/20/05 Ron Coulter Notice of Arbitration [393 Kb] -05/20/05 Ross McCall Notice of Arbitration [394 Kb] -05/20/05 Ryan Kasko Notice of Arbitration [393 Kb] -05/11/05 Barry Hillman Notice of Arbitration [392 Kb] -05/11/05 Ben Gardiner Notice of Arbitration [416 Kb] -05/11/05 Bernie Loman Notice of Arbitration [392 Kb] -05/11/05 Blair Bieman Notice of Arbitration [394 Kb] -05/11/05 Blake Holtman Notice of Arbitration [393 Kb] -05/11/05 Bruce Groenenboom Notice of Arbitration [403 Kb] -05/11/05 Butch Martin Notice of Arbitration [441 Kb] -05/11/05 Dale Pallister Notice of Arbitration [394 Kb] -05/11/05 Darwin Ullery Notice of Arbitration [412 Kb] -05/11/05 Dave Gardiner Notice of Arbitration [415 Kb] -05/11/05 Dave Johnston Notice of Arbitration [415 Kb] -05/11/05 Dave Matthies, Notice of Arbitration [421 Kb] -05/11/05 David Millsap Notice of Arbitration [394 Kb] -05/11/05 Doug Briggs Notice of Arbitration [394 Kb] -05/11/05 Doug Nieboer Notice of Arbitration [392 Kb] -05/11/05 Doug Shelswel Notice of Arbitration [394 Kb] -05/11/05 Ed Stronks Notice of Arbitration [413 Kb] -05/11/05 Eric Thacker Notice of Arbitration [394 Kb] -05/11/05 Eve Kraayenbrink Notice of Arbitration [415 Kb] -05/11/05 Firmin Declercq Notice of Arbitration [392 Kb] -05/11/05 Frank Zettler Notice of Arbitration [395 Kb] -05/11/05 G. Lee Hochstein Notice of Arbitration [374 Kb] -05/11/05 George Alton Notice of Arbitration [394 Kb] -05/11/05 George Maxwell Notice of Arbitration [394 Kb] -05/11/05 Glen Armitage Notice of Arbitration [392 Kb] -05/11/05 Grant Nelson Notice of Arbitration [393 Kb] -05/11/05 Harry Duban Notice of Arbitration [393 Kb] -05/11/05 Harry Vandersteen Notice of Arbitration [393 Kb] -05/11/05 Harry Welsch Notice of Arbitration [393 Kb] -05/11/05 Henry Van Hall Notice of Arbitration [392 Kb] -05/11/05 Herb Groenenboom Notice of Arbitration [392 Kb] -05/11/05 Herbert Serfas Notice of Arbitration [403 Kb] -05/11/05 Herman Stroeve Notice of Arbitration [449 Kb] -05/11/05 Ian MacLean Notice of Arbitration [394 Kb] -05/11/05 Jim Steed Notice of Arbitration [394 Kb] -05/11/05 Joe Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Schooten Notice of Arbitration [392 Kb] -05/11/05 John Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Vander Heyden Notice of Arbitration [392 Kb] -05/11/05 Julie Coe Notice of Arbitration [394 Kb] -05/11/05 Keith Scott Notice of Arbitration [392 Kb] -05/11/05 Larry Lehrbass Notice of Arbitration [394 Kb] -05/11/05 Leighton Kolk Notice of Arbitration [392 Kb] -05/11/05 Lloyd Sproule Notice of Arbitration [391 Kb] -05/11/05 Louis Ypma Notice of Arbitration [392 Kb] -05/11/05 Marty Wren Notice of Arbitration [392 Kb] -05/11/05 Mary Conlin Notice of Arbitration [395 Kb] -05/11/05 Murray Brodhagen Notice of Arbitration [394 Kb] -05/11/05 Nick Popovic Notice of Arbitration [394 Kb] -05/11/05 Paul Adams Notice of Arbitration [392 Kb] -05/11/05 Renus Van Hal Notice of Arbitration [392 Kb] -05/11/05 Richard Visser Notice of Arbitration [392 Kb] -05/11/05 Rients Wever Notice of Arbitration [392 Kb] -05/11/05 Robert Cooke Notice of Arbitration [415 Kb] -05/11/05 Robert Vander Heyden Notice of Arbitration [393 Kb] -05/11/05 Ryan Gibson Notice of Arbitration [392 Kb] -05/11/05 Steve McKague Notice of Arbitration [394 Kb] -05/11/05 Stuart Alton Notice of Arbitration [394 Kb] -05/11/05 Ward Takeda Notice of Arbitration [393 Kb] -05/11/05 Wayne Beattie Notice of Arbitration [394 Kb] -05/11/05 Wilfred Haines Notice of Arbitration [415 Kb] -03/16/05 Cor Van Raay Notice of Arbitration [396 Kb] -03/16/05 Joe Groenenboom Notice of Arbitration [392 Kb] -03/16/05 John Vander Heyden Notice of Arbitration [393 Kb] -03/16/05 Larry Nolan Notice of Arbitration [393 Kb] -03/16/05 Theodorus de Boer Notice of Arbitration [392 Kb]
http://www.state.gov/s/l/c14683.htm
POT CALLING KETTLE BLACK ;
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
LETS start with the UKBSEnvCJD only theory, lets look at UK exports to USA, Canada, and Mexico. the imported only theory. ...
