Thursday, December 17, 2015

Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738 10 December 2015


p.s. I forgot a few grams of suspect mad cow feed still in commerce in the USA since August 1997 ban that was nothing but ink on paper...see at the bottom...kindest regards, terry
Annual report of the Scientific Network on BSE-TSE 2015
 
Question Number:
 
EFSA-Q-2015-00738
 
Issued:
 
10 December 2015
 
Download Report (427.8 KB)
 
Abstract:
 
The EFSA Scientific Network on bovine spongiform encephalopathies and other transmissible spongiform encephalopathies (BSE-TSE) held its 10th meeting on 7 and 8 October 2015 in Parma. The meeting served as an opportunity to exchange scientific information on BSE-TSE related issues among EU Member States, countries from the European Free Trade Association (EFTA), EFSA, the European Commission and ad hoc participants. In this occasion, ad hoc representation included the World Animal Health Organisation (OIE), a scientific expert on genetic breeding for resistance to Classical scrapie in goats, and two scientific experts on human variant Creutzfeldt-Jakob disease (vCJD). The topics discussed included an update on BSE-TSE-related activities at national and international level and results from recent TSE-related research projects and risk assessments in several EU countries. In addition, the investigations of recent Classical BSE cases, the monitoring and control of Classical scrapie in small ruminants, and the distribution and trends of vCJD cases in humans were also discussed.
 
Summary:
 
Establishing a system of Networks of organisations operating in the fields within EFSA’s mission is among the tasks of EFSA, according to its founding regulation (Regulation (EC) No 178/2002), in order to facilitate a scientific cooperation framework by the coordination of activities, the exchange of information, the development and implementation of joint projects, the exchange of expertise and best practices. Additionally, the EFSA Science Strategy 2012–2016 set the objective of developing, together with Member States’ competent authorities, multi-annual work programmes focused on filling data gaps and setting priorities for data collections. To implement the above provisions various Networks were established. The Scientific Network on bovine spongiform encephalopathies and other transmissible spongiform encephalopathies (BSE-TSE) was launched in 2006. The BSE-TSE Network had its first meeting in 2006, and, following this, one meeting per year has been held.
 
The BSE-TSE Network is currently composed as follows: Network Members representing 27 EU MSs (Malta has not appointed a representative to this Network) and countries from the European Free Trade Association (EFTA). The European Commission Directorate-General of Health and Consumers and of Research and Innovation are also Observers of the Network.
 
The 10th meeting of the Network was held on 7–8 October 2015 in Parma. In this occasion, ad hoc representation included the World Animal Health Organisation (OIE), a scientific expert on genetic breeding for resistance to Classical scrapie in goats, and two scientific experts on human variant Creutzfeldt-Jakob disease (vCJD).
 
The topics discussed included an update on BSE-TSE-related activities at national and international level, results from recent TSE-related research projects and risk assessments in several EU countries, the investigations of recent Classical BSE cases, the monitoring and control of Classical scrapie in small ruminants, and the distribution and trends of vCJD cases in humans.
 
Published:
 
11 December 2015
 
snip...
 
1. Introduction
 
Background and Terms of Reference as provided by EFSA 1.1.
 
Art. 23 (g) of the EFSA founding regulation1 stipulates that EFSA shall establish a system of Networks of organisations operating in the fields within its mission and be responsible for their operation. Furthermore, Art. 23 (e) and Art. 33 provide for collection, collation, analysis and reporting on scientific and technical data in the fields within the Authority’s mission. The aim of such networking, as defined in Art. 36, is to facilitate a scientific cooperation framework by the coordination of activities, the exchange of information, the development and implementation of joint projects, the exchange of expertise and best practices. Additionally, since ‘in order to obtain data of adequate quality it is essential that data collections are planned over the medium to longer term’, the EFSA Science Strategy 2012–20162 set the objective of developing, together with the Member States’ competent authorities, multi-annual work programmes focused on filling data gaps and setting priorities for data collections.
 
To implement the above provisions of the founding regulation various Networks were established.
 
