Sunday, November 23, 2014

nvCJD aka mad cow disease Texas June 2014 NOT European linked

Sunday, November 23, 2014

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

 
http://vcjd.blogspot.com/2014/11/confirmed-variant-creutzfeldt-jakob.html


tss

Wednesday, November 12, 2014

National Creutzfeldt-Jakob Disease Awareness Week November 10-16

this week, and today especially, is National Creutzfeldt-Jakob Disease Awareness Week. but for myself and some others, everyday is National Creutzfeldt-Jakob Disease Awareness day for us, because we do this every day. I just made a promise, never forget, and never let them forget. ...tss

 

From: TSS Subject: National Creutzfeldt-Jakob Disease Awareness Week Date: November 6, 2005 at 6:22 pm PST

 

News Released: November 06, 2005 National Creutzfeldt-Jakob Disease Awareness Week

 

(PRLEAP.COM) "The purpose for National Creutzfeldt-Jakob Disease Awareness Week is to put a much-needed spotlight on this fatal disease," remarked Christy Brom, founder of CJD Aware!, a non-profit, information organization based in New Orleans. The organization was founded in the spring of 2002 after the death of Ms. Brom’s mother, Sara, from the sporadic form of Creutzfeldt-Jakob disease. Sara Brom was 66 years old when she died on November 12, 2000. "In 2002, organizations worldwide were invited by the CJD Support Network in Great Britain to join them in recognizing November 12 as International CJD Awareness Day," added Ms. Brom. "Our participation in this event began with support from Great Britain. Then in October, 2002, CJD Aware! decided to send a letter to the Governor of North Carolina requesting a signed CJD proclamation proclaiming November 10-16 as ‘Creutzfeldt-Jakob Disease Awareness Week’ in the state of North Carolina. We were very pleased when we received the proclamation from Governor Easley. Then one of my Board members, George B.K. Carr, Sr., suggested that we pursue a goal of CJD proclamations from the Governors in all 50-states. Since we began this campaign in 2002, we’re over half-way to our goal of all 50-states." "This cause is very near and dear to my heart," remarked Mr. Carr. "My wife, Bay, and I fully support Christy and her organization, CJD Aware!. Bay and I have known the Brom family for over 30-years, and were simply devastated when Sara died from this horrendous disease. It destroyed Sara’s intellect, her wonderful creativity and personality. We will do everything we can to get the word out about CJD, and we feel that ‘National CJD Awareness Week’ is one way of accomplishing this. That’s why we decided to send letters out to Governors of each state nationwide, in addition to the state of North Carolina. We’ve gotten a very positive feedback on this national campaign." CJD Aware! has made great strides since its inception in the spring of 2002. "This disease has no boundaries as far as location, race or age," added Ms. Brom. "We are here to assist any individual or organization who wishes information about Creutzfeldt-Jakob disease. The disease has been around since the 1920’s and, unfortunately, shows no sign of disappearing."

 


 

TSS

 


 


 

From: Terry S. Singeltary Sr. Sent: Monday, November 03, 2014 4:39 PM To: BSE-L@LISTS.AEGEE.ORG Subject: Re: [BSE-L] USA CJD TSE PRION UNIT, TEXAS, SURVEILLANCE UPDATE NOVEMBER 2014

 

if you notice, if you add up the vpspr 50 cases and the sporadic FFI 21 cases, and then add to the total sporadic cjd cases of 2660, this is where the total of 2731 sporadic cases come from...seems they are lumping them all together as total sporadic cjd cases, and leaving the sporadic cjd text completely out of the picture now. smoooth. covering all bases I presume, and they moved the goal post in the middle of the game, again. niice...we all didn't fall off a shrimp boat yesterday$$$ *** these kind always are interesting for me, those type determination pending cases, year after year ;

 

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

 

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

 


 

CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA

 

Monday, June 02, 2014 Confirmed Variant CJD Case in Texas

 


 

SO, 4 months after the fact and still no word on this case. no information what so ever. the silence is deafening $$$

 

Monday, November 3, 2014

 

The prion protein protease sensitivity, stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sporadic Creutzfeldt-Jakob disease

 


 


 

Tuesday, November 04, 2014

 

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

 


 

PLEASE REMEMBER ;

 

The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.

 

HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???

 

if not, why not...

 

Friday, November 30, 2007

 

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

 


 


 

Tuesday, November 04, 2014

 

The pathological and molecular but not clinical phenotypes are maintained after second passage of experimental atypical bovine spongiform encephalopathy in cattle

 


 

Tuesday, November 04, 2014

 

Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

 


 

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 ;

 


 

 kind regards, terry

Tuesday, November 04, 2014

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease

 

Jesu´ s de Pedro-Cuesta1*, Ignacio Mahillo-Fernandez1, Miguel Calero2, Alberto Ra´bano3, Mabel Cruz4, A° ke Siden4, Pablo Martı´nez-Martı´n1, Henning Laursen5, Marı´a Ruiz-Tovar1, Ka°re Mølbak6, on behalf of the EUROSURGYCJD Research Group"

 

1 Department of Applied Epidemiology, National Centre for Epidemiology, Carlos III Institute of Health; and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Madrid, Spain, 2 Carlos III Institute of Health, and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Majadahonda, Spain; and Alzheimer’s Disease Center, Reina Sofia Foundation, Madrid, Spain, 3 Alzheimer’s Disease Center, Reina Sofia Foundation, Madrid, Spain, 4 Karolinska Institute, Neurology Division, Stockholm, Sweden, 5 National Hospital, Copenhagen, Denmark, 6 Statens Serum Institut, Copenhagen, Denmark

 

Abstract

 

Introduction: Sporadic Creutzfeldt-Jakob disease (sCJD) might be transmitted by surgery. The purpose of this study was to investigate potential susceptibility to sCJD from surgery at juvenile age and in early adulthood.

 

Methods: From Danish and Swedish national registries we identified 167 definite and probable sCJD cases with onset from 1987 through 2003, and 835 age-, sex- and residence-matched controls along with their surgical histories. Main, anatomically or etiologically classified surgical procedures followed by a $20-year lag were analyzed using logistic regression, and stratified by age at first-registered surgical discharge.

 

Results: The risk of having a diagnosis of CJD depended strongly on age at first surgery with odds ratio (OR) of 12.80 (95% CI 2.56–64.0) in patients ,30 years, 3.04 (95% 1.26–7.33) in 30–39 years, and 1.75 (95% CI 0.89–3.45) in $40 years, for anatomically classified surgical procedures. Similar figures were obtained for etiologically classified surgical procedures.

