Wednesday, April 25, 2012

ACTUALITY – USDA Chief Veterinary Officer On Surveillance And Milk Safety and BSE aka MAD COW DISEASE

USDA Chief Veterinary Officer On Surveillance And Milk Safety

A new actuality is available on the USDA FTP site. The actuality can also be seen on USDA's YouTube channel.

Note for broadcasters: B-roll of cows follows Dr. Clifford’s actuality on the file available on the FTP site.

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User name: usdanews


Password: Newscontent1


Filename for TV Actuality: Clifford safeguards


The new file is in QuickTime Movie (H.264)




Please email bob.ellison@usda.gov if you have problems or suggestions.


Also, use this free ftp client if you have problems.





ACTUALITY – USDA Chief Veterinary Officer On Surveillance And Milk Safety





INFO: USDA Chief Veterinary Officer Dr. John Clifford explains the system of strong interlocking safeguards designed to protect human and animal health.


Dr. John Clifford, Chief Veterinary Officer For the United States of America:


Hello, I’m Dr. John Clifford, chief veterinary officer for the United States of America. At USDA, we oversee a system of strong interlocking safeguards that protect human and animal health, as well as food safety in the United States. Those safeguards include targeted surveillance activities. Through that surveillance program, on April 24th we confirmed the nation’s 4th case of bovine spongiform encephalopathy, or BSE, in a dairy cow on the west coast. BSE is a fatal disease affecting the central nervous system of adult cattle. We proactively test for BSE in order to detect the disease at the very low level of less than 1 case per million adult cattle, to assess any change in the BSE status of U.S. cattle, and to identify any rise in BSE prevalence in the country. Our targeted surveillance program has been in place since 1990. We currently test for BSE at levels 10 times greater than World Animal Health Organization standards. We test approximately 40,000 animals per year, taking those samples from cattle where the disease is most likely to be found. This includes animals that have clinical signs consistent with BSE, have other central nervous system abnormalities, die for unknown reasons, or cannot walk or move well. We collect samples from a variety of locations where the targeted groups of animals are found. The samples from the animal in question were taken at a rendering facility in California. Our surveillance works. We found this case of BSE. The carcass of the animal was held at the rendering facility and then will be destroyed. It was never presented for processing for human consumption. At no time did it present a risk to the food supply. Our food supply remains safe. With California being a large dairy state, there have been some concerns raised about milk. Let me assure you, our milk is safe to drink. Scientific research demonstrates that BSE cannot be transmitted in cow’s milk, even if that milk comes from a cow with BSE. The World Health Organization has stated that tests on milk from BSE-infected animals have not shown any BSE infectivity. Milk and milk products, are, therefore considered safe to consume. Let me assure consumers and our trading partners that ongoing BSE surveillance allows the USDA to detect BSE at very low levels in the U.S. cattle population. The safeguarding system is working. For updates on our ongoing investigation and more information about BSE in general, visit our website at www.usda.gov.







these folks should no now to never say never $$$



BOTTOM LINE, milk and atypical L-type BASE BSE, they have no clue yet. they must do transmission studies. with atypical L-type BASE BSE, this type is much more virulent. ...tss



MILK and Transmissible Spongiform Encephalopathy TSE PRION


Terry S. Singeltary Sr.


11/18/2011


TO date, and i imphasize 'to date', there has been no documented evidence of transmission of BSE via milk of BSE infected cow to another cow. however, with the limited testing done to date, on just the c-BSE, you cannot rule this out, especially with the atypical BSE L-type i.e. BASE, being much more virulent. Concern has been increasing due to fluids from TSE species i.e. blood, urine, and milk, and the fact that infectivity has been detected.



Prion infectivity has now been detected in blood, urine and milk.



please see ;




Seven main threats for the future linked to prions


The NeuroPrion network has identified seven main threats for the future linked to prions.


First threat


The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.


*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.


Second threat


In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.


Third threat


The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.


Fourth threat


Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,


whereas other countries, including the US,


Brazil, and Argentine do not have these constraints.


