Tuesday, June 23, 2015

Report on the monitoring and testing of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in the EU in 2013 Final version 18 May 2015

Report on the monitoring and testing of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in the EU in 2013 Final version 18 May 2015

 

1. SUMMARY

 

All the Member States of the EU 28 submitted information on the TSE testing of bovine, ovine and caprine animals. In addition, Norway and Switzerland also submitted information on their TSE testing programmes. Information submitted by Switzerland concerned only bovine animals.

 

1.1. Bovine animals

 

In 2013, a total of 3,135,958 bovine animals were tested in the EU 28 in the framework of the BSE monitoring programmes. 7 bovine animals turned out positive.

 

All of the 7 BSE cases identified in 2013 were submitted to discriminatory testing by the Member States. These tests confirmed 2 cases of classical BSE, 4 cases of atypical H-type BSE and 1 case of atypical L-type BSE. 996,779 risk bovine animals and 2,138,114 healthy animals slaughtered for human consumption were tested by rapid tests. 29 animals were tested in the framework of culling of animals with an epidemiological connection to a BSE case. In addition, 1,036 bovine animals were tested in the framework of passive surveillance (animals reported as official BSE suspects). 100 % of positive cases were detected by the active monitoring (testing of risk animals and healthy slaughtered cattle).

 

The 7 BSE cases detected in 2013 were found in France, Ireland, Poland and the United Kingdom. The number of BSE cases and the overall prevalence in tested animals decreased by respectively 61 % and 40 % in 2013 compared to 2012.

 

1.2. Ovine and caprine animals

 

In 2013, a total of 339,968 ovine and 132,926 caprine animals were tested in the EU 28 in the framework of the TSE monitoring programmes. 1,098 ovine and 1,792 caprine animals turned outpositive to classical scrapie.

 

339,697 ovine animals were tested by active monitoring, while 271 were animals reported as official TSE suspects and therefore subjected to laboratory examination. In caprine animals, the numbers of tests in the respective groups were 131,128 (active monitoring) and 1,798 (TSE suspects). Some 615 and 103 TSE cases in respectively sheep and goats confirmed in 2013 were subjected to discriminatory testing. None of them have been confirmed to be BSE.

 

Further information: Directorate-General for Health and Food Safety Unit G4; fax: +32-2-296.90.62;

 

e-mail: SANTE-TSE-MONITORING@ec.europa.eu

 

snip...

 

Comments on atypical BSE

 

The TSE regulation did not require the Member States to conduct discriminatory testing of all BSE cases before July 2013. The data in this report concerning previous years reflect the tests conducted by some Member States on a voluntary basis. The present results should therefore be interpreted with caution.

 

The present results suggest that the background noise of atypical BSE is between 5 and 8 detectable cases per year. For the first year, the number of Atypical BSE cases is higher than the number of Classical BSE cases.

 

L-BSE appears to be more frequent than H-BSE. In terms of target group, the proportion of atypical BSE cases (H and L together) appears to be higher in the fallen stock than in the healthy slaughtered cattle group.

 

Chart B10 also suggests that the average age of atypical L-type cases has been quite stable since 2001, while that of H-type cases may have been slowly increasing. When it comes to the average age in L-type BSE in 2013, one should however use great caution since it is based on a single case.

 

snip...

 

Comments on atypical cases

 

Atypical TSE cases were confirmed in several Member States. Atypical TSE even accounts quite consistently, year after year, for a large majority (if not 100%) of the TSE cases in some Member States, e.g. in sheep in DK, HU, PL, PT, NO, etc. In some other Member States, e.g. FR and UK (except for 2011 and 2013), the proportion of atypical TSE cases has been steadily growing since 2004, passing from a small share to a large majority of the TSE cases.

 

These results should however be interpreted with caution as the monitoring requirements have changed during this period and the testing and sampling methods have an influence on the detection of atypical cases.