 

Conclusions: Risk of surgical-acquired sCJD depends on age at exposure; this pattern is similar to age-specific profiles reported for CJD accidentally transmitted by human pituitary-derived growth hormone and susceptibility curves for variant CJD estimated after adjustment for dietary exposure to bovine spongiform encephalopathy. There might be an age-atexposure- related susceptibility to acquire all CJD forms, including sCJD from routine surgery.

 

SNIP...

 

Surgical history and risk of sCJD

 

A recent review of 18 case-control studies which examined links between medical procedures, particularly surgery and blood transfusion, and sCJD, identified many other associations, including protective ones, and highlighted diverse sources of potentially underlying bias [2]. The review concluded that potential methodological pitfalls in case-control studies on surgery and risk of sCJD were (a) the use of hospital controls and sampling controls close to or at the end of long case incidence periods, (b) exposure assessment in different lifetime periods for cases and controls and (c) potential confounding by concurrent procedures, particularly surgery and intra-operative blood transfusions. Three types of positive associations with decreasing biological plausibility were proposed. a) An increased frequency of surgery during the prodromal phase or early clinical course in sCJD was considered to be a stressful trigger of sCJD [22] or, alternatively, attributed to reverse causality by prodromal or subclinical disease [14]. b) Positive associations for SP and blood tranfusions, with the strongest evidence of an association based on latency analysis at .10- or .20-year lag, were consistent with the protracted incubation periods in human prion disease, but might have involved organs or tissues that are not known to be infectious in sCJD [9,10]. Although case-control studies must be interpreted with caution and there may be confounding of SP by BT, the positive findings in relation to SP and BT may indicate a true risk for sCJD c) As a third explanation, specific procedures at a shorter latency could be a risk factor, e.g. retinal surgery with about a mean 10-year lag or coronary surgery in the decade preceding sCJD onset. The interpretation of these findings required an assessment of specific, speculative hypotheses. Possibilities include the direct spread of prions to the retina, or the confounding by risk factors shared by coronary disease and sCJD [6,14]. For details we refer the reader to our abovementioned review.

 

Public Health implications

 

We have previously estimated a population-attributable proportion of surgically transmitted sCJD in Denmark and Sweden of 18%. This estimate was based mainly on surgery performed on middle-aged and elderly patients [6]. If susceptibility is age-related, as the present analysis indicate, the population-attributable fraction was underestimated. This idea is based on the fact that under-registration of SP prior to 1970 was highest for those first exposed at ages ,30 years, and that positive life-time surgical history in the UK at these ages reaches 60% [23]. Hence, risk of sCJD might be highest for ages at surgery not completely covered by our study. Estimating the public health impact would require a study update to be conducted after a 10-year interval, ie, at the present, to cover surgery at lower ages and infrequent, high-risk procedures such as neurosurgery.

 

Our results may imply that written recommendations for prevention, such as the need for single-use equipment, and for organizational measures may be particularly relevant for young surgical patients [24]. In addition, middle-aged and elderly patients inadvertently exposed to potentially contaminated instruments might not qualify as "at-risk persons for public health purposes", in view of their lower risk of acquiring sCJD. The results of this study would also support the need for EU Member States to implement continued surveillance of and public health research into all CJD forms, and the recording of patients’ complete surgical histories.

 

To sum up, the results of this study suggest that, in line with reported findings for iCJD and vCJD, there is an age-at-exposurerelated susceptibility for risk of sCJD from routine surgery. This observation is relevant for epidemiologic research, clinical guidance to prevent CJD transmission in medical settings, and CJD surveillance.

 

Figure 1. Potential age-at-exposure-related susceptibility for the following different CJD forms and exposures: (a) Age-susceptibility function for vCJD in the UK [12], and results from Table 1 for risk of sCJD from age at first hospital discharge associated with a registered, main surgical procedure, at a lag of $20 years. (b) Reported estimated risks relating to 5- to 10-year age groups, after adjustment for dietary exposure to bovine material and average incubation period established at 12.6 years for variant CJD in the UK [13], and plotted results from Table 1 for risk of sCJD from age at first hospital discharge associated with an etiologically reclassified higher-risk or lower-risk procedure, at a lag of $20 years. (c) Reported rate ratios of accidentally transmitted CJD (iCJD), for ever treatement vs never treatement with pituitary growth hormone (all treatments) at specific ages [11]. Reference: all other ages at treatment. (d) Reported rate ratios of accidentally transmitted CJD (iCJD) for ever treatment vs never treatment with pituitary growth hormone processed with the Hartree-modified Wilhelmi method (an hGH preparation associated with highest risk of iCJD among hGH-treated cohorts) at specific ages [11]. Reference: all other ages at treatment.

 

Citation: de Pedro-Cuesta J, Mahillo-Fernandez I, Calero M, Ra´bano A, Cruz M, et al. (2014) Towards an Age-Dependent Transmission Model of Acquired and Sporadic Creutzfeldt-Jakob Disease. PLoS ONE 9(10): e109412. doi:10.1371/journal.pone.0109412

 

Editor: Noriyuki Nishida, Nagasaki University Graduate School of Biomedical Sciences, Japan

 

Received June 11, 2014; Accepted August 30, 2014; Published October 3, 2014

 

Copyright: 2014 de Pedro-Cuesta et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. The data contains detailed information on treatment in hospitals at the individual level and it is unsuitable for public deposition. The data are available upon request to all interested researchers, and requests should be submitted to: Dr. Ka°re Mølbak (Epidemiology Department, Statens Serum Institute, Copenhagen, Denmark , KRM@ssi.dk, Artilleriva¨gen).

 

Funding: Funding was obtained from the EU Research Commission, Concerted Action QLRG3-CT-2002-81223, NEUROPRION and the Spanish Centro de Investigaciones en enfermedades Neurolo´ gicas (CIEN C03-06), and Consortium for Biomedical Research in Neurodegenerative Diseases (CIBERNED) networks, and from the Karolinska and Carlos III National Health Institutes. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

 

Competing Interests: The authors have declared that no competing interests exist.

 

* Email: jpedro@isciii.es

 

" Membership of the EUROSURGYCJD Research Group is provided in the Acknowledgments.

