Tuesday, December 29, 2015

Congress repeals country-of-origin labeling rule for beef and pork



Release No. 0345.15 Contact: USDA Office of Communications 202-720-4623


Statement from Agriculture Secretary Tom Vilsack on the Country of Origin Labeling Requirements for Beef and Pork


WASHINGTON, Dec. 18, 2015 – Agriculture Secretary Tom Vilsack today released the following statement regarding the language in the omnibus bill repealing the country of origin labeling requirements for beef and pork products.


"The omnibus bill repealed the country of origin labeling (COOL) requirements for muscle cuts of beef and pork, and ground beef and pork. Effective immediately, USDA is not enforcing the COOL requirements for muscle cut and ground beef and pork outlined in the January 2009 and May 2013 final rules."


USDA will be amending the COOL regulations as expeditiously as possible to reflect the repeal of the beef and pork provisions. In addition, all imported and domestic meat will continue to be subject to rigorous inspections by USDA to ensure food safety.




USDA is an equal opportunity provider and employer. To file a complaint of discrimination, write: USDA, Office of the Assistant Secretary for Civil Rights, Office of Adjudication, 1400 Independence Ave., SW, Washington, DC 20250-9410 or call (866) 632-9992 (Toll-free Customer Service), (800) 877-8339 (Local or Federal relay), (866) 377-8642 (Relay voice users).



USDA Looking at Voluntary COOL Program


Yesterday at 10:12 AM in Agriculture




LMAO !!!


yep, that voluntary mad cow feed ban worked so well, (NOT), we are now suppose to believe voluntary cool will work?


any voluntary move on COOL and that would/will be a joke.


USDA, OIE et al are already the laughing stock of the globe in animal disease, when it comes to the TSE prion disease aka mad cow type disease.


Veterinary Record 2015;177:381 doi:10.1136/vr.h5454 News and Reports One health THE World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research


THE World Organisation for Animal Health (OIE) and the Institut Pasteur have agreed to strengthen their cooperation in the fields of animal disease and zoonosis research, education, surveillance and control, in line with the One Health concept, through a new collaborative agreement.


The Institut Pasteur is



Veterinary Record 2015;177:379 doi:10.1136/vr.h5446


News and Reports


Defra seeks a dialogue on animal import controls Defra is seeking ‘ideas and discussion’ as part of a review in England of the Trade in Animals and Related Products Regulations 2011. The Regulations govern veterinary border controls for live animals and products of animal origin.



>THE World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research<


please forgive me if I don’t believe you $$$


I remember...


>>>PARIS -- The World Organization for Animal Health said on Wednesday it had lowered to the safest level the official risk of six countries for mad cow disease, a move expected to open international market access for their beef exports. These countries are France, Ireland, Switzerland, the Czech Republic, Cyprus and the Lichtenstein.<<<


THIS move is _not_ based on science, but on corporate profits and big ag. to say now that France is a "negligible risk", would be like saying North America is a "negligible risk", which is preposterous. not based on sound science, but on greed and special interest. the only _move_ this ‘’BSE mad cow negligible risk’’ assessment makes, is a move to increase global Transmissible Spongiform Encephalopathy prion mad cow type disease, via the legal trading of the TSE prion aka mad cow type disease via the BSE MRR i.e. Minimal Risk Region policy, a policy set up to fail from the start. please, for whatever God you pray to sake, please be warned.


‘’AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.’’




(Adopted by the International Committee of the OIE on 23 May 2006)


11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,



Tuesday, May 19, 2015


COUNTRY OF ORIGIN LABELING COOL H.R. 2393 Agriculture Chairman K. Michael Conaway (R-TX) Fears of US imports infected with mad cow disease is emerging as an issue in trans-Pacific trade talks



Wednesday, March 11, 2015


OIE and Centers for Disease Control and Prevention Reinforce Collaboration



Friday, April 4, 2014


China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures



Thursday, May 30, 2013


World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease


U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease




The OIE is nothing more than a trading brokerage for the Transmissible Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is still in the midst of a mad cow disease outbreak with atypical BSE cases still growing. mad cow disease is so bad in France, as with the USA, they stopped testing for mad cow disease (France altogether and the USA to figures so low, you would only detect a case of mad cow disease, only by chance).


from the inside looking out ;


Quote: Maybe familirise yourself with the OIE. The primary concern is animal health of the world they are the animal version of the WHO. It is a long way down from that ivory tower but here we go, until pressured by the USA representatives a country could not export animals for 6 years after finding a BSE/BASE positive animal so under the old rules the US would not be able to export anywhere in the world for another 4 1/2 years. Who got the risk levels system put in to allow some trade - your US representatives. You guys want to change rules - OK , but you do not get special rules that only apply to the US. As i have told you before Sand h I market all my own slaughter animals and you know that, so don't do the whole holier than thow act.