1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY other Countries list in PDF file)
USA -------- TOTALS ''8'' TONS CANADA -- TOTALS ''29'' TONS
1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA
USA ------- TOTALS ''358'' TONS
CANADA --TOTALS ''24'' TONS
BONE-IN BEEF AND VEAL
USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons above?)
UK EXPORT OF LIKE CATTLE TO USA AND CANADA
1986 TO 1996 USA TOTAL = 1297
1986 TO 1996 CAN TOTAL = 299
http://collections.europarchive.org/tna/20080102161741/http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987
CANADA -- 64,526 KG
UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED OR FROZEN OTHER THAN LIVER DEC 1987 YTD
USA -- 45,943 KG
UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988
CANADA -- 4,163 KG
PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE TO DEC 1988
USA -------- 28,609 KG CANADA -- 22,044 KG
MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989
USA -------- 17,880 KG MEXICO---- 33,444 KG
BONELESS MEAT OF BOVINE 1989
USA --------111,953 KG CANADA---1,800 KG MEXICO --- 1,143,387 KG
EDIBLE OFFAL OF BOVINE ANIMALS 1989
USA -------- 19,980 KG MEXICO--- 31,244 KG
MORE........
MEAT OF BOVINE ANIMALS BONELESS 1990
USA 146,443
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://collections.europarchive.org/tna/20081106012846/http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://collections.europarchive.org/tna/20080102193106/http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: S.J.Pearsall@esg.maff.gsi.gov.uk
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry
Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes
1980 1981 12 1982 1983 1984 10 1985 2 1986 1987 1988 1989 20 1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
====================================== END...TSS
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
Subject: Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Date: August 24, 2005 at 2:47 pm PST
August 24, 2005
Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Greetings APHIS ET AL,
My name is Terry S. Singeltary Sr.
I would kindly like to comment on [Docket No. 05-004-1] RIN 0579-AB93 ;
PROPOSED RULES
Exportation and importation of animals and animal products:
Whole cuts of boneless beef from-
Japan,
48494-48500 [05-16422]
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=0900006480086ebc&disposition=attachment&contentType=msw6
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
PLEASE SEE FULL TEXT HERE ;
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
http://madcowfeed.blogspot.com/2008/07/docket-no-03-080-1-usda-issues-proposed.html
Friday, August 22, 2008
MEXICO blocks Alberta cattle following the discovery of Canada's 14th case of mad cow disease
http://madcowtesting.blogspot.com/2008/08/mexico-blocks-alberta-cattle-following.html
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA
http://madcowtesting.blogspot.com/
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
please see full text ;
http://www.efsa.europa.eu/en/scdocs/doc/3rax1.pdf
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E. COMMISSION DECISION of 11 November 2009
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
snip...
http://collections.europarchive.org/tna/20080102185948/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
IN CONFIDENCE
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
http://collections.europarchive.org/tna/20080102233201/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
IN CONFIDENCE
PERCEPTIONS OF A SLOW VIRUS DISEASE IN ANIMALS IN THE USA
http://collections.europarchive.org/tna/20081106012811/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
2010
Rural and Regional Affairs and Transport References Committee The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Tuesday, March 16, 2010
COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA
COMMONWEALTH OF AUSTRALIA
Proof Committee Hansard
RRA&T 2 Senate Friday, 5 February 2010
RURAL AND REGIONAL AFFAIRS AND TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association
CARTER, Mr John Edward, Director, Australian Beef Association
CHAIR—Welcome. Would you like to make an opening statement?