In 2006 the Network on Microbiological Risk Assessment and the Network on bovine spongiform encephalopathies and other transmissible spongiform encephalopathies (BSE-TSE) convened, strengthening over time the scientific cooperation on issues of concern, anticipating and reducing the duplication of activities and hence avoiding divergence of opinions.
 
All these ongoing initiatives were supported by consultative processes, such as the review3 of the EFSA’s Strategy for cooperation and networking with Member States.4 In result EFSA identified four priority areas for the cooperation, notably: (i) exchange of scientific data and information, (ii) sharing of the risk assessment practices, (iii) harmonisation of risk assessment methodologies, and (iv) cooperation and coherence in communication. Meanwhile, the Management Board adopted a Decision5 governing the establishment and operation of EFSA Networks.
 
In 2013 the Network mandates expired. Owing to a need for a strong specific cooperation platform between EFSA and the Member States to provide advice, steer the process and help establishing a common vision, EFSA Advisory Forum at their meeting in December 2013 made recommendations with regard to the terms of reference of the Networks. Therefore it is now opportune to renew the mandates of the Networks operating in the remits of the Risk Assessment and Scientific Assistance (RASA) units.
 
The main overall goals of the Scientific Network on BSE-TSE are: to improve dialogue among participants; to build mutual understanding of risk assessment principles; to enhance knowledge on and confidence in the scientific assessments carried out in the EU; and to provide increased transparency in the current process among Member States and EFSA. The Network also aims to raise the harmonisation level of the risk assessments developed in the European Union (EU). The Scientific Network strengthens the scientific cooperation on BSE-TSE. It aims at anticipating and reducing the duplication of activities and hence avoiding divergence of opinions. The Network is a privileged environment to share data and methodologies facilitating harmonisation of assessment practices and to assist in anticipating emerging risks in the EU.
 
1 Regulation (EC) No 178/2002 of the European Parliament and the Council of 28 January 2002 laying down the general principles and requirements of food law, establishing the European Food Safety Authority and laying down procedures in matters of food safety. OJ L 31, 1.2.2002, p.1–24.
 
2 EFSA Science Strategy 2012-2016. Available online: http://www.efsa.europa.eu/en/corporate/pub/sciencestrategy12.htm
 
3 Interim Review of the Strategy for Cooperation and Networking between EU Member States and EFSA. Available online: http://www.efsa.europa.eu/en/keydocs/docs/msstrategyreview.pdf
 
4 MB 19.12.2006 – 6a Strategy for cooperation and networking. Available online: http://www.efsa.europa.eu/en/keydocs/docs/networksoperation.pdf
 
5 MB 18 03 10 – item 7 doc 6 Management Board Decision concerning the establishment and operation of European Networks of scientific organisations operating in the fields within the Authority’s mission. Available online: http://www.efsa.europa.eu/en/scdocs/doc/panelnetworksrop.pdf
 
Annual report of the Scientific Network on BSE-TSE
 
www.efsa.europa.eu/publications 6 EFSA Supporting publication 2015:EN-915
 
The specific objectives of the Scientific Network on BSE-TSE are:
 
a. identifying common themes and areas for mutual collaboration;
 
b. identifying and avoiding duplication and divergence of opinion;
 
c. identification of experts in specific areas and on special issues;
 
d. sharing of data availability and quality;
 
e. strengthening cooperation amongst risk assessors and risk managers;
 
f. exchanging information between EFSA, Member States and other stakeholder;
 
g. strengthening communication between EFSA and the EU Member States and among risk assessors, risk managers and stakeholders;
 
h. focusing attention on and streamlining of common research needs;
 
i. identifying potential emerging risks when addressing current issues.
 
EFSA may entrust to the Network certain tasks, in particular preparatory work for scientific opinions, scientific and technical assistance, and collection of data.
 
2. Annual meeting 2015
 
The Scientific Network on BSE-TSE was launched in 2006. The BSE-TSE Network had its first meeting in 2006, and, following this, one meeting per year has been held.
 