 

 

doi:10.1371/journal.pone.0109412.g001 Age-Dependent Induction of Acquired and Sporadic CJD PLOS ONE | www.plosone.org 5 October 2014 | Volume 9 | Issue 10 | e109412

 

SEE FULL TEXT ;

 


 

ONCE AGAIN, MANY THANKS TO PLOS ET AL FOR FULL TEXT ACCESS TO THE LAY PUBLIC...TSS

 

Monday, November 3, 2014

 

The prion protein protease sensitivity, stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sporadic Creutzfeldt-Jakob disease

 


 


 

Friday, January 10, 2014

 

*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???  ***

 


 

Monday, November 3, 2014

 

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

 

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

 

***6 Includes 11 cases in which the diagnosis is pending, and 19 inconclusive cases; ***7 Includes 12 (11 from 2014) cases with type determination pending in which the diagnosis of vCJD has been excluded. ***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

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

 

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

 


 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

Tuesday, February 11, 2014

 

Novant Health Forsyth Medical Center Information on potential CJD exposure

 


 

 

Tuesday, April 01, 2014

 

Questions linger in U.S. CJD cases 2005, and still do in 2014

 


 

Sunday, March 09, 2014

 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

 

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

 


 

Friday, February 14, 2014

 

Creutzfeldt-Jakob disease (CJD) biannual update (February 2014), with briefing on novel human prion disease National CJD Research and Surveillance Unit NCJDRSU

 


 

Thursday, April 17, 2014

 

Novant: Three more may have been exposed to disease CJD

 


 

Wednesday, April 02, 2014

 

Distinct origins of dura mater graft-associated Creutzfeldt-Jakob disease: past and future problems

 


 

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

 

*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***

 


 

Sunday, October 13, 2013

 

*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012

 


 

Sunday, July 06, 2014

 

Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study Conclusions—The a priori hypotheses were supported.

 

*Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.

 


 

Sunday, June 29, 2014

 

*** Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 


 

Wednesday, February 26, 2014

 

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 2004 THROUGHT PRION 2013 CONFERENCE ABSTRACT BOOKS

 


 

Thursday, January 23, 2014

 

Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]

 


 

Letters

 

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

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Terry S. Singeltary, Sr Bacliff, Tex

 

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

 

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

 

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

 


 

14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114

 

Session: International Scientific Exchange

 

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

 

T. Singeltary Bacliff, TX, USA

 

Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.

 

Methods: 12 years independent research of available data

 

Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.

 

Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

 


 

 Wednesday, May 16, 2012

 

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

 

Background

 

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

 

Methods

 

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

 

Results

 

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

 

Conclusions

 

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

 

end...tss

 

SEE FULL TEXT AND SOURCE REFERENCES ;

 

Wednesday, May 16, 2012

 

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

 

Proposal ID: 29403 ‘ACCEPTED’

 


 

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 ...

 


 


 

SEE FULL TEXT ;

 

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

 

Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003

 

Date: Tue, 29 Jul 2003 17:35:30 –0500

 

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

 

To: BSE-L@uni-karlsruhe.de

 

Volume 3, Number 8 01 August 2003

 

Previous

 

Next

 

Newsdesk

 

Tracking spongiform encephalopathies in North America

 

Xavier Bosch

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 


 

Singeltary submission to PLOS ;

 

No competing interests declared.

 

see full text ;

 


 

Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA

 

CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.

 

It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.

 


 

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

 

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

 

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

 

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

 

Something else I find odd, page 16;

 

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

 

A few more factors to consider, page 15;

 

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

 

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

 

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

 

Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.

 

To be continued...

 

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

 

Competing interests: None declared

 


 

Singeltary Response to USDA, and USDA RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT

 

Owens, Julie

 

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

 

Sent: Monday, July 24, 2006 1:09 PM

 

To: FSIS RegulationsComments

 

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98

 


 

FSIS, USDA, REPLY TO SINGELTARY

 


 

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

 


 

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

 


 

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 ***

 


 

Tuesday, August 12, 2014

 

MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014

 


 

Thursday, June 23, 2011

 

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

 


 

Wednesday, April 25, 2012 4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012

 


 

2012 ATYPICAL L-TYPE BSE BASE CALIFORNIA ‘confirmed’ Saturday, August 4, 2012

 

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

 


 

TSS

Monday, November 03, 2014

VPSPr stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sCJD

Monday, November 3, 2014

The prion protein protease sensitivity, stability and seeding activity in variably protease sensitive prionopathy brain tissue suggests molecular overlaps with sporadic Creutzfeldt-Jakob disease

 
 
kind regards, terry

Tuesday, September 30, 2014

Two suspected Creutzfeldt-Jakob Disease cases reported in Vietnam



Two Vietnamese men have been hospitalized with symptoms of the rare degenerative brain disorder known as Creutzfeldt – Jakob Disease (CJD); however, a definitive diagnosis could not be made, according to a Thanh Nien News report today.
Image/United States Army Center of Military History
Image/United States Army Center of Military History
Confirmation testing for CJD is not available in Vietnam, according to the report.
The two men, ages 44 and 86, from Binh Phuoc Province and Ho Chi Minh City, respectively, were treated for symptoms and released. There is no treatment for CJD.
According to the Centers for Disease Control and Prevention (CDC), Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.
The causative agents of TSEs are believed to be prions. The term “prions” refers to abnormal, pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular proteins called prion proteins that are found most abundantly in the brain.
Classic CJD is a human prion disease. It is a neurodegenerative disorder with characteristic clinical and diagnostic features. This disease is rapidly progressive and always fatal. Infection with this disease leads to death usually within 1 year of onset of illness.
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/
http://outbreaknewstoday.com/two-suspected-creutzfeldt-jakob-disease-cases-reported-in-vietnam-81488/#comment-1938
Vietnam hospitals reporst two suspected CJD cases
 
Thanh Nien News
 
Ho Chi Minh City - Tuesday, September 30, 2014 09:57 Email Print
 
Two Vietnamese men have been hospitalized with symptoms of the rare degenerative brain disorder known as Creutzfeldt – Jakob but doctors lack equipment to settle on a decisive diagnosis.
 
The HCMC Medical University Hospital received the first patient on August 20 -- a 44-year-old from Binh Phuoc Province, Tuoi Tre newspaper reported.
 
The second was an 86-year-old Ho Chi Minh City local who was admitted to the 115 People’s Hospital on September 6.
 
Both were discharged after being treated for their symptoms which haven't been precisely identified.
 
Even if doctors could be sure they suffer from CJD, which is a rare disease affecting about one in every million worldwide, no treatment is available.
 