 


 

THIS PARAGRAPH SUMS IT UP PRETTY MUCH ON THE USDA ET AL WEB PAGE ABOUT BSE TESTING IN THE USA, THE REST ON THIS PAGE IS SIMPLY BSe, I.E. bull sh!t encephalopathy i.e. political corporate store bought science $$$

 

Why is USDA "only" testing 40,000 samples a year?

 

USDA's surveillance strategy is to focus on the targeted populations where we are most likely to find disease if it is present. This is the most effective way to meet both OIE and our domestic surveillance standards. After completing our enhanced surveillance in 2006 and confirming that our BSE prevalence was very low, we concluded that 40,000 samples per year from these targeted, high risk populations would far exceed these standards. In fact, this sampling is ten times greater than OIE standards .

 


 

 

Bovine Spongiform Encephalopathy (BSE): Ongoing Surveillance Program

 

Last Modified: May 29, 2015 Print Current Monthly Test Results

 

APHIS reports ongoing surveillance test totals monthly.

 

The BSE ongoing surveillance program will sample approximately 40,000 animals each year. Under the program, USDA will continue to collect samples from a variety of sites and from the cattle populations where the disease is most likely to be detected, similar to the enhanced surveillance program procedures.

 

 

http://www.aphis.usda.gov/wps/portal/aphis/ourfocus/animalhealth/sa_animal_disease_information/sa_cattle_health/sa_bse/ct_about_bse/!ut/p/a1/lVLBkqIwEP2WOcwR04Qo4Yi6CrPqOFqzCheqiRGoBeJAHMu_n0BNbTmHcXdzSne_l37dLyQmexLX-F5kqAtVY9nF8Sh5eg6oPQYazrfeDwhXv2ZLvnCd54AZQGQAk7kfMHcBAIxTCKfjYOp6S4Bw1PNZyCl1DJ9vX0YQztar4YRSG-YjsiMxiUWtTzonEZ7yok2EqrWsdVIWaYPN9RFaTNS5SY5KnNs-wrqosExyiaXObzOHopXYyqSoj6qp-iH6skCtS3lLSFv5CEInmKqz7qJOx0kUBxJRIdHoZZZDXWax4cGxED1hbtL2kDMuHPtzbvjm-PC3vfVz365mbvtTw9suVi_BDOCn_Qm4t9oecEdDZES636rwGNn-59RP__AdaLOcLDPzLOrc6owg-7sG9eUvBvWZzpL9F4N2YxLP1Nvm1e90ZKVKzQfdTf4kTW-_Th1uejfyKBvZDHLVarK_XC6DTKmslAOhKnKqXivuXK3fGw7OsMzW62oT-Q8PH976i0M!/?1dmy&urile=wcm%3apath%3a%2Faphis_content_library%2Fsa_our_focus%2Fsa_animal_health%2Fsa_animal_disease_information%2Fsa_cattle_health%2Fsa_bse%2Fct_monthly_surv_test

 

 

when they started finding back to back atypical BSE around 2006 during the so called _enhanced_ BSE testing, where they were testing perfectly healthy cows they knew did not have BSE, they shut the testing down to numbers almost impossible to find BSE TSE prion disease, and the OIE knows this. if you don’t look, you don’t find, simple as that, problem solved $$$

 

 

 

it’s all about trade now, nothing else matters $$$

 

>>>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.’’

 

IN A NUT SHELL ;

 

(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,

 


 

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.

 

end...tss

 

please see ;

 

spontaneous atypical BSE ???

 

don’t let anyone fool you. spontaneous TSE prion disease is a hoax in natural cases, never proven.