The 10th meeting of the EFSA Scientific Network on BSE-TSE was held on 7–8 October 2015 in Parma (‘annual meeting 2015’).
 
The annual meeting 2015 was attended by representatives of 22 EU Member States (Austria, Belgium, Bulgaria, Croatia, Cyprus, the Czech Republic, Estonia, Finland, France, Germany, Greece, Hungary, Ireland, Italy, Luxembourg, the Netherlands, Poland, Romania, Slovakia, Slovenia, Spain and the United Kingdom) and by the representative of one EFTA country (Norway). The European Commission (Directorate-General Health and Consumers (DG SANTE)) was also present at the meeting. Further ad hoc attendees to this meeting included: Dr. Derek Belton (World Organisation for Animal Health (OIE)), Dr. Jan Langeveld, Dr. Maurizio Pocchiari and Dr. Maria Puopolo. Apologies were received from Network Members from Denmark, Latvia, Lithuania, Portugal, Sweden and Switzerland. Malta has not appointed a representative to this EFSA Network.
 
Topics discussed during the meeting are summarised in the following sections.
 
Follow-up from annual meeting 2014 2.1.
 
During the 2014 Network meeting, the Network expressed an interest to strengthen the collaboration of the Network with the OIE and other international organisations/agencies, and to consider the invitation of representatives from Third Countries in order to have insights on BSE-TSE related issues from a non-EU perspective (EFSA, 2014). In reply to these suggestions, OIE participation was confirmed for the 2015 Network meeting, and EFSA has taken contacts with the European Centre for Disease Prevention and Control (ECDC), inviting representatives from the ECDC former EuroCJD Network for participation in the 2015 Network meeting. Invitation of representatives from Third Countries will be considered in future meetings.
 
Update on Network Members’ and EFSA’s activities in the field of 2.2.TSE since the annual meeting 2014
 
The Members of the Network provided an update on the situation of classical and atypical TSE in their countries and summarised to the group the scientific activities in the field of TSE, including risk assessment activities, which had been undertaken in their respective countries since the previous Network meeting. Austria, the Czech Republic and France reported that the EFSA TSE infectivity (TSEi) Model presented during the 2014 Network Meeting, and provided by EFSA to the three countries upon request, was asked and possibly used for study/research purposes.
 
Annual report of the Scientific Network on BSE-TSE
 
www.efsa.europa.eu/publications 7 EFSA Supporting publication 2015:EN-915
 
The Secretariat of the EFSA Unit on Biological Hazards and Contaminants (BIOCONTAM) presented the EFSA activities in the field of TSE already completed and ongoing since the 2014 Network meeting. Completed activities include one Scientific Opinion of the Panel on Biological Hazards (BIOHAZ) on the zoonotic potential of ovine scrapie prions (EFSA BIOHAZ Panel, 2015). Ongoing activities include two mandates for scientific and technical assistance and a procurement activity: a) the evaluation of applications of Denmark, Finland and Sweden to be recognised as having a negligible risk status for classical scrapie; b) the revision of the BSE monitoring regime in Croatia; c) procurement activity on an experimental study on the infectivity of sheep embryos.
 
Results from search and safeguarding of TSE-resistant goats 2.3.
 
Dr. Jan Langeveld presented to the Network an overview on the results of several research projects carried out in the EU over 13 years, focusing on the work conducted in the last few years by the Goat-TSE-FREE consortium in relation to genetic resistance to TSE in goats. He presented the different goat genotypes identified in several EU countries and the association of genotype distribution and occurrence of scrapie. He presented results from experimental challenges of goats of different genotypes with different TSE agents and from the use of several mouse models to study TSE infectivity in goats. Dr. Jan Langeveld concluded that, based on current scientific evidence, the K222 allele and some other polymorphisms of the prion protein gene have shown to confer resistance to TSE in goats. The representative of Cyprus indicated that the studies on genetic resistance to classical scrapie in goats in Cyprus, presented to the 2014 Network meeting, have been progressing and that final results will be reported soon to the European Commission.
 
Update on UK/EU-RL activities and research projects 2.4.
 
