Thursday, December 1, 2016

The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015


The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015

Authors

  • European Food Safety Authority (EFSA),

  • Frank Boelaert,

  • Marta Hugas,

  • Angel Ortiz Pelaez,

  • Valentina Rizzi,

  • Pietro Stella,

  • Yves Van Der Stede

  • First published:
  • DOI: 10.2903/j.efsa.2016.4643V
  • Cited by: 0 articles


  • Requestor: European Commission
  • Question number: EFSA-Q-2015-00653
  • Acknowledgements: EFSA wishes to thank the following parties for the support provided for this report: European Commission (Lucie Carrouee, Eric Thevenard, Kris De Smet) who provided the data for extraction and review of the report; Dr Maria Nöremark (National Veterinary Institute, Sweden) and Dr Christian Ducrot (Unité d'Epidemiology Animale, INRA, France) for their scientific review of this report; EFSA staff members (Yves Van der Stede, Angel Ortiz Pelaez, Valentina Rizzi, Pietro Stella, Frank Boelaert) and the EFSA contractor: the Istituto Zooprofilattico Sperimentale del Piemonte (Unit Biostatistica Epidemiologia e Analisi del Rischio and staff: Giuseppe Ru, Francesco Ingravalle, Cristina Bona, Rosanna Desiato, Cristiana Maurella, Eleonora Aiassa).
  • Approved: 9 November 2016
Correspondence: zoonoses@efsa.europa.eu




Abstract

This report of EFSA presents the results of surveillance activities on transmissible spongiform encephalopathies (TSEs) in bovine animals, sheep and goats as well as genotyping data in sheep, carried out in 2015 in the EU and in three non-Member States (non-MS). Since 2001, approximately 114 million cattle in the EU have been tested for bovine spongiform encephalopathy (BSE) according Regulation (EC) 999/2001. In 2015, 1.4 million bovine animals were tested and five cases were detected in four MS (Ireland: one case; Slovenia: one case; Spain: one case; and the United Kingdom: two cases) and one case was detected in Norway. Two cases (in Ireland and the United Kingdom) were affected by classical BSE and both cases were born after the EU-wide feed ban enforced in 2001. The remaining four cases were atypical BSE cases (three H-BSE type and one L-BSE type). Since 2002, approximately 8.4 million small ruminants have been tested during the EU-wide surveillance for scrapie. In 2015, 319,638 sheep and 135,857 goats were tested. In total, 641 scrapie cases in sheep were detected in 18 MS while 1,052 scrapie cases in goats were detected in nine MS, respectively. In two non-MS (Iceland and Norway), 40 scrapie cases in sheep were detected. Although in a number of MS the decrease in classical scrapie is clear, at the EU level there is no clear decreasing trend in the occurrence of scrapie in small ruminants. Results obtained from genotyping in sheep confirm that cases of classical scrapie are clustered among certain genotypes, and animals with these genotypes seem to account for less than 20% of the European randomly sampled sheep population. In total, 580 samples from species other than domestic ruminants were tested for TSE in three MS, all with negative results.

Summary

This report of the European Food Safety Authority (EFSA) presents the detailed results of monitoring activities on transmissible spongiform encephalopathies (TSEs) in bovine animals, sheep and goats carried out during 2015 in the European Union (EU) and three non-Member States (non-MS) as well as a summary and trends of the monitoring between 2001 and 2015.

TSE monitoring data for bovine animals and small ruminants are reported by countries according to Regulation (EC) 999/2001 and consist of testing data (monthly reported) as well as case data (positive tested and/or confirmed positive animals). Data regarding the genotyping activities carried out on the ovine TSE cases, as well as on randomly selected sheep, were retrieved from the annual reports submitted by the Member States (MS) and non-MS in accordance with Article 6.4 of, and as specified in Chapter B.I of Annex III to, Regulation (EC) 999/2001, i.e. the TSE Regulation.

Descriptive statistics were used to analyse the data. Where possible, descriptions and calculations were stratified according to the available variables in the database, such as surveillance target group (healthy slaughtered animals, animals culled under bovine spongiform encephalopathy (BSE)/TSE control and eradication measures, etc.) or activity (passive vs active surveillance), country, year (since 2001 and 2002, respectively, for bovine animals and small ruminants), case type (i.e. classical BSE (C-BSE), atypical BSE (H-BSE or L-BSE), classical scrapie (CS) or atypical scrapie (AS)), flock status (infected/non-infected) and age class.