Doctor Vo Don of the 115 hospital and his colleague Tran Ngoc Tai from the other said the patients suffered rapidly progressive dementia and experienced problems moving or speaking.
 
The 86-year-old patient, only identified as P.V.L., could only lie still when he was admitted.
 
Family members said he started to forget things around two years ago and his memory grew progressively worse.
 
More than a month after he was admitted, his condition rapidly deteriorated. He had problems walking around and holding things in his hands.
 
L.B.H., the other patient, initially sought treatment at a Binh Phuoc hospital where doctors were baffled by the symptoms.
 
He went to two other hospitals in the city where doctors could not venture a diagnosis.
 
By the time he arrived at the University hospital in Ho Chi Minh City, he could hardly speak or raise his legs and arms.
 
Tests have been performed on the patients to rule out other treatable forms of dementia such as encephalitis or meningitis.
 
MRI scans showed their brains' electrical patterns have become irregular.
 
Doctors say the results are typical of the disease, which was once considered a human form of mad cow disease.
 
But the doctors say they need to conduct tests on samples of a brain protein called prion to decide for sure, and hospitals in Vietnam aren't equipped for that.
 
Prion proteins occur in both a normal form and an infectious form, which causes the disease.
 
The prions cause harm when they change into the infectious form and clump together, leading to neuron loss and other brain damage.
 
Tai said the disease usually occurs at people from between 55 to 60 years of age.
 
Victims of the disease forget what they've just said, then the way home and eventually cannot recognize their own children.
 
Gradually, they lapse into temper tantrums, behavioral disorders and mobility problems including seizures.
 
In less common cases among patients between 25 and 30, the victims suffer mobility before mental problems.
 
They too end up in a vegetative state, the doctor said.
 
Depending on nursing conditions, patients can survive for several months or several years and they usually die of complications such as ulceration and bacterial infections associated with lying still for long periods of time.
 
Tai said the cause of the disease is not known in around 85 percent of patients.
 
Another 10-15 percent inherit the disease and less than 1 percent are infected by other patients’ tissues or tainted medical equipment.
 
His hospital has seen four patients whom they believe suffer the disease in the past seven years..
 
Don meanwhile said his 115 hospital receives one to two suspected cases a year.
 
More :
 
Vietnam Ho Chi Minh City CJD Creutzfeldt – Jakob brain disease
 
 
USA 4TH CASE VCJD (aka nvCJD) HUMAN MAD COW, THE SILENCE IS DEAFENING BSE, CWD, AND SCRAPIE TSE PRION DISEASE
 
Greetings DSHS, Dr. Fishcer, et al,
 
I know that most in the USA could care less about the CJD TSE prion disease aka mad cow type disease. but there are some of us here that will never forget.
 
you can cover up what ever you want. we all know. I have seen it happen too many times here in Texas with BSE TSE prion, either the typical or the atypical strains, or with the feed, or, with cwd, or scrapie as that goes, but we are still here, and we will never forget...
 
kind regards, terry
 
Creutzfeld-Jacob Disease (CJD) Emerging & Acute Infectious Disease Branch Michael Fischer
 
Marilyn Felkner
 
512-776-7676
 
512-776-7676
 
Chronic Wasting Disease Zoonosis Control Branch Eric Fonken
 
512-776-2155
 
Lab tests have confirmed a diagnosis of variant Creutzfeldt-Jakob Disease (CJD) in a patient who recently died in Texas. Variant CJD is a rare, fatal brain disorder, first described in 1996 in the United Kingdom and associated with beef consumption overseas.
 
This is the fourth case ever reported in the United States. In each of the three previous cases, infection likely occurred outside the United States, including the United Kingdom and Saudi Arabia. The history of this fourth patient includes extensive travel to Europe and the Middle East, and infection likely occurred outside the United States. The CDC and DSHS continue to investigate the case.
 
There are no Texas public health concerns or threats associated with this case.
 
 
 
 
Last updated June 02, 2014
 
 
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
 
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
 
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
 
 
SO, 4 months after the fact and still no word on this case. no information what so ever. the silence is deafening $$$
 
Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
 
Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades.
 
The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
 
see ;
 
 
The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month.
 
nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment.
 
sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?
 
Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end
 
REFERENCES
 
Sunday, June 29, 2014
 
Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014
 
 
Tuesday, August 12, 2014
 
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST 2014
 
 
Singeltary Response to USDA, and USDA
 
RESPONSE TO SINGELTARY ON HARVARD BSE RISK ASSESSMENT
 
Owens, Julie
 
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
 
Sent: Monday, July 24, 2006 1:09 PM
 
To: FSIS RegulationsComments
 
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
 
 
FSIS, USDA, REPLY TO SINGELTARY
 
 
*** 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.
 
 
NOW, what is the latest on human risk factors to CWD strains ???
 
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
 
*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,
 
*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.
 
PPo2-27:
 
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
 
*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
 
PPo2-7:
 
Biochemical and Biophysical Characterization of Different CWD Isolates
 
*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.
 
 
Envt.07:
 
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease
 
***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.
 
 
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<
 
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
 
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
 
Wednesday, January 01, 2014
 
Molecular Barriers to Zoonotic Transmission of Prions
 
*** 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.
 
 
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
HD.13: CWD infection in the spleen of humanized transgenic mice
 
***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.
 
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier to conversion of human prion protein in the case of chronic wasting disease.
 
PRION2013 CONGRESSIONAL ABSTRACTS CWD
 
Sunday, August 25, 2013
 
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission
 
 
Friday, November 09, 2012
 
*** Chronic Wasting Disease CWD in cervidae and transmission to other species
 
 
there is in fact evidence that the potential for cwd transmission to humans can NOT be ruled out.
 
I thought your readers and hunters and those that consume the venison, should have all the scientific facts, personally, I don’t care what you eat, but if it effects me and my family down the road, it should then concern everyone, and the potential of iatrogenic transmission of the TSE prion is real i.e. ‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there from...like deer antler velvet and TSE prions and nutritional supplements there from, all a potential risk factor that should not be ignored or silenced. ...
 
the prion gods at the cdc state that there is ;
 
''no strong evidence''
 
but let's see exactly what the authors of this cwd to human at the cdc state ;
 
now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
 
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
 
From: TSS (216-119-163-189.ipset45.wt.net)
 
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
 
Date: September 30, 2002 at 7:06 am PST
 
From: "Belay, Ermias"
 
To:
 
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
 
Sent: Monday, September 30, 2002 9:22 AM
 
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Dear Sir/Madam,
 
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
 
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
 
Ermias Belay, M.D. Centers for Disease Control and Prevention
 
-----Original Message-----
 
From:
 
Sent: Sunday, September 29, 2002 10:15 AM
 
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
 
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
 
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
 
Thursday, April 03, 2008
 
A prion disease of cervids: Chronic wasting disease
 
2008 1: Vet Res. 2008 Apr 3;39(4):41
 
A prion disease of cervids: Chronic wasting disease
 
Sigurdson CJ.
 
snip...
 