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:
You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heidenhain variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:
The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.
Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:
snip...see full text 110 pages ;
http://www.aph.gov.au/hansard/senate/commttee/S12742.pdf
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
for those interested, please see much more here ;
http://docket-aphis-2006-0041.blogspot.com/2010/03/commonwealth-of-australia-hansard.html
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
****************PLEASE READ THE FOLLOWING CAREFULLY************
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Tuesday, December 14, 2010 TAFS1
Position Paper on Relaxation of the Feed Ban in the EU SUMMARY © TAFS, Berne, 2010
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/tafs1-position-paper-on-relaxation-of.html
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
Wednesday, June 16, 2010
Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
DID EVERYONE FILL OUT THEIR CJD QUESIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Atypical BSE in Cattle
BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
snip...see full text ;
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1
1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to:
John Collinge, E-mail: j.collinge@prion.ucl.ac.uk
Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
--------------------------------------------------------------------------------
Abstract
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
http://www.nature.com/emboj/journal/v21/n23/abs/7594869a.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
Sent: Saturday, December 11, 2010 3:17 PM Subject: Species-barrier-independent prion replication in apparently resistant species
Species-barrier-independent prion replication in apparently resistant species
Pertenece a: UCL University College London Eprints
Descripción: Transmission of prions between mammalian species is thought to be limited by a "species barrier," which depends on differences in the primary structure of prion proteins in the infecting inoculum and the host, Here we demonstrate that a strain of hamster prions thought to be nonpathogenic for conventional mice leads to prion replication to high levels in such mice but without causing clinical disease. Prions pathogenic in both mice and hamsters are produced. These results demonstrate the existence of subclinical forms of prion infection with important public health implications, both with respect to iatrogenic transmission from apparently healthy humans and dietary exposure to cattle and other species exposed to bovine spongiform encephalopathy prions, Current definitions of the species barrier, which have been based on clinical endpoints, need to be fundamentally reassessed.
Autor(es): Hill, AF - Joiner, S - Linehan, J - Desbruslais, M - Lantos, PL - Collinge, J -
Id.: 52395313
Versión: 1.0
Estado: Final
Palabras clave: TRANSMISSIBLE MINK ENCEPHALOPATHY, CREUTZFELDT - JAKOB - DISEASE, FATAL FAMILIAL INSOMNIA, STRAIN VARIATION, TRANSGENIC MICE, SCRAPIE INFECTIVITY, HAMSTER SCRAPIE, VARIANT CJD, BSE AGENT, PROTEIN -
Tipo de recurso: Article -
Tipo de Interactividad: Expositivo
Nivel de Interactividad: muy bajo
Audiencia: Estudiante - Profesor - Autor -
Estructura: Atomic
Coste: no
Copyright: sí
Requerimientos técnicos: Browser: Any -
Fecha de contribución: 10-dic-2010
Contacto:
http://biblioteca.universia.net/html_bura/ficha/params/id/52395313.html
for those interested, see more here with comments........
Saturday, December 11, 2010
Species-barrier-independent prion replication in apparently resistant species
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/species-barrier-independent-prion.html
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
Friday, December 17, 2010
PRION DISEASE Action Plan National Program 103 Animal Health 2012-2017
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/prion-disease-action-plan-national.html
DAY LATE, DOLLAR SHORT $$$
TSS
Dr. Earl Van Assen pleaded guilty to two counts of contravening the Health of Animals Act.
The United States Department of Agriculture placed severe restrictions on importing Canadian cattle following the “mad cow” scare early last decade. Restrictions have since been relaxed, but Canadian veterinarians are still required to certify that cattle bound for export to the U.S. were born after March 1999.