Since 2001, approximately 114 million bovine animals have been tested for BSE in the EU. There has been a decrease in the number of animals tested over time following amendments in the Regulation (EC) 999/2001. In 2015, around 1.4 million animals were tested in the EU. The number of positive BSE cases has also decreased over time, both in terms of absolute number of cases as well as the proportion of cases in tested animals. In 2015, only five BSE cases were detected in the EU, all among tested fallen stock from four different MS (Ireland, Slovenia, Spain and the United Kingdom). Two cases were C-BSE, both of them born after the EU-wide feed ban was enforced in 2001 (BARB cases). The remaining three cases in the EU were of atypical type (two H-BSE and one L-BSE, respectively). In addition, one case of H-BSE was detected in one non-MS (Norway).

A clear decline in the annual rate of cases per million tests performed was observed for the whole period of BSE monitoring in the EU (2001–2015). An increase in the age of the affected animals is observed and there is an accumulation of cases in animals born in the mid-1990s.

Since 2002, approximately 8.4 million small ruminants have been tested for scrapie in the EU. In 2015, approximately 300,000 sheep and 135,000 goats were tested. In 2015, 641 scrapie cases in sheep and 1,052 scrapie cases in goats were detected in the EU. The scrapie cases in sheep were detected in 18 MS, whereas caprine cases (± 90% reported by Cyprus) were detected in nine MS. In addition, 40 cases in sheep were detected in two out of the three reporting non-MS. There is no clear trend of improvement in the epidemiological situation of small ruminant TSEs overall in the countries included in the report, either in terms of the absolute number of cases or cases in tested animals. However, in some MS there is a decline of CS. The genotyping data confirm that CS in sheep is clustered among genetically susceptible animal while these animals account for less than 20% of the random sampled sheep.

In addition, 580 samples from species other than domestic animals were tested in three MS (Estonia, Finland and Hungary) in 2015 by, all with negative results.


snip...

4 Conclusions


In 2015, there was an almost 40% reduction in the total number of bovine samples tested compared with the previous year, moving from 2.3 to 1.4 million. Tests performed in cattle in the EU are mainly based on the exhaustive testing of risk animals over 48 months of age, which increases the probability of detecting cases even if at a very low rate, compared with random sampling of the slaughtered populations. Five BSE cases were reported by four different MS: one C-BSE case reported by both Ireland and the UK, and three atypical BSE cases – two H-type in Slovenia and the UK, and one L-type in Spain. One additional atypical case (H-type) has been detected in Norway.

The reliability of BSE categorisation by case type has improved over time in countries that detected BSE cases, because, samples from a large proportion of cases were submitted to discriminatory testing (either retrospectively or prospectively).

Surveillance data reflects, either in terms of absolute number of cases reported or prevalence, a pattern consistent with a decline in the European BSE epidemic. However, there were no differences in 2015 with respect to the recent previous years: a similar number of cases were detected, either of classical BSE (two and three cases in 2013 and 2014, respectively) or atypical BSE (five and eight cases in 2013 and 2014, respectively). The two C-BSE cases reported in 2015 were born in 2010 (Ireland) and 2009 (the UK), i.e. 14 and 13 years, respectively, after the enforcement of the feed ban in these countries (BARB cases).
Age-period analysis of the surveillance data confirms a decrease in the occurrence of C-BSE over time, associated with an increase in the age class with the highest prevalence over the years. This pattern indicates that the measures applied to control the main risk factors (e.g. feed ban) have been effective in reducing the burden of the disease. A similar conclusion is also justified by the fact that the highest level of detection occurred in animals born in 1995, when the decline commenced.

No cases of BSE have been detected in the last 7 years in cattle aged < 60 months. However, current monitoring of risk animals (i.e. AM, ES and FS) > 48 months of age allows for the detection of such cases. The detection of cases among young animals may represent an important early warning of a potential re-emergence of a BSE epidemic.

Since 2002, ca 8.4 million small ruminants have been tested in the frame of the EU-wide TSE surveillance. In 2015 a total of 319,638 sheep and 135,857 goats were tested. Among non-infected flocks in both species, there is a decreasing trend in the number of sheep and goats from non-infected flocks tested as TSE suspects (SU target group). There is high between-country heterogeneity with relation to the implementation of the surveillance activities as per the EU legislation. Considering the required samples to be taken within the SHC and NSHC target surveillance groups, 24 and 25 MS fulfilled the requirements in sheep and goats, respectively.