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
 
snip...
 
full text ;
 
 
 
 
***********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 ;
 
 
Thursday, October 10, 2013
 
*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************
 
 
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.
 
 
DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
 
Date: Fri, 16 May 2003 11:47:37 –0500
 
EMC 1 Terry S. Singeltary Sr. Vol #: 1
 
 
 
 
*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.
 
 
Monday, August 8, 2011
 
*** Susceptibility of Domestic Cats to CWD Infection ***
 
Oral.29: Susceptibility of Domestic Cats to CWD Infection
 
Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
 
Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu
 
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.
 
*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
 
 
 
AD.63:
 
Susceptibility of domestic cats to chronic wasting disease
 
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
 
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.
 
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
 
 
www.landesbioscience.com
 
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
 
 
 
FELINE SPONGIFORM ENCEPHALOPATHY FSE
 
 
 
Sunday, November 10, 2013
 
LARGE CJD TSE PRION POTENTIAL CASE STUDY AMONG HUMANS WHO TAKE DEER ANTLER VELVET WILL BE ONGOING FOR YEARS IF NOT DECADES, but who's cares $
 
 
Singeltary submission ;
 
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
 
DOCUMENT ID: APHIS-2006-0118-0411
 
***Singeltary submission
 
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards
 
>>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<<
 
Greetings USDA/APHIS et al,
 
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards.
 
I believe, and in my opinion, and this has been proven by scientific facts, that without a validated and certified test for chronic wasting disease cwd, that is 100% sensitive, and in use, any voluntary effort will be futile. the voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow surveillance program has failed terribly, as well as the testing for bse tse prion in cattle, this too has failed terrible. all this has been proven time and time again via OIG reports and GOA reports.
 
I believe that until this happens, 100% cwd testing with validated test, ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
 
In my opinion, and the opinions of many scientists and DNR officials, that these so called game farms are the cause of the spreading of chronic wasting disease cwd through much negligence. the game farms in my opinion are not the only cause, but a big factor. I kindly wish to submit the following to show what these factors are, and why interstate movement of cervids must be banned. ...
 
snip...see full text and PDF ATTACHMENT HERE ;
 
 
 
Sunday, June 23, 2013
 
National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)
 
***Terry S. Singeltary Sr. submission
 
 
Friday, November 22, 2013
 
Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids
 
***SINGELTARY SUBMISSION
 
The Scottish Parliament’s Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,
 
***and your email has been forwarded to the committee for information:
 
 
 
Friday, November 22, 2013
 
Wasting disease is threat to the entire UK deer population
 
 
Sunday, July 21, 2013
 
Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013
 
*** Singeltary Submission WG18417
 
 
Thursday, July 03, 2014
 
*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?
 
 
=============================================================================
 
Tuesday, July 01, 2014
 
*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM ***
 
 
=============================================================================
 
Ronnie Dunn Cross Examination, slaughtering cattle, or killing deer ?
 
IN THE UNITED STATES DISTRICT COURT FOR THE NORTHERN DISTRICT OF INDIANA SOUTH BEND DIVISION UNITED STATES OF AMERICA, vs. RUSSELL G. BELLAR, Defendant.
 
___________________________
 
)))))))))
 
Cause No.: 3:04cr00068-AS South Bend, Indiana January 4, 2005 9:30 a.m.
 
TRANSCRIPT EXCERPT OF JURY TRIAL (TESTIMONY OF: RONNIE DUNN AND RUSTY CAMP) BEFORE THE HONORABLE ALLEN SHARP
 
snip...
 
Ronnie Dunn Cross Examination
 
Q. Mr. Dunn, at one point I believe you told the federal agents that Mr. Bellar told you that this was a private deer farm and shooting deer on that farm was like slaughtering cattle; is that correct?
 
A. I don't know if I used the word "slaughter," but it was, yeah, like that.
 
Q. You don't know if that was your word, "slaughtering cattle"?
 
A. I don't know that.
 
Q. Well, did he give you the idea of killing cattle?
 
A. Yes, it was the same principle.
 
snip...
 
see full text ;
 
 
 
 
BUCK FEVER
 
 
Thursday, September 18, 2014
 
*** Risk behaviors in a rural community with a known point-source exposure to chronic wasting disease
 
 
Saturday, September 20, 2014
 
*** North Carolina Captive cervid licenses and permits Senate Bill 744 Singeltary Submission
 
Description The proposed changes to 15A NACA 10H .0301 would allow the Commission to issue new captivity licenses and permits for the purpose of holding cervids in captivity and allow certified herd owners to sell or transfer cervids to any licensed facility. Also, mandatory testing for CWD will be raised from all cervids that die at age 6 months or older to all cervids that die at age 12 months or older.
 
 
North Carolina Captive cervid licenses and permits Senate Bill 744 Singeltary Submission
 
*** p.s. please add this to my submission, very important information...
 
Saturday, February 04, 2012
 
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
 
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.
 
*** Two of the six fawns with CWD detected were 5 to 6 months old.
 
All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
 
Saturday, February 04, 2012
 
*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
 
 
*** Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
 
 
SNIP...SEE FULL TEXT ;
 
Saturday, September 20, 2014
 
*** North Carolina Captive cervid licenses and permits Senate Bill 744 Singeltary Submission
 
 
Thursday, September 11, 2014
 
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
 
How they voted: attempt to override veto of ag bill fails in the House
 
 
Thursday, September 11, 2014
 
*** TEXAS ANIMAL HEALTH COMMISSION 390th COMMISSION MEETING AGENDA (CWD movement restriction zone) September 16, 2014 8:30 A.M.
 