“Some people might feel this is not a big deal,” Crown attorney Christina Cheater told Judge John Guy. “The wrongful certification of cattle... has the potential to cause serious disruption to the export of cattle to the U.S.”
Court heard Van Assen submitted certification documents in February 2009 for 42 cows claiming he inspected the animals and found them suitable for export. Following a subsequent investigation, Van Assen admitted he accepted the word of the farmer exporting the cattle and did not inspect all the animals himself.
Veterinarians are expected to establish a cow’s age in one of three ways: through birth records, a visual inspection or an examination of its teeth.
“Unfortunately, Dr. Van Assen didn’t do any of these things,” Cheater said.
There is no indication any of the exported cattle was diseased, Cheater said.
“But the problem is the USDA is going to look at this very seriously because we are unable to protect our border,” she said.
Defence lawyer Greg Brodsky said Van Assen is guilty of carelessness, not deceit.
“He did make random checks,” Brodsky said. “This wasn’t him trying to fool anybody.”
http://www.winnipegsun.com/news/manitoba/2010/12/21/16639166.html
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA
http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html
Monday, August 30, 2010
Bovine Spongiform Encephalopathy (BSE) CANADA Import Policy for Bovine Animals and Their Products (TAHD-DSAT-IE-2005-9-2) Import Policy updates August
http://madcowtesting.blogspot.com/2010/08/bovine-spongiform-encephalopathy-bse.html
Thursday, August 19, 2010
SCRAPIE CANADA UPDATE Current as of 2010-07-31 The following table lists sheep flocks and/or goat herds confirmed to be infected with scrapie in Canada in 2010.
Current as of: 2010-07-31
http://nor-98.blogspot.com/2010/08/scrapie-canada-update-current-as-of.html
Friday, September 24, 2010 BSE
Surveillance Continues to Benefit Canadian Cattle Producers September 24, 2010 - Notice to Industry
http://madcowtesting.blogspot.com/2010/09/bse-surveillance-continues-to-benefit.html
Saturday, October 2, 2010
BSE surveillance front and centre: CFIA and USA
http://madcowtesting.blogspot.com/2010/10/bse-surveillance-front-and-centre-cfia.html
Cases Regarding the Border Closure due to BSE Concerns
Several Canadian claimants have submitted notices of arbitration under the UNCITRAL Arbitration Rules alleging that the United States has violated NAFTA Chapter Eleven by closing the border to the importation of Canadian cattle after the discovery in 2003 of a case of bovine spongiform encephalopathy (BSE or mad cow disease) in a cow in Alberta, Canada. Claimants are Canadian citizens and corporations that own and operate cattle feeding, feedlot and transportation businesses in Canada, which they allege were damaged by the border closure.
Claimants allege that the border closure violates NAFTA Article 1102 (national treatment). The notices of arbitration seek damages of varying amounts, ranging from CAN$38,000 to CAN$95 million. The total amount of damages sought by claimants is approximately US$235 million.
On January 28, 2008, the tribunal issued its Award on Jurisdiction, dismissing the claims against the United States in their entirety. The tribunal’s award, and other documents in the case, appear below.