However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.


Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.


Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.


Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.









Goat BSE: Proposal for Improvement of Goat TSE Discriminative Diagnosis and Susceptibility based Assessment of BSE Infectivity in Goat Milk and Meat



Funded by EU, DEFRA This project is run by a consortium of ten research teams in seven EU countries.



In light of the known ability of the BSE agent to cross the animal/human species barrier, recent evidence establishing the presence of BSE in goat is especially alarming, as it represents a new potential risk of food-born contamination to human consumers of goat milk and meat products. The main objective is to determine the tissue distribution of BSE after oral exposure of goats and to do this while simultaneously generating data on genetic susceptibility in the most common used production breeds. This proposal aims at (i) providing data for the evaluation of human risk associated with goat BSE, (ii) providing pathogenesis data and biological material from first and second passage BSE in goats, (iii) evaluating the possibility of BSE self-maintenance in goat herds through maternal or horizontal transmission, (iv) validating and improving our ability to detect caprine BSE and discriminate it from scrapie in goats. Our approach will establish the influence of PrP gene polymorphisms on scrapie and BSE susceptibility so that genetics could potentially be used for the control of field TSE outbreaks in goats. We will also document European field TSE strain variability in goats by recruiting a large number of TSE goat isolates from affected European countries. Already established or specifically created animal models (strain typing) and biochemical tools (PrPSc typing), will be tested for their ability to efficiently discriminate goat BSE/scrapie. Finally, by measuring infectivity in various tissues collected from goats at different stages of BSE infection, we will provide essential data for quantitative risk assessment.









Vet. Res. (2010) 41:48 Original article




Pathogenesis of natural goat scrapie: modulation by host PRNP genotype and effect of co-existent conditions




Lorenzo González1*, Stuart Martin1, Stephen A.C. Hawkins2, Wilfred Goldmann3, Martin Jeffrey1 and Sílvia Sisó1


1 Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, Penicuik, Midlothian EH26 0PZ, United Kingdom 2 VLA-Weybridge, Addlestone, Surrey KT15 3NB, United Kingdom 3 The Roslin Institute and R(D)SVS University of Edinburgh, Roslin, Midlothian EH25 9PS, United Kingdom


* Corresponding author: l.gonzalez@vla.defra.gsi.gov.uk


Received: 13 January 2010 Accepted: 7 April 2010


Abstract


After detection of a high prevalence of scrapie in a large dairy goat herd, 72 infected animals were examined by immunohistochemistry with prion protein (PrP) antibody Bar224 to study the pathogenesis of the infection. Tissues examined included the brain and thoracic spinal cord (TSC), a wide selection of lymphoreticular system (LRS) tissues, the distal ileum and its enteric nervous system (ENS), and other organs, including the mammary gland. The whole open reading frame of the PRNP gene was sequenced and antibodies to caprine arthritis-encephalitis virus (CAEV) infection were determined. Unexpectedly, accumulation of disease-associated PrP (PrPd) in the brain was more frequent in methionine carriers at codon 142 (24/32, 75.0%) than amongst isoleucine homozygotes (14/40, 35.0%). The latter, however, showed significantly greater amounts of brain PrPd than the former (average scores of 9.3 and 3.0, respectively). A significant proportion of the 38 goats that were positive in brain were negative in the ENS (44.7%) or in the TSC (39.5%). These results, together with the early and consistent involvement of the circumventricular organs and the hypothalamus, point towards a significant contribution of the haematogenous route in the process of neuroinvasion. Chronic enteritis was observed in 98 of the 200 goats examined, with no association with either scrapie infection or presence of PrPd in the gut. Lymphoproliferative interstitial mastitis was observed in 13/31 CAEV-positive and scrapie-infected goats; PrPd in the mammary gland was detected in five of those 13 goats, suggesting a possible contribution of CAEV infection in scrapie transmission via milk.