 

all one has to do is look at France. France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow disease in numbers they could find any with, after those atypical BSE cases started showing up. shut down the testing to numbers set up by OIE that are so low, you could only by accident find a case of BSE aka mad cow disease. and this brilliant idea by the WHO et al, to change the name of mad cow disease, thinking that might change things is preposterous. it’s all about money now folks, when the OIE, USDA and everyone else went along and made the TSE prion disease aka mad cow type disease a legal trading commodity by the BSE MRR policy, I would say everyone bit off more then they can chew, and they will just have to digest those TSE Prions coming from North America, and like it, and just prey you don’t get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE prion disease in the decades to come, and or pass it to some other poor soul via the iatrogenic medical surgical tissue friendly fire mode of transmission i.e. second hand transmission. it’s real folks, just not documented much, due to lack of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is tracked down and documented, and put into the academic and public domain, which very seldom happens. ...

 

As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.

 


 

FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$

 

so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

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, Val erie 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...TSS

 

===============

 

O.08: H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism: Clinical and pathologic features in wild-type and E211K cattle following intracranial inoculation

 

S Jo Moore, M Heather West Greenlee, Jodi Smith, Eric Nicholson, Cathy Vrentas, and Justin Greenlee United States Department of Agriculture; Ames, IA USA

 

In 2006 an H-type bovine spongiform encephalopathy (BSE) case was reported in an animal with an unusual polymorphism (E211K) in the prion protein gene. Although the prevalence of this polymorphism is low, cattle carrying the K211 allele are predisposed to rapid onset of H-type BSE when exposed. The purpose of this study was to investigate the phenotype of this BSE strain in wild-type (E211E) and E211K heterozygous cattle. One calf carrying the wild-type allele and one E211K calf were inoculated intracranially with H-type BSE brain homogenate from the US 2006 case that also carried one K211 allelle. In addition, one wild-type calf and one E211K calf were inoculated intracranially with brain homogenate from a US 2003 classical BSE case. All animals succumbed to clinical disease. Survival times for E211K H-type BSE inoculated catttle (10 and 18 months) were shorter than the classical BSE inoculated cattle (both 26 months). Significant changes in retinal function were observed in H-type BSE challenged cattle only. Animals challenged with the same inoculum showed similar severity and neuroanatomical distribution of vacuolation and disease-associated prion protein deposition in the brain, though differences in neuropathology were observed between E211K H-type BSE and classical BSE inoculated animals. Western blot results for brain tissue from challenged animals were consistent with the inoculum strains. ***This study demonstrates that the phenotype of E211K H-type BSE remains stable when transmitted to cattle without the E211K polymorphism, and exhibits a number of features that differ from classical BSE in both wild-type and E211K cattle.

 

==============

 

***This study demonstrates that the phenotype of E211K H-type BSE remains stable when transmitted to cattle without the E211K polymorphism, and exhibits a number of features that differ from classical BSE in both wild-type and E211K cattle.***

 

PLEASE SEE ;

 

Wednesday, May 27, 2015

 

BSE Case Associated with Prion Protein Gene Mutation

 


 

==============

 

P.108: Successful oral challenge of adult cattle with classical BSE

 

Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada

 

Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults.

 

Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease.

 

At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, 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.

 

Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. We are further examining explanations for the unusual disease presentation in the third challenged animal.

 

========================

 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

================

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

ALSO, PLEASE SEE ;

 

31 Jan 2015 at 20:14 GMT

 

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

 

31 Jan 2015 at 20:14 GMT

 


 


 

Saturday, May 30, 2015

 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 


 


 

Wednesday, June 10, 2015

 

Zoonotic Potential of CWD Prions

 

LATE-BREAKING ABSTRACTS

 


 

please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS No documents available. Attachments View All (1) Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission View Attachment:

 


 

Thursday, May 28, 2015

 

OIE cuts six European countries' mad cow risk level, while increasing risk factors for humans to the BSE TSE PRION DISEASE around the globe

 


 

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

 

Posted by Terry S. Singeltary Sr. on May 20, 2015 at 9:00am

 


 

Sunday, June 14, 2015

 

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

 


 

spontaneous atypical BSE ???

 

if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$

 

As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.