-01/28/08 Award on Jurisdiction [575 Kb] -10/10/07 Transcript of the Hearing on the Preliminary Issue - Day Two [166 Kb] -10/09/07 Transcript of the Hearing on the Preliminary Issue - Day One [260 Kb] -08/03/07 Procedural Order No. 3 [26 Kb] -07/05/07 Claimants' Rejoinder on the Preliminary Issue [849 Kb] -05/01/07 U.S. Reply on the Preliminary Issue [245 Kb] -03/01/07 Article 1128 Submission of Mexico [47 Kb] -01/30/07 Claimants' Response on the Preliminary Question [2303 Kb] -12/01/06 U.S. Memorial on the Preliminary Issue [167 Kb] -11/07/06 Procedural Order No. 2 [62 Kb] -10/20/06 Procedural Order No. 1 [122 Kb] -06/02/05 Jim McNall Notice of Arbitration [393 Kb] -06/02/05 Leslie Smith Notice of Arbitration [393 Kb] -06/02/05 Michael Sears Notice of Arbitration [393 Kb] -06/02/05 Rex Vandenberg Notice of Arbitration [393 Kb] -06/02/05 Richard Hiebert Notice of Arbitration [392 Kb] -06/02/05 Rod Oosterbroek Notice of Arbitration [392 Kb] -06/02/05 TER Cattle Notice of Arbitration [393 Kb] -05/20/05 Andrew Oosterbroek Notice of Arbitration [392 Kb] -05/20/05 Brad Hopkins Notice of Arbitration [396 Kb] -05/20/05 Brent Byers Notice of Arbitration [395 Kb] -05/20/05 Brent Fisher Notice of Arbitration [393 Kb] -05/20/05 Byron Sedore Notice of Arbitration [394 Kb] -05/20/05 Chris Irwin Notice of Arbitration [394 Kb] -05/20/05 Cornelius Van Hal Notice of Arbitration [392 Kb] -05/20/05 Darren Johnston Notice of Arbitration [394 Kb] -05/20/05 Dave Knapp Notice of Arbitration [394 Kb] -05/20/05 David Hewitt Notice of Arbitration [394 Kb] -05/20/05 Donald Procter Notice of Arbitration [394 Kb] -05/20/05 George Adams Notice of Arbitration [392 Kb] -05/20/05 Glen Thompson Notice of Arbitration [392 Kb] -05/20/05 Graham Alexander Notice of Arbitration [394 Kb] -05/20/05 Helmut Friesen Notice of Arbitration [393 Kb] -05/20/05 James Wiskerke Notice of Arbitration [392 Kb] -05/20/05 Joseph Daunt Notice of Arbitration [394 Kb] -05/20/05 Keith Kerr Notice of Arbitration [394 Kb] -05/20/05 Ken Andreychuk Notice of Arbitration [396 Kb] -05/20/05 Kevin Freiburger Notice of Arbitration [394 Kb] -05/20/05 Larry Brodersen Notice of Arbitration [392 Kb] -05/20/05 Lee Robson Notice of Arbitraiton [450 Kb] -05/20/05 Maria Vanden Elzen Notice of Arbitration [413 Kb] -05/20/05 Murray Johnston Notice of Arbitration [395 Kb] -05/20/05 NFL Holdings Notice of Arbitration [456 Kb] -05/20/05 Paul Gowing Notice of Arbitration [394 Kb] -05/20/05 Paul MacIntyre Notice of Arbitration [394 Kb] -05/20/05 Peter Schwenk Notice of Arbitration [448 Kb] -05/20/05 Peter Vander Heyden Notice of Arbitration [415 Kb] -05/20/05 Robert Emerson Notice of Arbitration [394 Kb] -05/20/05 Robert Laidlaw Notice of Arbitration [393 Kb] -05/20/05 Ron Coulter Notice of Arbitration [393 Kb] -05/20/05 Ross McCall Notice of Arbitration [394 Kb] -05/20/05 Ryan Kasko Notice of Arbitration [393 Kb] -05/11/05 Barry Hillman Notice of Arbitration [392 Kb] -05/11/05 Ben Gardiner Notice of Arbitration [416 Kb] -05/11/05 Bernie Loman Notice of Arbitration [392 Kb] -05/11/05 Blair Bieman Notice of Arbitration [394 Kb] -05/11/05 Blake Holtman Notice of Arbitration [393 Kb] -05/11/05 Bruce Groenenboom Notice of Arbitration [403 Kb] -05/11/05 Butch Martin Notice of Arbitration [441 Kb] -05/11/05 Dale Pallister Notice of Arbitration [394 Kb] -05/11/05 Darwin Ullery Notice of Arbitration [412 Kb] -05/11/05 Dave Gardiner Notice of Arbitration [415 Kb] -05/11/05 Dave Johnston Notice of Arbitration [415 Kb] -05/11/05 Dave Matthies, Notice of Arbitration [421 Kb] -05/11/05 David Millsap