The representative of the United Kingdom (UK) presented to the Network an update of the results of 2015 TSE surveillance in the UK, also including a recent case of classical BSE in a cow, currently under investigation. She presented results of studies on atypical BSE transmission to sheep and of studies investigating the presence of prion accumulation in human appendices. She also updated the Network on the activities of the EU Reference Laboratory (EU-RL) for TSE, including results from studies on the diagnostic sensitivity of rapid tests for the detection of TSE in goats.
 
Investigation on the origin of a case of Classical BSE in Ireland 2.5.
 
The representative of Ireland updated the Network on the classical BSE case detected in a 5-year-old cow in June 2015 in Ireland. He presented the results of the epidemiological investigation aimed at detecting the origin of the case, which has not produced so far evidence to support horizontal transmission of classical BSE to the cow following to environmental exposure or feed, vertical transmission or iatrogenic transmission.
 
Investigation on the existence of spontaneous cases of Classical 2.6.BSE
 
The representatives of Poland and Germany presented to the Network the results of joint studies on classical BSE isolates from cattle and comparison with atypical BSE cases using biochemical characterisation and mouse bioassay. Recent ANSES activities on TSE 2.7.
 
The representative of France updated the Network on the most recent TSE risk assessments carried out by The French Agency for Food, Environmental and Occupational Health & Safety (ANSES). In particular, he presented the results of an assessment of the surveillance programmes for TSE in small ruminants in France, of two assessments of the human TSE transmission risks linked to a possible change of the list of specified risk material, and of one assessment of the risks linked to the use of ruminant fat in animal feed.
 
Annual report of the Scientific Network on BSE-TSE
 
www.efsa.europa.eu/publications 8 EFSA Supporting publication 2015:EN-915
 
Practical problems and challenges with the design of TSE 2.8.surveillance in small ruminants
 
The representative of Croatia updated the Network on the TSE surveillance in small ruminants in his country. Surveillance in small ruminants started in Croatia in 2002 and the number of animals tested increased only in 2010–2015. Despite almost 11,000 tests in sheep and 3,000 tests in goats, classical scrapie has never been detected, and only two cases of atypical scrapie (in 2013 and 2015) have been detected. Also considering the epidemiological situation in neighbouring countries, he concluded that it seems surprising that classical scrapie has not been detected in Croatia so far. A discussion followed on relevant issues that Croatia may consider when studying the situation and designing and implementing a surveillance programme aimed at maximising the chances to detect classical scrapie if present, including: a) investigation on genotypes of the small ruminant population; b) implementation of risk-based active surveillance (e.g. focused on fallen stock); c) use of incentives to encourage reporting and presentation of animals for testing; d) consideration to breeding for genetic resistance.
 
Distribution and trends of vCJD and associated risk factors 2.9.
 
Dr. Maurizio Pocchiari, representative of the former EuroCJD Network, managed by the ECDC, presented to the Network a recent analysis on the distribution and trends of human vCJD cases. He discussed vCJD case definition, clinical and diagnostic features, including differences between EU countries, and risk factors for vCJD development. Dr. Pocchiari recommended continued surveillance of all forms of CJD in the EU, also to allow a better study and comparison of human and animal TSE epidemiological data.
 
Update on the OIE activities in the field of TSE 2.10.
 
Dr. Derek Belton, representative of the OIE, explained to the Network the procedure for setting OIE standards and provided an update on the recent activities carried out at the OIE in relation to TSE. In 2015 the OIE Terrestrial Animal Health Code was updated to specifically exclude atypical BSE from the OIE process of official BSE risk status recognition ‘as a condition believed to occur spontaneously in all cattle populations at a very low rate’. Update on the activities of the European Commission in the field of 2.11.TSE
 
The representative of the European Commission (DG SANTE) updated the Network on the recent TSE-related risk management activities in the European Commission, as a follow-up of the TSE Road Map 2, in relation to feed ban, specified risk material, TSE surveillance in cattle and small ruminants, and other measures on scrapie eradication and intra-EU trade. The European Commission is planning to send EFSA new mandates in relation to genetic resistance to classical scrapie in goats and an update on a past EFSA risk assessment of the BSE risk in processed animal proteins. Representatives of Member States and of the European Commission discussed recent developments of the TSE surveillance and control measures implemented in the EU and their possible impact.
 