 
Wednesday, September 17, 2014
 
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant Health Inspection Service Veterinary Services ***
 
 
Friday, September 05, 2014
 
*** CFIA CWD and Grain Screenings due to potential risk factor of spreading via contamination of grain, oil seeds, etc. ***
 
 
Wednesday, September 17, 2014
 
*** Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant Health Inspection Service Veterinary Services ***
 
 
Sunday, September 21, 2014
 
INFORM: Cervid Health and States Indemnity FY 2015
 
 
Wednesday, September 17, 2014
 
Cost benefit analysis of the development and use of ante-mortem tests for transmissible spongiform encephalopathies
 
 
Sunday, August 24, 2014
 
*** USAHA 117TH ANNUAL MEETING USDA-APHIS–VS CWD Herd Certification Program Goals TSE PRION October 17 – 23, 2013
 
 
*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.
 
*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.
 
PRION 2014 CONFERENCE
 
CHRONIC WASTING DISEASE CWD
 
A FEW FINDINGS ;
 
Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.
 
We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.
 
The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.
 
Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.
 
Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.
 
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
 
Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.
 
Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.
 
see full text and more ;
 
Monday, June 23, 2014
 
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
 
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
 
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
 
 
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
 
 
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
 
 
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
 
 
PPo4-4:
 
Survival and Limited Spread of TSE Infectivity after Burial
 
PPo4-4:
 
Survival and Limited Spread of TSE Infectivity after Burial
 
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
 
Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.
 
The authors gratefully acknowledge funding from DEFRA.
 
 
 
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE transmission Project Code: M03024 ***
 
02/08/2011
 
The project confirmed that U.K red deer are susceptible to both oral and intra-cerebral inoculation with the cattle BSE agent. Six clinically positive (from 26-42 months post inoculation) i.c inoculated and one (56 months post inoculation) orally dosed deer that tested positive for TSE by immunohistochemistry and Western blotting using several primary antibodies demonstrated widespread accumulation of disease specific prion protein in the central nervous system, peripheral nervous system and enteric nervous system but none in lymphoreticular system. All showed several brain sites positive for disease specific prion protein and presented immunohistochemistry and Western blotting phenotypes with similarities to BSE in sheep, goats and cattle but unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep. The vacuolar pathology and distribution of disease specific prion protein in red deer resembled that of CWD in most major respects however we have shown that BSE can be clearly differentiated from CWD by existing immunohistochemical and biochemical methods that are in routine use.
 
The knowledge gained as a result of this work will permit rapid and accurate diagnosis should a TSE ever be detected in European red deer and will also enable effective disease control methods to be quickly put in place.
 
 
Results
 
We confirmed that U.K red deer are susceptible to both oral and intra-cerebral inoculation with the cattle BSE agent. Six clinically positive (from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested positive for TSE by IHC and WB using several primary antibodies demonstrated widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in LRS. All showed several brain sites positive for disease specific PrP and presented IHC and WB phenotypes with similarities to BSE in sheep, goats and cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar pathology and distribution of PrPd BSE in red deer resembled that of CWD in most major respects however we have shown that BSE can be clearly differentiated from CWD by existing immunohistochemical and biochemical methods that are in routine use.
 
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann; Roslin NPD.
 
Negative controls and the remaining 5 orally dosed deer culled at 72mpi tested negative by IHC and Western blot however analysis of the PrP ORF of these deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q to E polymorphism at codon 226 that may influence the efficiency of oral transmission (not published).
 
In the experimental BSE challenge of red deer six out of six deer succumbed to BSE when challenged by intracerebral routes but only one of six deer challenged by the oral route succumbed to infection. Deer killed at 190 days or 365 days post oral challenge showed no evidence of abnormal PrP accumulation when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E polymorphism at codon 226. The table shows the distribution of these codon 226 polymorphisms within experimental challenge groups.
 
snip...
 
 
Research article Open Access
 
Immunohistochemical and biochemical characteristics of BSE and CWD in experimentally infected European red deer (Cervus elaphus elaphus)
 
Stuart Martin*1, Martin Jeffrey1, Lorenzo González1, Sílvia Sisó1, Hugh W Reid2, Philip Steele2, Mark P Dagleish2, Michael J Stack3, Melanie J Chaplin3 and Aru Balachandran4 Address: 1Veterinary Laboratories Agency (VLA-Lasswade), Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 2Moredun Research Institute, Pentlands Science Park, Bush Loan, Penicuik, Midlothian, EH26 0PZ, UK, 3VLA-Weybridge, Addlestone, Surrey, KT15 3NB, UK and 4Animal Diseases Research Institute, Canadian Food Inspection Agency, Ottawa, Ontario, K2H 8P9, Canada
 
Abstract
 
Background: The cause of the bovine spongiform encephalopathy (BSE) epidemic in the United Kingdom (UK) was the inclusion of contaminated meat and bone meal in the protein rations fed to cattle. Those rations were not restricted to cattle but were also fed to other livestock including farmed and free living deer. Although there are no reported cases to date of natural BSE in European deer, BSE has been shown to be naturally or experimentally transmissible to a wide range of different ungulate species. Moreover, several species of North America's cervids are highly susceptible to chronic wasting disease (CWD), a transmissible spongiform encephalopathy (TSE) that has become endemic. Should BSE infection have been introduced into the UK deer population, the CWD precedent could suggest that there is a danger for spread and maintenance of the disease in both free living and captive UK deer populations. This study compares the immunohistochemical and biochemical characteristics of BSE and CWD in experimentally-infected European red deer (Cervus elpahus elaphus).
 
Results: After intracerebral or alimentary challenge, BSE in red deer more closely resembled natural infection in cattle rather than experimental BSE in small ruminants, due to the lack of accumulation of abnormal PrP in lymphoid tissues. In this respect it was different from CWD, and although the neuropathological features of both diseases were similar, BSE could be clearly differentiated from CWD by immunohistochemical and Western blotting methods currently in routine use.
 
Conclusion: Red deer are susceptible to both BSE and CWD infection, but the resulting disease phenotypes are distinct and clearly distinguishable.
 
SNIP...
 
Results
 
Clinical disease
 
All six deer challenged i.c. with BSE developed clinical disease between 794 and 1260 days post-inoculation with a mean incubation period of 1027 days. A detailed description of the clinical signs was provided in an earlier report [8]. Briefly, affected deer showed variable degrees of ataxia, anorexia, circling and apparent blindness, together with failure of seasonal change of coat, weight loss and 'panic attacks'. In addition, one of six red deer orally dosed with BSE developed clinical disease 1740 days after challenge, and this animal presented with a short clinical duration of two days; the other five deer from this group remain healthy at the time of writing (65 months after challenge). Sequential rectal biopsies taken at five different time points from orally and i.c. inoculated deer were negative for PrPd.
 