Notice of Arbitration [394 Kb] -05/11/05 Doug Briggs Notice of Arbitration [394 Kb] -05/11/05 Doug Nieboer Notice of Arbitration [392 Kb] -05/11/05 Doug Shelswel Notice of Arbitration [394 Kb] -05/11/05 Ed Stronks Notice of Arbitration [413 Kb] -05/11/05 Eric Thacker Notice of Arbitration [394 Kb] -05/11/05 Eve Kraayenbrink Notice of Arbitration [415 Kb] -05/11/05 Firmin Declercq Notice of Arbitration [392 Kb] -05/11/05 Frank Zettler Notice of Arbitration [395 Kb] -05/11/05 G. Lee Hochstein Notice of Arbitration [374 Kb] -05/11/05 George Alton Notice of Arbitration [394 Kb] -05/11/05 George Maxwell Notice of Arbitration [394 Kb] -05/11/05 Glen Armitage Notice of Arbitration [392 Kb] -05/11/05 Grant Nelson Notice of Arbitration [393 Kb] -05/11/05 Harry Duban Notice of Arbitration [393 Kb] -05/11/05 Harry Vandersteen Notice of Arbitration [393 Kb] -05/11/05 Harry Welsch Notice of Arbitration [393 Kb] -05/11/05 Henry Van Hall Notice of Arbitration [392 Kb] -05/11/05 Herb Groenenboom Notice of Arbitration [392 Kb] -05/11/05 Herbert Serfas Notice of Arbitration [403 Kb] -05/11/05 Herman Stroeve Notice of Arbitration [449 Kb] -05/11/05 Ian MacLean Notice of Arbitration [394 Kb] -05/11/05 Jim Steed Notice of Arbitration [394 Kb] -05/11/05 Joe Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Schooten Notice of Arbitration [392 Kb] -05/11/05 John Stroeve Notice of Arbitration [423 Kb] -05/11/05 John Vander Heyden Notice of Arbitration [392 Kb] -05/11/05 Julie Coe Notice of Arbitration [394 Kb] -05/11/05 Keith Scott Notice of Arbitration [392 Kb] -05/11/05 Larry Lehrbass Notice of Arbitration [394 Kb] -05/11/05 Leighton Kolk Notice of Arbitration [392 Kb] -05/11/05 Lloyd Sproule Notice of Arbitration [391 Kb] -05/11/05 Louis Ypma Notice of Arbitration [392 Kb] -05/11/05 Marty Wren Notice of Arbitration [392 Kb] -05/11/05 Mary Conlin Notice of Arbitration [395 Kb] -05/11/05 Murray Brodhagen Notice of Arbitration [394 Kb] -05/11/05 Nick Popovic Notice of Arbitration [394 Kb] -05/11/05 Paul Adams Notice of Arbitration [392 Kb] -05/11/05 Renus Van Hal Notice of Arbitration [392 Kb] -05/11/05 Richard Visser Notice of Arbitration [392 Kb] -05/11/05 Rients Wever Notice of Arbitration [392 Kb] -05/11/05 Robert Cooke Notice of Arbitration [415 Kb] -05/11/05 Robert Vander Heyden Notice of Arbitration [393 Kb] -05/11/05 Ryan Gibson Notice of Arbitration [392 Kb] -05/11/05 Steve McKague Notice of Arbitration [394 Kb] -05/11/05 Stuart Alton Notice of Arbitration [394 Kb] -05/11/05 Ward Takeda Notice of Arbitration [393 Kb] -05/11/05 Wayne Beattie Notice of Arbitration [394 Kb] -05/11/05 Wilfred Haines Notice of Arbitration [415 Kb] -03/16/05 Cor Van Raay Notice of Arbitration [396 Kb] -03/16/05 Joe Groenenboom Notice of Arbitration [392 Kb] -03/16/05 John Vander Heyden Notice of Arbitration [393 Kb] -03/16/05 Larry Nolan Notice of Arbitration [393 Kb] -03/16/05 Theodorus de Boer Notice of Arbitration [392 Kb]
http://www.state.gov/s/l/c14683.htm
POT CALLING KETTLE BLACK ;
Thursday, November 18, 2010
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html
LETS start with the UKBSEnvCJD only theory, lets look at UK exports to USA, Canada, and Mexico. the imported only theory. ...
1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY other Countries list in PDF file)
USA -------- TOTALS ''8'' TONS CANADA -- TOTALS ''29'' TONS
1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA
USA ------- TOTALS ''358'' TONS
CANADA --TOTALS ''24'' TONS
BONE-IN BEEF AND VEAL
USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons above?)