Future EFSA involvement in drafting the Annual report on TSE 2.12.monitoring in the EU
 
The EFSA BIOCONTAM Secretariat updated the Network on the future transfer from the European Commission to EFSA of the responsibility for the preparation of the annual report on animal TSE surveillance in the EU (as of 2016, with respect to the analysis of 2015 data), and related data collection (as of 2017, with respect to 2016 data). In relation to 2015, no changes are expected for Member States on the collection and transmission of data to the European Commission, while in future years EFSA will reflect on the opportunity to adjust the requirements and the system for data collection.
 
Annual report of the Scientific Network on BSE-TSE
 
www.efsa.europa.eu/publications 9 EFSA Supporting publication 2015:EN-915
 
Information on a Workshop on TSE in Italy 2.13.
 
The representatives of Italy provided to the Network information with respect to a Workshop on TSE that is going to take place on 10 December 2015 in Turin (Italy), organised by the Italian National Reference Centre for TSE, and intended for EU Candidate and Potential Candidate Countries.
 
3. Planned Network activities for 2016
 
Network members were invited to provide, also after the meeting, suggestions for improvement of the functioning of the Network and possible issues for future discussion in the Network.
 
The next meeting of the EFSA Network on BSE-TSE will be organised during the third quarter of 2016.
 
snip...
 
 
 
Maximizing profits is all that is going on now, thanks to the OIE BSE MRR policy, the legal trading of all strains of TSE prion disease globally. ...Terry S. Singeltary Sr.
 
atypical BSE spontaneous sporadic ???
 
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...
 
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
Singeltary et al
 
31 Jan 2015 at 20:14 GMT
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
 
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
 
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
 
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
 
see page 176 of 201 pages...tss
 
 
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.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of scrapie prions to primate after an extended silent incubation period
 
Authors
 
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -
 
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.
 
Interpretive Summary:
 
The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. 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.
 
Technical Abstract:
 
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
 
***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.
 
 
*** 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. ...
 
 
 
 
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
 
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.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Evaluation of the zoonotic potential of transmissible mink encephalopathy
 
Authors
 
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.
 
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease
 
Authors
 
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
 
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
 
 
***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.
 
snip...
 
R. BRADLEY
 
 
1: J Infect Dis 1980 Aug;142(2):205-8
 
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
 
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
 
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
 
snip...
 
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
 
PMID: 6997404
 
 
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
 
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
 
snip...
 
76/10.12/4.6
 
 
Nature. 1972 Mar 10;236(5341):73-4.
 
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
 
Gibbs CJ Jr, Gajdusek DC.
 
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
 
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
 
C. J. GIBBS jun. & D. C. GAJDUSEK
 
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
 
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
 
 
Singeltary Comment
 
*** Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ;
 
 
Monday, November 30, 2009
 
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
 
 
 
 
Thursday, December 20, 2012
 
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED
 
 
Friday, February 04, 2011
 
NMLB and USDA allow scrapie prion infected mutton to enter food chain on the Navajo Reservation in New Mexico
 
 
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
 
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. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
 
==========================================
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.
 
==================
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
==================
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.
 
================
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
================
 
 
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015 ***
 
 
*** CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015 ***
 
 
*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015 ***
 
 
*** NOTICE: Environmental Impact Statement on Large Livestock Carcasses TSE Prion REPORT December 14, 2015 ***
 
 
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
 
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
 
CJD9/10022
 
October 1994
 
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ
 
Dear Mr Elmhirst,
 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
 
 
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
 
R. G. WILL
 
1984
 
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
 
snip...
 
 
IN CONFIDENCE
 
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASES IN THE USA
 
GAH WELLS
 
REPORT OF A VISIT TO THE USA APRIL-MAY 1989
 
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.
 