Surveillance activities carried out in 2015 in the EU 28 led to the detection of 641 and 1,052 scrapie cases in sheep and goats, respectively. Ovine scrapie was reported by 18 MS and caprine scrapie by nine MS, even though in the case of goats 90% of the cases were reported by Cyprus.

There is no clear overall trend of improvement in the epidemiological situation of scrapie in small ruminants either in terms of absolute number of cases or proportion of cases. However, in a number of countries a decreasing trend in the annual ratios of CS/AS was observed.

Genotyping data consistently confirm the association between genotype and CS and that the proportion of susceptible animals in the sampled population has decreased over the recent years.

In 2015, 580 samples from species other than domestic ruminants (including wild animals) were tested in three MS and one non-MS (Estonia, Finland, Hungary and Norway); no positives were reported.


snip...see full text ;


http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2016.4643/full


Low incidence of TSEs in the EU, says EFSA report





EFSA has published its first EU summary report on the monitoring of Transmissible Spongiform Encephalopathies (TSEs) in cattle, sheep and goats. Previously, the annual reports on TSEs were compiled by the European Commission.
TSEs are a group of diseases that affect the brain and nervous system of humans and animals.  With the exception of Classical BSE, there is no scientific evidence that other TSEs can be transmitted to humans.
A low number of BSE cases in cattle were detected in EU Member States, none of which entered the food chain.
Some of the main findings of the report are:
  • Five cases of BSE in cattle have been reported in the EU, out of about 1.4 million animals tested.
  • 641 cases of scrapie in sheep (out of 319,638 tested) and 1,052 in goats have been reported (out of 135,857 tested) in the EU.
This report provides results on data collected by all EU Member States, Iceland, Norway and Switzerland for 2015 on the occurrence of bovine spongiform encephalopathy (BSE) in cattle and scrapie in sheep and goats – two forms of TSEs.


http://www.oie.int/animal-health-in-the-world/bse-situation-in-the-world-and-annual-incidence-rate/10-13-number-of-reported-cases-worldwide-excluding-the-united-kingdom-copy-1/


interesting, not a word on the outbreak of Chronic Wasting Disease CWD TSE Prion disease in cervids in Europe, and potential zoonotic risk factors there from. see ;


Wednesday, November 09, 2016

Norway and Finland Rule Changes for importation and exportation of deer to limit the spread of skrantesjuke (CWD)



MAJOR FINDINGS FOR NORWAY !

Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Author
item Moore, Sarah item Kunkle, Robert item West greenlee, Mary item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
Submitted to: Emerging Infectious Diseases Publication Type: Peer reviewed journal Publication Acceptance Date: 8/29/2016 Publication Date: N/A Citation:
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.

Monday, September 05, 2016
*** Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway ***


Sunday, November 13, 2016

Horizontal Transmission of Chronic Wasting Disease in Reindeer CDC Volume 22, Number 12—December 2016




SUNDAY, OCTOBER 02, 2016

What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016






Thursday, September 22, 2016

NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke



Saturday, September 03, 2016

NORWAY Regulation concerning temporary measures to reduce the spread of Chronic Wasting Disease (CWD) as 4th case of skrantesjuke confirmed in Sogn og Fjordane



Wednesday, August 31, 2016

*** NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU



Wednesday, August 31, 2016

NORWAY CONFIRMS 4TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN SECOND CARIBOU



Tuesday, August 02, 2016

Chronic wasting disease of deer – is the battle to keep Europe free already lost?


*** Chronic Wasting Disease (CWD) in a moose from Selbu in Sør-Trøndelag Norway ***



Thursday, July 07, 2016

Norway reports a third case Chronic Wasting Disease CWD TSE Prion in 2nd Norwegian moose

14/06/2016 - Norway reports a third case



Saturday, July 16, 2016

Chronic wasting Disease in Deer (CWD or Spongiform Encephalopathy) The British Deer Society 07/04/2016

Red Deer Ataxia or Chronic Wasting Disease CWD TSE PRION?

could this have been cwd in the UK back in 1970’S ???