UK EXPORT OF LIKE CATTLE TO USA AND CANADA
1986 TO 1996 USA TOTAL = 1297
1986 TO 1996 CAN TOTAL = 299
http://collections.europarchive.org/tna/20080102161741/http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf
UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987
CANADA -- 64,526 KG
UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED OR FROZEN OTHER THAN LIVER DEC 1987 YTD
USA -- 45,943 KG
UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988
CANADA -- 4,163 KG
PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE TO DEC 1988
USA -------- 28,609 KG CANADA -- 22,044 KG
MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989
USA -------- 17,880 KG MEXICO---- 33,444 KG
BONELESS MEAT OF BOVINE 1989
USA --------111,953 KG CANADA---1,800 KG MEXICO --- 1,143,387 KG
EDIBLE OFFAL OF BOVINE ANIMALS 1989
USA -------- 19,980 KG MEXICO--- 31,244 KG
MORE........
MEAT OF BOVINE ANIMALS BONELESS 1990
USA 146,443
http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf
UK Exports of Live Cattle by Value 1986-96
USA 697 LIVE CATTLE
CANADA 299 LIVE CATTLE
http://collections.europarchive.org/tna/20081106012846/http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf
UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995
USA 24 TONS
CANADA 83 TONS
http://collections.europarchive.org/tna/20080102193106/http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf
HOWEVER, my files show 44 tons of greaves for USA. ...TSS
Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: S.J.Pearsall@esg.maff.gsi.gov.uk
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: flounder@wt.net (Receipt Notification Requested) (Non Receipt Notification Requested)
Terry
Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes
1980 1981 12 1982 1983 1984 10 1985 2 1986 1987 1988 1989 20 1990
Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222).
Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C
====================================== END...TSS
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
https://lists.aegee.org/cgi-bin/wa?A2=ind0306&L=BSE-L&P=R1740&X=1ABE7910CF6C11F2D0&Y=flounder9%40verizon.net&m=10864
Subject: Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Date: August 24, 2005 at 2:47 pm PST
August 24, 2005
Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION
Greetings APHIS ET AL,
My name is Terry S. Singeltary Sr.
I would kindly like to comment on [Docket No. 05-004-1] RIN 0579-AB93 ;
PROPOSED RULES
Exportation and importation of animals and animal products:
Whole cuts of boneless beef from-
Japan,
48494-48500 [05-16422]
http://www.regulations.gov/fdmspublic/ContentViewer?objectId=0900006480086ebc&disposition=attachment&contentType=msw6
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed
PLEASE SEE FULL TEXT HERE ;
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA
http://madcowfeed.blogspot.com/2008/07/docket-no-03-080-1-usda-issues-proposed.html
Friday, August 22, 2008
MEXICO blocks Alberta cattle following the discovery of Canada's 14th case of mad cow disease
http://madcowtesting.blogspot.com/2008/08/mexico-blocks-alberta-cattle-following.html
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA
http://madcowtesting.blogspot.com/
The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.
http://www.oie.int/boutique/extrait/06heim937950.pdf
P.9.21
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *It also suggests a similar cause or source for atypical BSE in these countries.
http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.europa.eu/EFSA/efsa_locale-1178620753812_1211902594180.htm
Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
please see full text ;
http://www.efsa.europa.eu/en/scdocs/doc/3rax1.pdf
Monday, November 23, 2009
BSE GBR RISK ASSESSMENTS UPDATE NOVEMBER 23, 2009 COMMISSION OF THE EUROPEAN COMMUNITIES AND O.I.E. COMMISSION DECISION of 11 November 2009
http://docket-aphis-2006-0041.blogspot.com/2009/11/bse-gbr-risk-assessments-update.html
Tuesday, November 02, 2010
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Monday, November 22, 2010
Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control
REVIEW ARTICLES
http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
snip...
http://collections.europarchive.org/tna/20080102185948/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
IN CONFIDENCE
IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?
http://collections.europarchive.org/tna/20080102233201/http://www.bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
IN CONFIDENCE
PERCEPTIONS OF A SLOW VIRUS DISEASE IN ANIMALS IN THE USA
http://collections.europarchive.org/tna/20081106012811/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
2010
Rural and Regional Affairs and Transport References Committee The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
http://madcowusda.blogspot.com/2009/09/mad-cow-usa-1997-video.html
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.html
Tuesday, March 16, 2010
COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA
COMMONWEALTH OF AUSTRALIA
Proof Committee Hansard
RRA&T 2 Senate Friday, 5 February 2010
RURAL AND REGIONAL AFFAIRS AND TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association
CARTER, Mr John Edward, Director, Australian Beef Association
CHAIR—Welcome. Would you like to make an opening statement?