Key words: scrapie / goat / prion neuroinvasion / transmissible spongiform encephalopathy / CAEV


© The British Crown, published by INRA/EDP Sciences, 2010








6 January 2010 -


The public “TSEs in goats” website Link:






Since December 2006 a new EU funded project has started that has been essentially developed from NeuroPrion TSEgoat task group members and their progress: “GoatBSE: Proposal for improvement of goat TSE discriminative diagnosis and susceptibility based assessment of BSE infectivity in goat milk and meat.” (European STREP project FOOD-CT-2006-36353, frame work 6, area Thematic priority: Food quality and safety). In this project the focus of study is about consequences of an infection with BSE in goats for disease transmission and product safety.








Sheep with Scrapie and Mastitis Transmit Infectious Prions through the Milk?



Ciriaco Ligios1,†, Maria Giovanna Cancedda1, Antonello Carta2, Cinzia Santucciu1, Caterina Maestrale1, Francesca Demontis1, Mariangela Saba1, Cristiana Patta1, James C. DeMartini3, Adriano Aguzzi4,†,* and Christina J. Sigurdson4,5,6,†,*


+ Author Affiliations


1Istituto Zooprofilattico Sperimentale della Sardegna, Sassari, Italy


2Research Unit of Genetics and Biotechnology, DIRPA, AGRIS Sardinia, Olmedo, Italy


3Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado


4Institute of Neuropathology, UniversitätsSpital Zürich, Zürich, Switzerland


5 Department of Pathology, School of Medicine, University of California, San Diego, California


6Department of Pathology, Microbiology, and Immunology, University of California, Davis, California


Next Section ABSTRACT


Prions are misfolded proteins that are infectious and naturally transmitted, causing a fatal neurological disease in humans and animals. Prion shedding routes have been shown to be modified by inflammation in excretory organs, such as the kidney. Here, we show that sheep with scrapie and lentiviral mastitis secrete prions into the milk and infect nearly 90% of naïve suckling lambs. Thus, lentiviruses may enhance prion transmission, conceivably sustaining prion infections in flocks for generations. This study also indicates a risk of prion spread to sheep and potentially to other animals through dietary exposure to pooled sheep milk or milk products.











EFSA Journal 2011; 9(1):1945 Suggested citation:


EFSA Panel on Biological Hazards (BIOHAZ);


Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans.



EFSA Journal 2011;9(1):1945. [111 pp.] doi:10.2903/j.efsa.2011.1945. Available online: www.efsa.europa.eu/efsajournal © European Food Safety Authority, 2011 SCIENTIFIC OPINION Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans1 EFSA Panel on Biological Hazards (BIOHAZ)2, 3 European Food Safety Authority (EFSA), Parma, Italy European Centre for Disease Prevention and Control (ECDC)4, 5 Stockholm, Sweden


More recent EFSA opinions focused on the human exposure risk to TSEs through consumption of products deriving from small ruminants (ovine and caprine carcasses below six months, milk and milk products), but only focused on human exposure, without discussing the zoonotic potential of small ruminants TSEs (EFSA, 2008a, 2008c). A recent EFSA opinion (EFSA Panel on Biological Hazards (BIOHAZ), 2010a) provided updated data on the TSE infectivity distribution in small ruminant tissues. It also estimated the relative reduction of BSE infectivity load that can be achieved in the carcass of a small ruminant through the implementation of the current or alternative policies in terms of removal of Specified Risk Material (SRM). The zoonotic potential of TSE agents in small ruminants is, however, not discussed in the opinion.


The TSE agent disseminates to the CNS (brain and spinal cord) apparently via the Enteric Nervous System and its nerves fibers (Andreoletti et al., 2000; Jeffrey et al., 2001; van Keulen et al., 2002), which is considered to accumulate TSE agents until around half of the incubation period. From there the agent could redistribute (centrifugally) to the peripheral nervous system and skeletal muscle (Andreoletti et al., 2004). Additionally, infectivity was also reported to be present in blood (Hunter et al., 2002), and in blood and in milk and colostrum (from the first lactation) from animals during incubation (Konold et al., 2008; Lacroux et al., 2008). In blood, the infectious agent can be detected as early as at 3 months of age and persists throughout the incubation period (Andreoletti et al., 2007).