 


 

so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

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

 


 

Thursday, August 12, 2010

 

Seven main threats for the future linked to prions

 

***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...

 


 

Monday, October 10, 2011

 

EFSA Journal 2011 The European Response to BSE: A Success Story

 

snip...

 

*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. 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...

 


 


 

***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.

 


 

Tuesday, December 16, 2014

 

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

 

Abstract

 

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

 


 

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.

 

snip...

 

R. BRADLEY

 


 

Friday, January 30, 2015

 

*** Scrapie: a particularly persistent pathogen ***

 


 

Monday, November 30, 2009

 

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

 


 

I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS

 

Sunday, April 12, 2015

 

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

 


 

Friday, May 22, 2015

 

Chronic Wasting Disease and Program Updates - 2014 NEUSAHA Annual Meeting 12-14 May 2014

 


 

Comment from Terry Singeltary This is a Comment on the Food and Drug Administration (FDA) Notice: Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained and Fed On-Farm; Availability

 

For related information, Open Docket Folder Docket folder icon

 

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Show agency attachment(s) Attachments View All (0)

 

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Comment View document:

 


 


 

WI

 

REASON

 

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

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

Terry S. Singeltary Sr.

 

*** See attached file(s) No documents available. Attachments View All (1) Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Terry Singeltary Comment View Attachment:

 


 

Sunday, April 5, 2015

 

*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 ***

 


 

Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 Singeltary Comment

 

Greetings FDA et al,

 

I wish to comment on Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180.

 

Once again, I wish to kindly bring up the failed attempt of the FDA and the ruminant to ruminant mad cow feed ban of August 4, 1997. This feed ban is still failing today, as we speak. Even more worrisome, is the fact it is still legal to feed cervids to cervids in the USA, in fact, the FDA only _recommends_ that deer and elk considered to be of _high_ risk for CWD do not enter the animal food chain, but there is NO law, its only voluntary, a recipe for a TSE prion disaster, as we have seen with the ruminant to ruminant feed ban for cattle, where in 2007, one decade post August 1997 mad cow feed ban, where in 2007 10,000,000 POUNDS OF BANNED BLOOD LACED MEAT AND BONE MEAL WHEN OUT INTO COMMERCE, TO BE FED OUT. Since 2007, these BSE feed ban rules have been breached time and time again. tons and tons of mad cow feed went out in Alabama as well, where one of the mad cows were documented, just the year before in 2006, and in 2013 and 2014, breaches so bad (OAI) Official Action Indicated were issued. those are like the one issued where 10 million pounds of banned blood laced meat and bone meal were fed out.

 

What is the use of having a Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180, if it cannot be enforced, as we have seen with a mandatory ruminant to ruminant feed ban?

 

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

 


 

19 May 2010 at 21:21 GMT

 

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

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE

 


 

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1

 


 


 

PLEASE SEE FULL TEXT SUBMISSION ;

 


 

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

 

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

 

REASON

 

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

 

VOLUME OF PRODUCT IN COMMERCE

 

42,090 lbs.

 

DISTRIBUTION

 

WI

 

REASON

 

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

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

Terry S. Singeltary Sr.

 

*** See attached file(s) No documents available. Attachments View All (1) Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Terry Singeltary Comment View Attachment:

 


 

Sunday, April 5, 2015

 

*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 ***

 


 

Sunday, January 11, 2015

 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 


 

This is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products

 

For related information, Open Docket Folder Docket folder icon

 

--------------------------------------------------------------------------------

 

Show agency attachment(s) AttachmentsView All (0) Empty

 

--------------------------------------------------------------------------------

 

Comment View document:Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;

 

I believe that there is more risk to the world from Transmissible Spongiform Encephalopathy TSE prion aka mad cow type disease now, coming from the United States and all of North America, than there is risk coming to the USA and North America, from other Countries. I am NOT saying I dont think there is any risk for the BSE type TSE prion coming from other Countries, I am just saying that in 2015, why is the APHIS/USDA/FSIS/FDA still ignoring these present mad cow risk factors in North America like they are not here?