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:
You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heidenhain variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:
The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.
Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:
snip...see full text 110 pages ;
http://www.aph.gov.au/hansard/senate/commttee/S12742.pdf
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
for those interested, please see much more here ;
http://docket-aphis-2006-0041.blogspot.com/2010/03/commonwealth-of-australia-hansard.html
http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html
****************PLEASE READ THE FOLLOWING CAREFULLY************
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
Tuesday, December 14, 2010 TAFS1
Position Paper on Relaxation of the Feed Ban in the EU SUMMARY © TAFS, Berne, 2010
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/tafs1-position-paper-on-relaxation-of.html
Tuesday, June 1, 2010
USA cases of dpCJD rising with 24 cases so far in 2010
http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html
Wednesday, June 16, 2010
Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html
Tuesday, December 14, 2010
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010
http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html
DID EVERYONE FILL OUT THEIR CJD QUESIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
http://cjdquestionnaire.blogspot.com/
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Atypical BSE in Cattle
BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
snip...see full text ;
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1
1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to:
John Collinge, E-mail: j.collinge@prion.ucl.ac.uk
Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
--------------------------------------------------------------------------------
Abstract
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
http://www.nature.com/emboj/journal/v21/n23/abs/7594869a.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
Sent: Saturday, December 11, 2010 3:17 PM Subject: Species-barrier-independent prion replication in apparently resistant species
Species-barrier-independent prion replication in apparently resistant species
Pertenece a: UCL University College London Eprints
Descripción: Transmission of prions between mammalian species is thought to be limited by a "species barrier," which depends on differences in the primary structure of prion proteins in the infecting inoculum and the host, Here we demonstrate that a strain of hamster prions thought to be nonpathogenic for conventional mice leads to prion replication to high levels in such mice but without causing clinical disease. Prions pathogenic in both mice and hamsters are produced. These results demonstrate the existence of subclinical forms of prion infection with important public health implications, both with respect to iatrogenic transmission from apparently healthy humans and dietary exposure to cattle and other species exposed to bovine spongiform encephalopathy prions, Current definitions of the species barrier, which have been based on clinical endpoints, need to be fundamentally reassessed.
Autor(es): Hill, AF - Joiner, S - Linehan, J - Desbruslais, M - Lantos, PL - Collinge, J -
Id.: 52395313
Versión: 1.0
Estado: Final
Palabras clave: TRANSMISSIBLE MINK ENCEPHALOPATHY, CREUTZFELDT - JAKOB - DISEASE, FATAL FAMILIAL INSOMNIA, STRAIN VARIATION, TRANSGENIC MICE, SCRAPIE INFECTIVITY, HAMSTER SCRAPIE, VARIANT CJD, BSE AGENT, PROTEIN -
Tipo de recurso: Article -
Tipo de Interactividad: Expositivo
Nivel de Interactividad: muy bajo
Audiencia: Estudiante - Profesor - Autor -
Estructura: Atomic
Coste: no
Copyright: sí
Requerimientos técnicos: Browser: Any -
Fecha de contribución: 10-dic-2010
Contacto:
http://biblioteca.universia.net/html_bura/ficha/params/id/52395313.html
for those interested, see more here with comments........
Saturday, December 11, 2010
Species-barrier-independent prion replication in apparently resistant species
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/species-barrier-independent-prion.html
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html
Friday, December 17, 2010
PRION DISEASE Action Plan National Program 103 Animal Health 2012-2017
http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/prion-disease-action-plan-national.html
DAY LATE, DOLLAR SHORT $$$
TSS
Subscribe to:
Posts (Atom)