Finally, protection measures applied all along the food chain against small ruminants TSEs in the EU mainly rely at operational level on specified risk material (SRM) removal, i.e exclusion from food chain of tissues that can contain a high infectious load. However, for practical reasons, the SRM measures do not imply discarding from the food chain of all the infectious tissues and animal products that could contain infectivity (EFSA, 2008c). Moreover, infectivity was recently identified in tissues like skeletal muscles or in products like milk from small ruminants incubating scrapie, tissues that were previously considered to be non infectious.









Commentary


In vitro amplification of prions from milk in the detection of subclinical infections


Volume 3, Issue 4 October/November/December 2009 Pages 236 - 239 http://dx.doi.org/10.4161/pri.3.4.10425


Kevin C. Gough, Claire A. Baker, Maged Taema and Ben C. Maddison


View affiliations


Prions can be amplified by serial protein misfolding cyclic amplification (sPMCA) from the milk of a high proportion of apparently healthy, scrapie exposed sheep with PRNP genotypes not previously associated with high disease penetrance1. These data strongly suggest the widespread presence of subclinical scrapie infections within scrapie-exposed flocks containing sheep with a range of susceptible PRNP genotypes. These data also lead to the hypothesis that similar subclinical disease states may be common for other animal and human prion diseases. Furthermore, the application of sPMCA to milk provides a method to detect such subclinical disease. Here, we describe the high level amplification of bovine spongiform encephalopathy (BSE) prions from both ovine and bovine origin, a methodology that will facilitate the detection of any prions secreted within bovine and ovine milk during subclinical and clinical BSE disease.







Prion Protein in Milk


Nicola Franscini,1 Ahmed El Gedaily,1 Ulrich Matthey,1 Susanne Franitza,1 Man-Sun Sy,2 Alexander Bürkle,3 Martin Groschup,4 Ueli Braun,5 and Ralph Zahn1


Conclusions/Significance


In view of a recent study showing evidence of prion replication occurring in the mammary gland of scrapie infected sheep suffering from mastitis, the appearance of PrPC in milk implies the possibility that milk of TSE-infected animals serves as source for PrPSc.











WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010



snip...



Since the publication in 2006 of Annex 1 (Major Categories of Infectivity) in the ‘‘WHO Guidelines on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies’’, some tissues (ovary, uterus, mammary glands/udder, skin, adipose tissue, and heart/pericardium) and body fluids (saliva, milk, urine, and feces) in which infectivity had not been detected, have since been found to contain infectivity or PrPTSE and therefore have there been moved from the category of ‘‘tissues with no detectable infectivity’’ ’’ to the category of ‘‘lower-infectivity tissues.’’






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.











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




Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...










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...









PLoS One. 2012; 7(2): e31449.

Published online 2012 February 21. doi: 10.1371/journal.pone.0031449

PMCID: PMC3283643

Infectivity in Skeletal Muscle of Cattle with Atypical Bovine Spongiform Encephalopathy

The present data offer novel information on the tropism of the BASE agent and highlight relevant public health issues. While the transmission barrier for classical BSE is high in most species, BASE prions are readily transmissible to a variety of mammals including non-human primates [11]–[13], [35]. Accordingly, the possibility of spreading of BASE prions through skeletal muscle to other species should be taken into account and evaluated in risk analysis studies.






PINK SLIME LFTB MSM MRM BSE TSE PRION




Saturday, April 21, 2012



HISD seeks refund on burgers with 'pink slime'














Wednesday, March 14, 2012





PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP














Sunday, August 28, 2011






Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

http://sciencebushwhacked.blogspot.com/2011/08/rick-perry-texas-bse-aka-mad-cow.html
BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!
Tuesday, April 24, 2012




MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA







Wednesday, April 25, 2012








4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012






http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/4th-mad-cow-disease-usa-california.html







Wednesday, April 25, 2012




USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 – 2012




http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/usa-mad-cow-disease-and-cjd-there-from.html









America's Mad Cow crisis by John Stauber





http://www.commondreams.org/view/2012/04/26-1








layperson
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net
Posted by at No comments:

USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 - 2012

USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999-2012




Re: vCJD in the USA * BSE in U.S.