 

North America has more strains of TSE prion disease, in more species (excluding zoo animals in the early BSE days, and excluding the Feline TSE and or Canine TSE, because they dont look, and yes, there has been documented evidence and scientific studies, and DEFRA Hound study, that shows the canine spongiform encephalopathy is very possible, if it has not already happened, just not documented), then any other Country in the world. Mink TME, Deer Elk cervid CWD (multiple strains), cBSE cattle, atypical L-type BSE cattle, atypical H-type BSE cattle, atyical HG type BSE cow (the only cow documented in the world to date with this strain), typical sheep goat Scrapie (multiple strains), and the atypical Nor-98 Scrapie, which has been linked to sporadic CJD, Nor-98 atypical Scrapie has spread from coast to coast. sporadic CJD on the rise, with different strains mounting, victims becoming younger, with the latest nvCJD human mad cow case being documented in Texas again, this case, NOT LINKED TO EUROPEAN TRAVEL CDC.

 

typical BSE can propagate as nvCJD and or sporadic CJD (Collinge et al), and sporadic CJD has now been linked to atypical BSE, Scrapie and atypical Scrapie, and scientist are very concerned with CWD TSE prion in the Cervid populations. in my opinion, the BSE MRR policy, which overtook the BSE GBR risk assessments for each country, and then made BSE confirmed countries legal to trade mad cow disease, which was all brought forth AFTER that fateful day December 23, 2003, when the USA lost its gold card i.e. BSE FREE status, thats the day it all started. once the BSE MRR policy was shoved down every countries throat by USDA inc and the OIE, then the legal trading of Scrapie was validated to be a legal trading commodity, also shoved through by the USDA inc and the OIE, the world then lost 30 years of attempted eradication of the BSE TSE prion disease typical and atypical strains, and the BSE TSE Prion aka mad cow type disease was thus made a legal trading commodity, like it or not. its all about money now folks, trade, to hell with human health with a slow incubating disease, that is 100% fatal once clinical, and forget the fact of exposure, sub-clinical infection, and friendly fire there from i.e. iatrogenic TSE prion disease, the pass it forward mode of the TSE PRION aka mad cow type disease. its all going to be sporadic CJD or sporadic ffi, or sporadic gss, or now the infamous VPSPr. ...problem solved $$$

 

the USDA/APHIS/FSIS/FDA triple mad cow BSE firewall, well, that was nothing but ink on paper.

 

for this very reason I believe the BSE MRR policy is a total failure, and that this policy should be immediately withdrawn, and set back in place the BSE GBR Risk Assessments, with the BSE GBR risk assessments set up to monitor all TSE PRION disease in all species of animals, and that the BSE GBR risk assessments be made stronger than before.

 

lets start with the recent notice that beef from Ireland will be coming to America.

 

Ireland confirmed around 1655 cases of mad cow disease. with the highest year confirming about 333 cases in 2002, with numbers of BSE confirmed cases dropping from that point on, to a documentation of 1 confirmed case in 2013, to date. a drastic decrease in the feeding of cows to cows i.e. the ruminant mad cow feed ban, and the enforcement of that ban, has drastically reduced the number of BSE cases in Europe, minus a few BABs or BARBs. a far cry from the USDA FDA triple BSE firewall, which was nothing more than ink on paper, where in 2007, in one week recall alone, some 10 MILLION POUNDS OF BANNED POTENTIAL MAD COW FEED WENT OUT INTO COMMERCE IN THE USA. this is 10 years post feed ban. in my honest opinion, due to the blatant cover up of BSE TSE prion aka mad cow disease in the USA, we still have no clue as to the true number of cases of BSE mad cow disease in the USA or North America as a whole. ...just saying.