With all due respect, it is obvious that you know little about the OIE and how it actually works. Having been to their offices in Paris and talked personally with the Head of the Animal Test Section, you would choke if you knew how many lobby groups attend that office daily. There is a steady stream of paid lobby groups that have one goal in life and that is to sway the Section Heads of each department within the OIE to suit the needs of different jurisdictions around the world, which curiously enough, also includes the USA and Canada. Anyone can go there and chat with them - providing they can provide valid cause to be let in. To say that the only goal of the OIE is animal health is actually only part of their function. They are more than that and my discussions with Dr. Diaz there has showed me that. But to blindly make a statement regarding what they do when you have no idea what they actually do is like eating the skin of the orange and not knowing what is actually under.


Interestingly you state that the US Government applied pressure (to the OIE) I assume and that is a great example of the lobby groups doing their job. So, at the end of the day, one can safely assume that it is the pressure applied by certain influential lobby groups that will determine a likely outcome to an apparent OIE directive. Man alive, isn't it great to live in a democracy wherein the people get to make the choices and not just some "other" interested party or group - say like........Cargill or Tyson for example?


So, one last question, question?


Who wags the tail of that dog?? And for what reason other than one that is purely associated with trade and international agreements and greed?


And you think it is so simply explainable.




Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD)


Distribution of infectivity in animal tissue and body fluids




A.2.1 The following table (Table A2) presents a guide to the possible presence of TSE infectivity in various tissues and body fluids of cattle (exposed naturally or experimentally and orally to first passage BSE agent), sheep and goats (exposed naturally to scrapie agents and potentially to the BSE agent) irrespective of the stage of incubation. Table A2 has been updated in June 2010 taking account of the updated WHO Guidelines published in 2010 (WHO, 2010).


*** A.2.2 This is the first time that the WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD). CWD has not been reported in Europe despite some surveillance for it and there are no specific regulations in force. Should information on TSE infectivity in CWD be required, for example in regard to Cervidae in zoos or in animals in transit through our ports,*** please see updated 2010 WHO Guidelines.


The inclusion of infectivity data in CWD in these Tables was considered important for three reasons: 1) CWD is continuing its spread to new regions of North America, 2) infectivity has been convincingly demonstrated in several bodily secretions and excretions of infected deer and 3) CWD is the only form of animal Transmissible Spongiform Encephalopathies (TSE) that exists in the wild and, although not presently considered to be an important concern for human, could pose serious problems of control in the future, especially as a potential source of infection in other animal species.





Monday, May 05, 2014


*** Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing ***



Wednesday, March 11, 2015


OIE and Centers for Disease Control and Prevention Reinforce Collaboration



Friday, April 4, 2014


China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures



Thursday, May 30, 2013


World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease


U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease




 It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.



it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.



Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.




The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...



In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells


3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...




10 years post mad cow feed ban August 1997




Date: March 21, 2007 at 2:27 pm PST






Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007




Cattle feed delivered between 01/12/2007 and 01/26/2007




Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.


Firm initiated recall is ongoing.




Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.




42,090 lbs.














The firm does not utilize a code - only shipping documentation with commodity and weights identified.




Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.




Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.




9,997,976 lbs.




ID and NV





16 years post mad cow feed ban August 1997




Sunday, December 15, 2013





17 years post mad cow feed ban August 1997


Tuesday, December 23, 2014





Sunday, June 14, 2015


Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion



*** Monday, October 26, 2015 ***





Saturday, January 31, 2015


European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route



I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...




In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.


***However, this recommendation is guidance and not a requirement by law.




31 Jan 2015 at 20:14 GMT


*** Ruminant feed ban for cervids in the United States? ***


31 Jan 2015 at 20:14 GMT



*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;



Monday, October 26, 2015





Thursday, July 24, 2014


*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations



Saturday, December 12, 2015





December 28, 2015 at 2:21am


*** Australian government assessing risk of importing beef from US, Japan and the Netherlands



***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.


***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.


***IBNC Tauopathy or TSE Prion disease, it appears, no one is sure


Posted by flounder on 03 Jul 2015 at 16:53 GMT



Sunday, October 25, 2015


*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***


Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats


SUMMARY: We are reopening the comment period for our proposed rule that would revise completely the scrapie regulations, which concern the risk groups and categories established for individual animals and for flocks, the use of genetic testing as a means of assigning risk levels to animals, movement restrictions for animals found to be genetically less susceptible or resistant to scrapie, and recordkeeping requirements. This action will allow interested persons additional time to prepare and submit comments.