SEE FULL TEXT ;



Tuesday, April 12, 2016

The first detection of Chronic Wasting Disease (CWD) in Europe free-ranging reindeer from the Nordfjella population in South-Norway.



Saturday, April 9, 2016

The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)

Department for Environment, Food and Rural Affairs



Wednesday, September 28, 2016

Norway sides with OIE, decides to expose millions of consumers to the ATYPICAL BSE SRM TSE Prion aka mad cow type disease



Thursday, January 29, 2015

Atypical H-TYPE BSE Case Confirmed in Norway



Friday, June 3, 2016

The epidemiological evolution of prion infection on bovine in Romania, in the period of 2010 – 2015



Wednesday, November 09, 2016

Chronic Wasting Disease (CWD) Program Standards - Review and Comment By Terry S Singeltary Sr. November 9, 2016
http://chronic-wasting-disease.blogspot.com/2016/11/chronic-wasting-disease-cwd-program_9.html

CHRONIC WASTING DISEASE CWD AND SCRAPIE TSE PRION ZOONOSIS UPDATE

 *** WDA 2016 NEW YORK ***
 We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
 Student Presentations Session 2
 The species barriers and public health threat of CWD and BSE prions
 Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
 Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.

Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf

PRION 2016 TOKYO
 Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.

PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016
http://prion2016.org/dl/newsletter_03.pdf

Cervid to human prion transmission
Kong, Qingzhong

Case Western Reserve University, Cleveland, OH, United States

Abstract

Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:

(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;

(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;

(3) Reliable essays can be established to detect CWD infection in humans;and

(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.

Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.

Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.

Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.

Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.

Funding Agency Agency National Institute of Health (NIH)

Institute National Institute of Neurological Disorders and Stroke (NINDS)

Type Research Project (R01)

Project # 1R01NS088604-01A1

Application # 9037884

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

Program Officer Wong, May

Project Start 2015-09-30

Project End 2019-07-31

Budget Start 2015-09-30

Budget End 2016-07-31

Support Year 1

Fiscal Year 2015

Total Cost $337,507

Indirect Cost $118,756

Institution

Name Case Western Reserve University

Department Pathology

Type Schools of Medicine

DUNS # 077758407

City Cleveland

State OH

Country United States

Zip Code 44106

http://grantome.com/grant/NIH/R01-NS088604-01A1


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

We hypothesize that:

(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;

(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;

(3) Reliable essays can be established to detect CWD infection in humans;and

(4) *** CWD transmission to humans has already occurred. *** We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

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

Key Molecular Mechanisms of TSEs

Zabel, Mark D.

Colorado State University-Fort Collins, Fort Collins, CO, United States Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims. 1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion. 2. Determine whether CD21/35 and C1q differentially bind distinct prion strains 3. Monitor the effects of CD21/35 on prion trafficking in real time and space 4. Assess the role of CD21/35 in incunabular prion trafficking

Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations.

Funding Agency Agency National Institute of Health (NIH)

Institute National Institute of Allergy and Infectious Diseases (NIAID)

Type High Priority, Short Term Project Award (R56)