 

Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom)

 

Country/Year

 

snip...please see attached pdf file, with references of breaches in the USA triple BSE mad cow firewalls, and recent science on the TSE prion disease. ...TSS

 

No documents available. AttachmentsView All (1) Empty Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission View Attachment:

 


 

Sunday, January 11, 2015

 

Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission

 


 

Tuesday, February 17, 2015

 

*** Could we spot the next BSE?, asks BVA President ***

 


 

UK EXPORTS OF MBM TO WORLD

 


 


 


 

OTHERS BEEF AND VEAL

 


 


 


 


 


 


 


 


 


 

Tuesday, September 2, 2014

 

COOL UPDATE September 2, 2014

 


 

Thursday, March 26, 2015

 

National Scrapie Eradication Program Monthly Report - February 2015

 


 

SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012

 

Summary Report BSE 2012

 

Executive Summary

 


 

Saturday, August 4, 2012

 

Final Feed Investigation Summary - California BSE Case - July 2012

 


 

Saturday, August 4, 2012

 

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

 


 

 

 

2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $

 

 May 4, 2004

 

Statement on Texas Cow With Central Nervous System Symptoms

 

On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

 

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

 

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

 

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...

 


 

 USDA regulations, any cow that exhibits signs of central nervous system (CNS)

 

According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

May 13,2004

 

Page 2

 

snip...

 

The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5

 

This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:

 


 

 

 

-------- Original Message --------

 

Subject: re-USDA's surveillance plan for BSE aka mad cow disease

 

Date: Mon, 02 May 2005 16:59:07 -0500

 

From: "Terry S. Singeltary Sr."

 

To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us

 

Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............

 

snip...

 

There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

 

Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

 

Date: June 14, 2005 at 1:46 pm PST In

 

Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:

 

Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS

 

 MAD COW IN TEXAS NOVEMBER 2004. ...TSS

 

 

 

-------- Original Message --------

 

 Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 17:12:15 –0600

 

 From: "Terry S. Singeltary Sr."

 

 To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>

 

 Greetings Carla,still hear a rumor;

 

 Texas single beef cow not born in Canada no beef entered the food chain?

 

 and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???

 

 terry

 

 -------- Original Message --------

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Fri, 19 Nov 2004 11:38:21 –0600

 

 From: Carla Everett

 

 To: "Terry S. Singeltary Sr." References: <[log in to unmask]>

 

 The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas. Carla At 09:44 AM 11/19/2004, you wrote:>Greetings Carla,>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from>TEXAS. can you comment on this either way please?>>thank you,>Terry S. Singeltary Sr.>>

 

 

 

-------- Original Message --------

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett

 

 To: "Terry S. Singeltary Sr."

 

References: ...sniptss

 

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,

 

 you wrote:

 

 >why was the announcement on your TAHC site removed?

 

 >>Bovine Spongiform Encephalopathy:

 

 >November 22: Press Release title here

 

 >>star image More BSE information

 

 >>>>terry

 

 >>Carla Everett wrote:

 

 >>>no confirmation on the U.S.' inconclusive test...

 

 >>no confirmation on location of animal.>>>>>>

 

 ==========================

 

 -------- Original Message --------

 

 Director, Public Information Carla Everett ceverett@tahc.state.tx.us

 

 Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

 

 Date: Mon, 22 Nov 2004 17:12:15 –0600

 

 From: "Terry S. Singeltary Sr."

 

 To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>

 

 Greetings Carla,still hear a rumor;

 

 Texas single beef cow not born in Canada no beef entered the food chain?

 

 and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???

 

 terry

 

 ==============================

 


 


 

 

 

USDA did not test possible mad cows

 

By Steve Mitchell

 

United Press International

 

Published 6/8/2004 9:30 PM

 

WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims ittested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.

 


 


 

 

 

""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

 

 THIS WAS DONE FOR A REASON!