DATES: The comment period for the proposed rule published on September 10, 2015 (80 FR 54660-54692) is reopened. We will consider all comments that we receive on or before December 9, 2015. ...







WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I kindly submit the following ;


>>>The last major revision of the scrapie regulations occurred on August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket No. 97-093-5) a final rule amending part 79 by imposing additional restrictions on the interstate movement of sheep and goats.<<<


Indeed, much science has changed about the Scrapie TSE prion, including more science linking Scrapie to humans. sadly, politics, industry, and trade, have not changed, and those usually trump sound science, as is the case with all Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing animals and the OIE. we can look no further at the legal trading of the Scrapie TSE prion both typical and atypical of all strains, and CWD all stains. With as much science of old, and now more new science to back this up, Scrapie of all types i.e. atypical and typical, BSE all strains, and CWD all strains, should be regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE, and all trading partners to take heed to the latest science on the TSE prion disease, all of them, and seriously reconsider the blatant disregards for human and animal health, all in the name of trade, with the continued relaxing of TSE Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set up to fail in the first place. If the world does not go back to the ‘BSE RISK ASSESSMENTS’, enhance, and or change that assessment process to include all TSE prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’ PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they will continue to mutate and spread among species of human and animal origin, and they will continue to kill. ...


please see ;


O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations


Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France


Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.


*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,


***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),


***is the third potentially zoonotic PD (with BSE and L-type BSE),


***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.




***thus questioning the origin of human sporadic cases***





***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.


***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.





Title: Evaluation of the zoonotic potential of transmissible mink encephalopathy




item Comoy, Emmanuel - item Mikol, Jacqueline - item Ruchoux, Marie-Madeleine - item Durand, Valerie - item Luccantoni-Freire, Sophie - item Dehen, Capucine - item Correia, Evelyne - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Torres, Juan Maria - item Brown, Paul - item Deslys, Jean-Philippe -


Submitted to: Pathogens Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 30, 2013 Publication Date: July 30, 2013 Citation: Comoy, E.E., Mikol, J., Ruchoux, M., Durand, V., Luccantoni-Freire, S., Dehen, C., Correia, E., Casalone, C., Richt, J.A., Greenlee, J.J., Torres, J.M., Brown, P., Deslys, J. 2013. Evaluation of the zoonotic potential of transmissible mink encephalopathy. Pathogens. 2:(3)520-532.


Interpretive Summary: Cases of bovine spongiform encephalopathy (BSE) or mad cow disease can be subclassified into at least 3 distinct disease forms with the predominate form known as classical BSE and the others collectively referred to as atypical BSE. Atypical BSE can be further subdivided into H-type and L-type cases that are distinct from classical BSE and from each other. Both of the atypical BSE subtypes are believed to occur spontaneously, whereas classical BSE is spread through feeding contaminated meat and bone meal to cattle. Transmissible mink encephalopathy (TME) is another prion disease that transmits to cattle and show similarities to L-type BSE when subjected to laboratory testing. The purpose of this study was to use non-human primates (cynomologous macaque) and transgenic mice expressing the human prion protein to determine if TME could represent a potential risk to human health. TME from two sources (cattle and raccoons) was able to infect non-human primates and transgenic mice after exposure by the intracranial route. This result suggest that humans may be able to replicate TME prions after an exposure that allows infectious material access to brain tissue. At this time, it is unknown whether non-human primates or transgenic mice would be susceptible to TME prions after oral exposure. The results obtained in these animal models were similar to those obtained for L-type BSE. Although rare, the existence of TME and that it transmits to cattle, non-human primates, and transgenic mice suggest that feed bans preventing the feeding of mammalian tissues to cattle should stay in place and that regular prion surveillance during the slaughter should remain in place. Parties with interest in the cattle and beef industries and regulatory officials responsible for safe feeding practices of cattle will be interested in this work. Technical Abstract: Successful transmission of Transmissible Mink Encephalopathy (TME) to cattle supports the bovine hypothesis to the still controversial origin of TME outbreaks. Human and primate susceptibility to classical Bovine Spongiform Encephalopathy (c-BSE) and the transmissibility of L-type BSE to macaques assume a low cattle-to-primate species barrier: we therefore evaluated the zoonotic potential of cattle-adapted TME. In less than two years, this strain induced in cynomolgus macaques a neurological disease similar to L-BSE and distinct from c-BSE. TME derived from another donor species (raccoon) induced a similar disease with shorter incubation periods.