Project # 1R56AI122273-01A1

Application # 9211114

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

Program Officer Beisel, Christopher E

Project Start 2016-02-16

Project End 2017-01-31

Budget Start 2016-02-16

Budget End 2017-01-31

Support Year 1

Fiscal Year 2016

Total Cost

Indirect Cost Institution Name Colorado State University-Fort Collins

Department Microbiology/Immun/Virology

Type Schools of Veterinary Medicine

DUNS # 785979618 City Fort Collins

State CO

Country United States

Zip Code 80523

http://grantome.com/grant/NIH/R56-AI122273-01A1


PMCA Detection of CWD Infection in Cervid and Non-Cervid Species

Hoover, Edward Arthur

Colorado State University-Fort Collins, Fort Collins, CO, United States

Abstract Chronic wasting disease (CWD) of deer and elk is an emerging highly transmissible prion disease now recognized in 18 States, 2 Canadian provinces, and Korea. We have shown that Infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces, and in the tissues generating those body fluids and excreta, thereby leading to facile transmission by direct contact and environmental contamination. We have also shown that CWD can infect some non-cervid species, thus the potential risk CWD represents to domestic animal species and to humans remains unknown. Whether prions borne in blood, saliva, nasal fluids, milk, or excreta are generated or modified in the proximate peripheral tissue sites, may differ in subtle ways from those generated in brain, or may be adapted for mucosal infection remain open questions. The increasing parallels in the pathogenesis between prion diseases and human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, add relevance to CWD as a transmissible protein misfolding disease. The overall goal of this work is to elucidate the process of CWD prion transmission from mucosal secretory and excretory tissue sites by addressing these questions: (a) What are the kinetics and magnitude of CWD prion shedding post-exposure? (b) Are excreted prions biochemically distinct, or not, from those in the CNS? (c) Are peripheral epithelial or CNS tissues, or both, the source of excreted prions? and (d) Are excreted prions adapted for horizontal transmission via natural/trans-mucosal routes? The specific aims of this proposal are: (1) To determine the onset and consistency of CWD prion shedding in deer and cervidized mice; (2); To compare the biochemical and biophysical properties of excretory vs. CNS prions; (3) To determine the capacity of peripheral tissues to support replication of CWD prions; (4) To determine the protease- sensitive infectious fraction of excreted vs. CNS prions; and (5) To compare the mucosal infectivity of excretory vs. CNS prions. Understanding the mechanisms that enable efficient prion dissemination and shedding will help elucidate how horizontally transmissible prions evolve and succeed, and is the basis of this proposal. Understanding how infectious misfolded proteins (prions) are generated, trafficked, shed, and transmitted will aid in preventing, treating, and managing the risks associated with these agents and the diseases they cause.

Public Health Relevance Chronic wasting disease (CWD) of deer and elk is an emergent highly transmissible prion disease now recognized throughout the USA as well as in Canada and Korea. We have shown that infected deer harbor and shed high levels of infectious prions in saliva, blood, urine, and feces thereby leading to transmission by direct contact and environmental contamination. In that our studies have also shown that CWD can infect some non-cervid species, the potential risk CWD may represents to domestic animal species and humans remains unknown. The increasing parallels in the development of major human neurodegenerative conditions, such as Alzheimer's and Parkinson's diseases, and prion diseases add relevance to CWD as a model of a transmissible protein misfolding disease. Understanding how infectious misfolded proteins (prions) are generated and transmitted will aid in interrupting, treating, and managing the risks associated with these agents and the diseases they cause.

Funding Agency Agency National Institute of Health (NIH)

Institute National Institute of Neurological Disorders and Stroke (NINDS)

Type Research Project (R01)

Project # 4R01NS061902-07

Application # 9010980

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)

Program Officer Wong, May Project Start 2009-09-30

Project End 2018-02-28

Budget Start 2016-03-01

Budget End 2017-02-28

Support Year 7

Fiscal Year 2016

Total Cost $409,868

Indirect Cost $134,234 Institution Name Colorado State University-Fort Collins

Department Microbiology/Immun/Virology

Type Schools of Veterinary Medicine

DUNS # 785979618 City Fort Collins

State CO

Country United States

Zip Code 80523

http://grantome.com/grant/NIH/R01-NS061902-07


LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249
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.***

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

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf


*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm


http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html


*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249


*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf


***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

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).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf


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

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf


Monday, May 02, 2016

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html


*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD


http://chronic-wasting-disease.blogspot.com/2014/06/prion-2014-chronic-wasting-disease-cwd.html


http://chronic-wasting-disease.blogspot.com/2016/07/colorado-chronic-wasting-disease-cwd.html


http://chronic-wasting-disease.blogspot.com/


Monday, May 02, 2016

*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html

 Saturday, April 23, 2016

PRION 2016 TOKYO

Saturday, April 23, 2016

 SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

 Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

 To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

 Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with ef?ciency comparable to that of cattle BSE. While the ef?ciency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 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

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf

 *** 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.

 http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

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 long 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***
 ***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.

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
 http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html

Tuesday, August 9, 2016

Concurrence with OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2015-0055]

BILLING CODE: 3410-34-P DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service
http://bovineprp.blogspot.com/2016/08/concurrence-with-oie-risk-designations.html
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016 
Saturday, July 16, 2016
Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10
WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.
THIS is absolutely insane. it’s USDA INC.
Thursday, August 4, 2016
Secretary's Advisory Committee on Animal Health [Docket No. APHIS-2016-0046] 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
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.

http://jama.jamanetwork.com/article.aspx?articleid=1031186

Terry S. Singeltary Sr.

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