All four deer orally challenged with CWD started to show behavioural changes between 577 and 586 days post challenge;
 
these progressed to definite neurological disease between 742 and 760 days post-challenge (Table 1).
 
Clinical signs were similar to the BSE challenged deer and included nervousness, weight loss, excessive salivation, roughness of coat, and progressive ataxia. All these CWD inoculated deer showed PrPd accumulation in the secondary follicles of rectal biopsies taken at 7 months post infection.
 
Conclusion
 
European red deer are susceptible to infection with the cattle BSE agent, not only by the intra-cerebral but also by the oral route, and although the clinical signs and spong- iform change are similar to those of CWD in the same species, these two infections can be easily differentiated. The lack of lymphoid involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the predominantly intracellular accumulation of PrPd are features of deer BSE that are in contrast with those of deer CWD. However, only one of six deer developed disease after alimentary exposure to 25 g of a BSE brain pool homogenate after an incubation period of nearly 5 years; this suggests a strong species barrier but if a TSE in European red deer should ever be identified then BSE/CWD discrimination would be an urgent priority. To determine whether there are potential naturally occurring BSE-like strains and to determine the degree to which there is strain variation, it would be necessary to examine many more naturally occurring CWD cases. These results will support the ongoing European surveillance for natural TSEs in red deer and the further assessment of potential risk to human health.
 
Published: 27 July 2009 BMC Veterinary Research 2009, 5:26 doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009 This article is available from: http://www.biomedcentral.com/1746-6148/5/26 © 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
 
 
Monday, May 05, 2014
 
*** Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing ***
 
 
snip...
 
Friday, December 14, 2012
 
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
 
snip...
 
In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
 
Animals considered at high risk for CWD include:
 
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
 
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
 
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
 
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
 
*** Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
 
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
 
snip...
 
 
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
 
EMC 1 Terry S. Singeltary Sr. Vol #: 1
 
 
 
see my full text submission here ;
 
 
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
 
 
Tuesday, September 16, 2014
 
mad cow scaremongers consumerfreedom.com December 20, 2003 article and a 2014 review
 
 
Wednesday, September 10, 2014
 
Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated guidance on decontamination of gastrointestinal endoscopy equipment
 
Research and analysis
 
 
CWD STRAINS TO HUMANS ???
 
*** 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).
 
 
as I said, what if ?
 
*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***
 
 
===========================================
 
Thursday, January 2, 2014
 
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
 
WHAT IF ?
 
 
Saturday, April 19, 2014
 
Exploring the zoonotic potential of animal prion diseases: In vivo and in vitro approaches
 
 
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
 
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***
 
 
Sunday, October 13, 2013
 
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
 
 
Tuesday, April 01, 2014
 
*** Questions linger in U.S. CJD cases 2005, and still do in 2014
 
 
Monday, March 29, 2010
 
CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER
 
URGENT, PLEASE NOTE ;
 
>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<
 
 
 
CJD NE TEXAS CLUSTER
 
Creutzfeldt-Jakob Disease in Northeast Texas
 
J.A. Rawlings,*1 K.A. Hendricks1, O.M. Nuno1, D.A. Brown1, D.A. Evans2, Texas Department of Health, 1Austin and 2Tyler, Texas Creutzfeldt-Jacob Disease (CJD), a transmissible spongiform encephalopathy, is caused by prions composed of proteinaceous material devoid of nucleic acid. CJD occurs sporadically (generally 1 case/1,000,000 population per year) in older patients (average age of 65) and is characterized by rapidly progressive dementia, accompanied by severe muscle spasms and incoordination. Death usually occurs within 3 to 12 months (average 7 months). CJD activity in Texas, which has a population of nearly 19 million, appeared to be typical. The statewide death rate for 1995 and 1996 was just under 1/1,000,000. In April of 1997, the Texas Department of Health became aware of an increased number of possible CJD cases in a 23-county area of NE Texas with a population of just over one million. After review of medical and pathology records, four patients were identified with definite classic CJD and three were identified with probable CJD. Dates of death for the eight patients were from April, 1996 through mid-July 1997. The patients were from 46 through 65 years of age; four were male and three were female. A case-control study to identify risks for CJD in NE Texas has been initiated. http://www.jifsan.umd.edu/tse/Rawlings.htm
 
we get them young cases of tse prion disease in Texas, that is not related to anything $$$ money and politics will buy anything, especially junk science... sporadic ffi and sporadic gss ;
 
NOT THIS CASE !!! but another one a while back in Texas...see ;
 
We report a case of a 33-year-old female who died of a prion disease for whom the diagnosis of sFI or FFI was not considered clinically. Following death of this patient, an interview with a close family member indicated the patient's illness included a major change in her sleep pattern, corroborating the reported autopsy diagnosis of sFI.
 
 
sporadic FFI or nvCJD Texas style ???
 
 
Creutzfeldt-Jakob Disease Surveillance in Texas
 
 
Sunday, July 11, 2010
 
CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
Thursday, August 12, 2010
 
Seven main threats for the future linked to prions
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
 
Second threat
 
snip...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
snip...
 
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
 
snip...
 
 
 
***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
 
 
Monday, May 19, 2014
 
Variant CJD: 18 years of research and surveillance
 
 
Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
 
 
 
 
full text with source references ;
 
 
re-Human Prion Diseases in the United States
 
Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
 
Views & Reviews
 
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
 
Ermias D. Belay, MD, Ryan A. Maddox, MPH, Pierluigi Gambetti, MD and Lawrence B. Schonberger, MD
 
+ Author Affiliations
 
From the Division of Viral and Rickettsial Diseases (Drs. Belay and Schonberger and R.A. Maddox), National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA; and National Prion Disease Pathology Surveillance Center (Dr. Gambetti), Division of Neuropathology, Institute of Pathology, Case Western Reserve University, Cleveland, OH.
 
Address correspondence and reprint requests to Dr. Ermias D. Belay, 1600 Clifton Road, Mailstop A-39, Atlanta, GA 30333.
 
 
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?
 
 
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. FREE FULL TEXT
 
 
 
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.
 
 
Saturday, January 2, 2010
 
Human Prion Diseases in the United States January 1, 2010 ***FINAL***
 
 
14th ICID International Scientific Exchange Brochure -
 
Final Abstract Number: ISE.114
 
Session: International Scientific Exchange
 
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
 
T. Singeltary
 
Bacliff, TX, USA
 
Background:
 
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
 
Methods:
 
12 years independent research of available data
 
Results:
 
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
 
Conclusion:
 
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
 
 
re-Human Prion Diseases in the United States
 
Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
I kindly disagree with your synopsis for the following reasons ;
 
snip...
 