SNIP...
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.
 
 
***atypical spontaneous BSE in France LOL***
 
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
 
 
***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
 
 
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)
 
*** Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
 
 
07 02:27 AM
 
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy
 
*** Terry S. Singeltary Sr. said:
 
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
 
snip...see full text ;
 
 
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
 
BSE101/1 0136
 
IN CONFIDENCE
 
CMO
 
From: . Dr J S Metiers DCMO
 
4 November 1992
 
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
 
snip...
 
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
 
 
*** CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015 ***
 
 
USDA Announces Preliminary Concurrence with OIE Risk Designations for BSE in 16 Countries USDA Animal and Plant Health Inspection Service sent this bulletin at 12/04/2015 11:15 AM EST
 
USDA Announces Preliminary Concurrence with World Animal Health Organization Risk Designations for Bovine Spongiform Encephalopathy in 16 Countries
 
December 4, 2015—The United States Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS) is preliminarily concurring with the World Organization for Animal Health’s (OIE) bovine spongiform encephalopathy (BSE) risk designations for 16 countries. The OIE recognizes these regions as being of negligible risk for BSE. APHIS reviewed the information supporting the OIE’s risk designations for these regions and agrees with the OIE designations.
 
The 16 countries are: Bulgaria, Cyprus, Czech Republic, Estonia, France, India, Korea (Republic of), Hungary, Latvia, Liechtenstein, Luxembourg, Malta, Portugal, Romania, Slovakia, and Switzerland.
 
The OIE recommendations regarding each of the above countries can be viewed online.
 
APHIS considers all countries of the world to fall into in one of three BSE risk categories: negligible risk, controlled risk, or undetermined risk. Any region that is not classified by APHIS as presenting either negligible risk or controlled risk for BSE is considered to present an undetermined risk.
 
Under the regulations, APHIS may classify a region for BSE in one of two ways. One way is for countries that have not received a risk classification from the World Organization for Animal Health (OIE) to request classification by APHIS. The other way is for APHIS to concur with the classification given to a country by the OIE.
 
This notice is available for 60 days for review and comment. APHIS will consider all comments received on or before February 2, 2016. After reviewing any comments we receive, we will announce our final determination regarding the BSE classification of these countries in the Federal Register.
 
 
LMAO !!! pot calling kettle black. BSE MRR policy equals the legal trading of all strains of TSE Prion aka mad cow disease. any consumers death there from are now acceptable $$$
 
these blogs are for educational use. I do not advertise or make money from them.
 
MOM DOD December 14, 1997 confirmed hvCJD, just made a promise to mom, never forget, and never let them forget.
 
carry on with this charade or masquerade God save the industry at all cost mentality $$$ but be sure, history should be very cruel to those that have been involved, with no soul or courage to come forward. ...terry
 
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
 
Original
 
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
 
 
 
P.S. I forgot a few grams of banned potential mad cow protein in commerce here in the USA since the August 1997 mad cow feed ban...just saying, nothing else matters except trade $$$
 
P.S.
 
 
10 years post mad cow feed ban August 1997
 
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
 
Date: March 21, 2007 at 2:27 pm PST
 
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
 
PRODUCT
 
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
 
CODE
 
Cattle feed delivered between 01/12/2007 and 01/26/2007
 
RECALLING FIRM/MANUFACTURER
 
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
 
Firm initiated recall is ongoing.
 
REASON
 
Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
42,090 lbs.
 
DISTRIBUTION
 
WI
 
___________________________________
 
PRODUCT
 
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
 
CODE
 
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
 
RECALLING FIRM/MANUFACTURER
 
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
 
REASON
 
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
 
VOLUME OF PRODUCT IN COMMERCE
 
9,997,976 lbs.
 
DISTRIBUTION
 
ID and NV
 
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
 
 
16 years post mad cow feed ban August 1997
 
2013
 
Sunday, December 15, 2013
 
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
 
 
17 years post mad cow feed ban August 1997
 
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
 
 
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 ***
 
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 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
 
 
 
Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net
 
 
 

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