*** L-BSE and cattle-adapted TME were also transmissible to transgenic mice expressing human PrP. Interestingly, secondary transmissions to transgenic mice expressing bovine PrP showed the maintenance of prion strain features for the three tested bovine prion strains (cattle TME, c-BSE and L-BSE) regardless of intermediate host.


*** Thus, TME is the third animal prion strain transmissible to both macaques and humanized transgenic mice, suggesting zoonotic potentials that should be considered in the risk analysis of animal prion diseases for human health.


*** Moreover, the similarities between TME and L-BSE are highly suggestive of a link between those strains, and of the presence of L-BSE decades prior to its identification in USA and Europe.



Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies 2014 Annual Report


1a.Objectives (from AD-416): 1. Investigate the pathobiology of atypical transmissible spongiform encephalopathies (TSEs) in natural hosts. A. Investigate the pathobiology of atypical scrapie. B. Investigate the pathobiology of atypical bovine spongiform encephalopathy (BSE). 2. Investigate the horizontal transmission of TSEs. A. Assess the horizontal transmission of sheep scrapie in the absence of lambing. B. Determine routes of transmission in chronic wasting disease (CWD) infected premises. C. Assess oral transmission of CWD in reindeer. 3. Investigate determinants of CWD persistence. A. Determine CWD host range using natural routes of transmission. B. Investigate the pathobiology of CWD.


1b.Approach (from AD-416): The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of accumulation, routes of infection, environmental persistence, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include clinical exams, histopathology, immunohistochemistry and biochemical analysis of proteins. The enhanced knowledge gained from this work will help mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.


3.Progress Report: Research efforts directed toward meeting objective 1 of our project plan, Investigate the pathobiology of atypical transmissible spongiform encephalopathies (TSEs) in natural hosts, include work in previous years starting with the inoculation of animals for studies designed to address the pathobiology of atypical scrapie, atypical bovine spongiform encephalopathy (BSE), as well as a genetic version of BSE. Animals inoculated with atypical scrapie have not yet developed disease. Atypical BSE animals have developed disease and evaluation of the samples is currently underway. Animals inoculated with a genetic version of BSE have developed disease and the manuscript has been published (2012). In addition, we have investigated the possibility that atypical scrapie was present earlier than previously detected in the national flock by analyzing archived field isolates using methods that were unavailable at the time of original diagnosis. Sample quality was sufficiently degraded that modern methods were not suitable for evaluation. In research pertaining to objective 2, Investigate the horizontal transmission of TSEs, we have initiated a study to determine if cohousing non-lambing scrapie inoculated sheep is sufficient to transmit scrapie to neonatal lambs. At this time, scrapie free ewes have lambed in the presence of scrapie inoculated animals and the lambs are cohoused with these inoculated animals.


4.Accomplishments 1. Evaluated enzyme immunoassay for rapid identification of prion disease in livestock. Scrapie of sheep and bovine spongiform encephalopathy of cattle are diseases that cause damage to the central nervous system including the retina in the eye. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state and is resistant to breakdown by the host cells. Current diagnostic methods require the testing of brain material, which can be difficult to collect and may lead to contamination of the environment and exposure of personnel to the infectious agent. Eyes can be readily collected without opening the skull. ARS researchers at Ames, Iowa demonstrated that the enzyme immunoassay results using eyes of negative controls or samples collected from sheep or cattle with clinical signs were in agreement with approved confirmatory assays (western blot or immunohistochemistry). These results indicate the retina is a useful tissue for rapid diagnosis of prion disease in clinically ill sheep and cattle and could be considered to greatly increase the number of samples submitted for prion disease diagnosis with a minimal investment of time and limited exposure of personnel to prion agents.


2. Evaluated E211K cattle as a model for inherited human prion disease. Prion diseases cause damage to the central nervous system of animals and humans. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state and is resistant to breakdown by the host cells and thus accumulates and damages those cells. Some forms of prion disease are genetic and can be inherited. Current models of genetic prion disease in humans rely on mouse models expressing either the human prion protein (E200K) or a combination of both mouse and human sequences. In addition to being an entirely artificial system these mouse models have a short lifespan making them a less than ideal system to study a naturally occurring genetic disorder with a long incubation time and late onset of disease. Cattle, however, exhibit a number of similarities to humans with regard to prion disease and perhaps most notable is the late onset of genetic prion disease. ARS researchers at Ames, Iowa have produced cattle containing both 1 and 2 chromosome copies of the cattle prion gene (E211K) and evaluated many aspects of this prion protein from cattle including protein stability, protein expression levels and ratios, as well as evidence of oxidative stress. Taken together, these results highlight the differences between mouse models of genetic prion disease and a naturally occurring prion disease system in cattle and suggest that cattle will provide a more relevant understanding of genetic prion disease in humans than do current rodent models.