15 November 1999 Terry S Singeltary, NA




In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.


Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.




My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;




vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.




The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?


CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.


So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.




No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;


Since 1990 the U.S. has raised 1,250,880,700 cattle;


Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;


There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;


Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;


Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.


I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.


Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.


It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........


The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.


Terry S. Singeltary Sr.


P.O. Box 42, Bacliff, Texas 77518 USA


flounder@wt.net


Competing interests:None declared










U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000 Terry S Singeltary


In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;


"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."


Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.


Something else I find odd, page 16;


"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."


A few more factors to consider, page 15;


"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."


"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."


"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."


Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.


Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.


To be continued...


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA


Competing interests:None declared








Letters


JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Terry S. Singeltary, Sr Bacliff, Tex


Since this article does not have an abstract, we have provided the first 150 words of the full text.


KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.


References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.









Looking further into this 'continuous rendering'. I first wrote about it here ;





U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...


2 January 2000


snip...


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;


"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."


Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.


Something else I find odd, page 16;


"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."


A few more factors to consider, page 15;


snip...








Qualitative Analysis of BSE Risk Factors in the United States


February 13, 2000 at 3:37 pm PST


(BSE red book)









DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:









"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.


Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.


"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...

















Suspect symptoms


What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?


28 Mar 01


Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.


Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.


Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD. "This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.


Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.


Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.


As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.


"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.


But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.


People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.


But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."


There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.


Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.







Published March 26, 2003


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


Terry S. Singeltary, retired (medically)


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?


Published March 26, 2003







Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch


My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally , he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling teeth , Singeltary argues. You get it when they want you to have it, and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings ; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure . The USA should develop a system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters two of whom were friends who died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans ; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further . Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat . He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited .








THE PATHOLOGICAL PROTEIN


BY Philip Yam


Yam Philip Yam News Editor Scientific American www.sciam.com


Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.


CHAPTER 14


Laying Odds


Are prion diseases more prevalent than we thought?


Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?


Revisiting Sporadic CJD


It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.


Singeltary has similar inclinations. ...


snip...


THE PATHOLOGICAL PROTEIN


Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9


June 2003


BY Philip Yam


CHAPTER 14 LAYING ODDS


Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.


























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.







CJD Singeltary submission to PLOS ;


No competing interests declared.


see full text ;






http://www.plosone.org/annotation/listThread.action?root=363








Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
















full text with source references ;








Tuesday, November 08, 2011


Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper


Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.









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 Heinemann 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:


snip...see full text 110 pages ;







for those interested, please see much more here ;







Friday, January 6, 2012


OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease









BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009




Subject: Re: Hello Dr. Gibbs...........


Date: Wed, 29 Nov 2000 14:14:18 –0500


From: "Clarence J. Gibbs, Jr., Ph.D."


To: "Terry S. Singeltary Sr." References: <3a254430.9fb97284@wt.net>


Hi Terry:


326 E Stret N.E., Washington, D. C. 20002.


Better shrimp and oysters than cards!!!!


Have a happy holiday and thanks for all the information you bring to the screen.


Joe Gibbs


==========









Tuesday, April 24, 2012


MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA






***atypical L-type BASE BSE***




Wednesday, April 25, 2012



4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012








Saturday, March 5, 2011


MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA







Sunday, February 12, 2012


National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas







Wednesday, March 28, 2012


VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $








Thursday, April 12, 2012



Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010



Eurosurveillance, Volume 17, Issue 15, 12 April 2012




Research articles






America's Mad Cow Crisis by John Stauber


http://www.commondreams.org/view/2012/04/26-1







layperson



Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

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