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.
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"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
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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.
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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.
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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...
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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
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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
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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.
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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
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