 

 THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

 

TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED

 

THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP

 

JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED

 

OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER

 

TEXAS MAD COW

 

THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;

 

During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.

 


 

Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.

 

snip...

 

Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.

 

Trace Herd 4 The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.

 

Trace Herd 5 The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.

 

Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.

 

Trace Herd 7 The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.

 


 

 Tuesday, November 02, 2010

 

*** BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

 


 

THE SECRET MAD COW POSITIVE TEST, THAT WAS COVERED UP

 

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

 

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

 

snip...

 

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

 


 

 PAUL BROWN COMMENT TO ME ON THIS ISSUE

 

Tuesday, September 12, 2006 11:10 AM

 

"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."

 

end...tss

 

Saturday, May 26, 2012

 

Are USDA assurances on mad cow case 'gross oversimplification'?

 

SNIP...

 

What irks many scientists is the USDA’s April 25 statement that the rare disease is “not generally associated with an animal consuming infected feed.”

 

The USDA’s conclusion is a “gross oversimplification,” said Dr. Paul Brown, one of the world’s experts on this type of disease who retired recently from the National Institutes of Health. "(The agency) has no foundation on which to base that statement.”

 

“We can’t say it’s not feed related,” agreed Dr. Linda Detwiler, an official with the USDA during the Clinton Administration now at Mississippi State.

 

In the May 1 email to me, USDA’s Cole backed off a bit. “No one knows the origins of atypical cases of BSE,” she said

 

The argument about feed is critical because if feed is the cause, not a spontaneous mutation, the California cow could be part of a larger outbreak.

 

SNIP...

 


 

Saturday, August 4, 2012

 

*** Final Feed Investigation Summary - California BSE Case - July 2012

 


 

in the url that follows, I have posted

 

SRM breaches first, as late as 2011.

 

then

 

MAD COW FEED BAN BREACHES AND TONNAGES OF MAD COW FEED IN COMMERCE up until 2007, when they ceased posting them.

 

then,

 

MAD COW SURVEILLANCE BREACHES.

 

Friday, May 18, 2012

 

Update from APHIS Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States Friday May 18, 2012

 


 

2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006

 


 


 


 

 Sunday, November 23, 2014

 

 

 

*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***

 

 

 


 

 

 

Friday, May 29, 2015

 

GAO FEDERAL VETERINARIANS US Federal Government Is Unprepared for a Large-Scale Animal Disease Outbreak

 


 

Monday, February 23, 2015

 

20th BSE Case Raises New Concerns about Canada's Feeding Practices and Voluntary Testing Program; Highlights Importance of COOL

 


 

Friday, February 20, 2015

 

A BSE CANADIAN COW MAD COW UPDATE Transcript - Briefing (February 18, 2015)

 


 

EDMONTON - Some of former Alberta premier Ralph Klein's most colourful quotes — and the reactions they elicited:

 

SNIP...

 

"This all came about through the discovery of a single, isolated case of mad cow disease in one Alberta cow on May 20th. The farmer — I think he was a Louisiana fish farmer who knew nothing about cattle ranching. I guess any self-respecting rancher would have shot, shovelled and shut up, but he didn't do that." — Klein recalls how the mad cow crisis started and rancher Marwyn Peaster's role. The premier was speaking at the Western Governors Association meeting in Big Sky, Mont. September 2004.

 

"The premier meant that in an ironic or almost a sarcastic way." — Klein spokesman Gordon Turtle.

 

---

 

"You would have to eat 10 billion meals of brains, spinal cords, ganglia, eyeballs and tonsils." — Klein speaking in Montreal in January 2005 on the risk of humans contracting mad cow disease.

 

---

 

"I would offer $5 billion to have a Japanese person to come over here and eat nothing but Alberta beef for a year. And if he gets mad cow disease, I would be glad to give him $5 billion — make it $10 billion — Canadian." — Klein speaking after Japan closed its borders to Canadian beef.