Review Publications Smith, J.D., Greenlee, J.J. 2014. Detection of misfolded prion protein in retina samples of sheep and cattle by use of a commercially available enzyme immunoassay. American Journal of Veterinary Research. 75(3):268-272. Haldar, S., Beveridge, A.J., Wong, J., Singh, A.J., Galimberti, D., Borroni, D., Zhu, X., Blevins, J., Greenlee, J., Perry, G., Mukhopadhyay, C.K., Schmotzer, C., Singh, N. 2014. A low-molecular-weight ferroxidase is increased in the CSF of sCJD Cases: CSF ferroxidase and transferrin as diagnostic biomarkers for sCJD. Antioxidants & Redox Signaling. 19(14):1662-1675.





Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease




item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -


Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.




Monday, November 16, 2015


*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***




*** Evidence for zoonotic potential of ovine scrapie prions


Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics




Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.


Subject terms: Biological sciences• Medical research At a glance



***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.***


***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.***


why do we not want to do TSE transmission studies on chimpanzees $


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.







Wednesday, December 16, 2015


*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission



 Tuesday, December 15, 2015


*** Chronic Wasting Disease will cause a Wyoming deer herd to go virtually extinct in 41 years, a five-year study predicts


Study: Chronic Wasting Disease kills 19% of deer herd annually



 North America CWD TSE Prion Out of Control


Saturday, December 12, 2015





the tse prion aka mad cow type disease is not your normal pathogen.


The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.


you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.


the TSE prion agent also survives Simulated Wastewater Treatment Processes.


IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.


you can bury it and it will not go away.


The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.


it’s not your ordinary pathogen you can just cook it out and be done with.


that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?


to the breeders and industry that care more about their bottom dollar, ignore science, and the ones crying about their poor deer being slaughtered...crying me a river$$$




Sunday, August 23, 2015


TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas


from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss



Wednesday, March 18, 2015


*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015 (8 cases CWD in wild to date Texas)



Wednesday, March 25, 2015


*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015




Thursday, December 24, 2015


*** Infectious disease spread is fueled by international trade ***



Saturday, December 12, 2015


NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015



Saturday, December 12, 2015





Thursday, December 24, 2015


Revisiting the Heidenhain Variant of Creutzfeldt-Jakob Disease: Evidence for Prion Type Variability Influencing Clinical Course and Laboratory Findings


Article type: Research Article



Congress is all set to give NIH it's largest increase in 12 years.


Included in the bill: $350 million increase for Alzheimer’s research and an $85 million increase for the BRAIN Initiative, the project to map the human brain.


Full story at: http://ow.ly/VYKBv


great news, with not a minute to spare...


Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy



07 02:27 AM


Terry S. Singeltary Sr. said:


re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy


Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)



I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.


snip...see full text ;





BSE101/1 0136






From: . Dr J S Metiers DCMO


4 November 1992




1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.


2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.


what are the implications for public health?


3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.






BSE101/1 0137


4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.


J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2



>>> The only tenable public line will be that "more research is required’’ <<<


>>> possibility on a transmissible prion remains open<<<


O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?


Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease


Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014



*** Singeltary comment PLoS ***


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Posted by flounder on 05 Nov 2014 at 21:27 GMT



Wednesday, September 2, 2015


Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses in an Alzheimer’s Disease Database



Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


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


Terry S. Singeltary, Sr Bacliff, Tex


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



26 March 2003


Terry S. Singeltary, retired (medically) CJD WATCH


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



2 January 2000


British Medical Journal


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



15 November 1999


British Medical Journal


vCJD in the USA * BSE in U.S.



The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI


Tracking spongiform encephalopathies in North America




Xavier Bosch


“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...



Suspect symptoms


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


28 Mar 01


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...



Sunday, August 09, 2009


CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009



Tuesday, August 18, 2009


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



The Pathological Protein:


Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases


Philip Yam


''Answering critics like Terry Singeltary, who feels that the US undercounts CJD, Schonberger _conceded_ that the current surveillance system has errors but stated that most of the errors will be confined to the older population''....end




RIP MOM DOD December 14, 1997 confirmed Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD...
































these blogs are for educational use. I do not advertise or make money from them.


MOM DOD 12/14/97 confirmed hvCJD, just made a promise to mom, never forget, and never let them forget...


kindest regards, terry


Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net

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