 

---

 


 


 

Thursday, February 10, 2011

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

 


 

Wednesday, August 11, 2010

 

REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Thursday, August 19, 2010

 

REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

 


 

Friday, March 4, 2011

 

Alberta dairy cow found with mad cow disease

 


 

Tuesday, May 21, 2013

 

Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$

 


 

Thursday, March 29, 2012 atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

 

NIAA Annual Conference April 11-14, 2011San Antonio, Texas http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html

 

Increased Atypical Scrapie Detections

 

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

 


 

Current as of: 2015-01-31

 

Sheep flocks and/or goat herds confirmed to be infected with classical scrapie in Canada in 2015 Date confirmed Location Animal type infected January 5 Ontario Goat

 


 


 

P03.141

 

Aspects of the Cerebellar Neuropathology in Nor98

 

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

 

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

 


 

PR-26

 

NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS

 

R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway

 

Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.

 

*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.

 

119

 


 

A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes

 

Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations

 

*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway

 

***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)

 

Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. *** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

 


 

Monday, December 1, 2008

 

When Atypical Scrapie cross species barriers

 

Authors

 

Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.

 

Content

 

Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.

 

The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.

 

Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.

 

Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

 

(i) the unsuspected potential abilities of atypical scrapie to cross species barriers

 

(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier

 

These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.

 


 

Friday, February 11, 2011

 

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

 


 

RESEARCH

 

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos

 

To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.

 

SNIP...

 

Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.

 

How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantifi ed, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confi rmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.

 

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011

 


 

Tuesday, February 10, 2015

 

Alberta Canada First case of chronic wasting disease found in farm elk since 2002

 


 

Saturday, March 21, 2015

 

***Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing

 


 

Tuesday, May 26, 2015

 

*** Minimise transmission risk of CJD and vCJD in healthcare settings Last updated 15 May 2015 ***

 


 

Tuesday, April 21, 2015

 

Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING SCHEDULED FOR June 1, 2015

 


 

Saturday, April 18, 2015

 

*** vCJD TEXAS CDC Emerging Infectious Diseases May 2015 Baylor College of Medicine Neuroscience 2014 case of human form of “mad cow disease” highlights need for continued surveillance

 


 

Saturday, May 09, 2015

 

*** Psychiatric Symptoms in Patients With Sporadic Creutzfeldt-Jakob Disease ***

 


 

Sunday, May 3, 2015

 

PRION2015 FORT COLLINS

 


 

Transmissible Spongiform Encephalopthy TSE Prion Disease

 

*** Kuru Video

 

Kuru: The Science and The Sorcery

 


 

*** Scrapie Video

 


 

*** Human Mad Cow Video

 


 

*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video

 


 

2014

 

***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.

 

***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.

 

*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].

 

snip...

 


 

Monday, October 10, 2011

 

EFSA Journal 2011 The European Response to BSE: A Success Story

 

snip...

 

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far

 

*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded.

 

*** 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...

 


 

Sunday, November 23, 2014

 

*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***

 


 

Monday, November 3, 2014

 

USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014

 

National Prion Disease Pathology Surveillance Center Cases Examined1 (October 7, 2014)

 

***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases;

 

***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

***50 cases of Variably Protease-Sensitive Prionopathy (VPSPr)

 

***and 21 cases of sporadic Fatal Insomnia (sFI).

 


 

Thursday, January 15, 2015

 

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

 


 

Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

 

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

 

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

 

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

 

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

 

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

 

Saturday, January 17, 2015

 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

 


 

*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report ***

 


 

*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO

 


 


 


 


 

Saturday, December 13, 2014

 

Terry S. Singeltary Sr. Publications TSE prion disease

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

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

 

snip...

 


 

lost my mom to the Heidenhain Variant of Creutzfeldt Jakob Disease hvCJD 12/14/97 confirmed. I just made a promise to mom, never forget (I could never ever forget what I saw), and never let them forget...

 

layperson

 

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

 

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