I would kindly like to add to my initial concerns, something I brought up years ago, and I believe that still hold true today, more so even than when I first stated these concerns in 2003 ;
 
routine passive mortality CJD surveillance USA ?
 
THIS has been proven not to be very useful in the U.K.;
 
THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)
 
snip...
 
One reason for this was the _inaccuracy_ in coding of cases correctly certified as CJD Coding is carried out by staff who are not medically qualified and it is not surprising that coding errors occur in the processing of large numbers of certificates. In 1982, 12,000 certificates per week were processed at the office of population censuses and surveys by 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of both inter- and intra-observer coding errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH certification and coding discovered in this study _support_ the introduction of a more accurate system of death certificates and a more detailed and specific coding system...
 
snip...
 
 
Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr. R. Will
 
snip...
 
IDENTIFICATION OF CASES
 
Cases of CJD may be identified from death certificates, but this alone is unlikely to provide adequate monitoring. ERRORS are made in certification and diagnosis; in the Oxford study death certificates were obtained on a series of known confirmed cases and CJD was mentioned in only 66% of certificates. In another series of 175 certified cases, 42 patients were judged not to have suffered from CJD after examination of case notes (7)...
 
full text;
 
 
snip...see my full text submission here ;
 
re-Human Prion Diseases in the United States
 
Posted by flounder on 01 Jan 2010 at 18:11 GMT
 
 
2001-2002ish
 
greetings TSE PRION WORLD,
 
i am reminded of a few things deep throat told me years ago;
 
*** The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people.........
 
Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie..... why???? than the UK... then would the same mechanisms that make different strains of scrapie here make different strains of BSE... if the patterns are different in sheep and mice for scrapie..... could not the BSE be different in the cattle, in the mink, in the humans....... I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........ bse..... scrapie
 
Scrape the damn slide and put it into mice..... wait..... chop up the mouse brain and and spinal cord........ put into some more mice..... dammit amplify the thing and start the damned research..... This is NOT rocket science... we need to use what we know and get off our butts and move.... the whining about how long everything takes..... well it takes a whole lot longer if you whine for a year and then start the research!!!
 
Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde..... for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year....... it is a big fat sponge... the agent continues to eat the brain ...... you can't make slides anymore because the agent has never stopped........ and the old slides that are stained with Hemolysin and Eosin...... they get holier and holier and degenerate and continue... what you looked at 6 months ago is not there........ Gambetti better be photographing every damned thing he is looking at.....
 
***Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........ if you want to move this thing along and shake the earth.... then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........ I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........ forget any action........ it is ALL gonna be sporadic!!! And, if there is a case....... there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats.... and this may be their biggest downfall...***
 
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here.......... knocked me out of my chair........ you must keep pushing. If I was a power person.... I would be demanding that there be at least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the wood work as there is money to be made!!!
 
In short: "FIRE AT WILL"!!! for the very dumb.... who's "will"! "Will be the burden to bare if there is any coverup!"
 
again it was said years ago and it should be taken seriously.... BSE will NEVER be found in the US!
 
As for the BSE conference call... I think you did agreat service to freedom of information and making some people feign integrity... I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
 
You need to watch your back........ but keep picking at them....... like a buzzard to the bone... you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
 
================================================
 
*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 SINGELTARY HACKS IN (DEEP THROAT ABOVE HELPED ME GET IN)
 
 
 
Mad cow disease: Could it be here?
 
Man's stubborn crusade attracts experts' notice By Carol Christian | August 5, 2001
 
 
yes, cjd is popping up in more and more places it seems. I think in 55 year and older, it's now 1 in 9,000.
 
see ;
 
lifetime risk of developing sporadic CJD is about 1 in 30,000, jumps to 1 in 9,000 in 50 years of age and above
 
IN REALITY, sporadic CJD is 1 in 9,000 in 50 years of age and above, and that's with a inadequate or what I call passive surveillance system. see below ;
 
Dr. William Shulaw, a veterinarian with The Ohio State University extension service, is involved in a nationwide program to eradicate scrapie, the form of BSE found in sheep.
 
Shulaw said the chances of a person getting sporadic Creutzfeldt- Jakob disease is about one in a million. But that's the total population, infants, children, adults and the elderly.
 
Chances increase to one in 9,000 when the group is restricted to those age 50 and older.
 
 
 
 
NOW, remember, the federal government lied to us for 100 years about other long incubating disease i.e. tobacco and asbestos, just to protect the industry. ...
 
just saying...
 
kind regards, terry
 
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
 
Monday, June 02, 2014
 
Confirmed Human BSE aka mad cow Variant CJD vCJD or nvCJD Case in Texas
 
fact is, BSE cases in Europe of the past years have dropped dramatically due to feed ban that was enforced, and extensive BSE testing, in large numbers. just the opposite has happened in the USA. it’s all been documented. there is ample evidence that there is as much of a chance (if not more), that this victim contracted human mad cow disease from sources right here in the USA. this PR push to alienate a USA source factor for human BSE in the USA is a PR stunt by the USDA inc., and not justified now, in my opinion. compare BSE testing figures in the EU compared to the USA, compare mad cow feed ban breaches, and you will see. hell, the 2004 enhanced BSE surveillance program was flawed so bad, the top Prion God at the NIH TSE prion expert Paul Brown, says he does not trust anything from the USDA since Texas covered up a mad cow for 7 months, on a 48 hour confirmation turn around. it’s all documented below in link. USDA inc shut down the mad cow testing after so many atypical BSE cases started showing up.
 
yes, another foreigner comes to the USA, or another USA citizens does some traveling, and all of a sudden, it’s a foreign disease. evidently, these folks never eat anything in the USA, and contracts nvcjd. right. just like the last one in 2005. really? here are the facts of the TEXAS MAD COW, MAD COW FEED in Texas, CJD CLUSTER in Texas, CJD CASE IN 38 YEAR OLD WOMAN THAT APPARENTLY WORKED ON THE SLAUGHTER LINE FOR TYSON in Texas, AND OTHER STRANGE TSE PRION DISEASE IN VERY YOUNG VICTIMS HERE IN TEXAS with long duration of illness from onset of clinical symptoms to death, CALLED SPORADIC FFI (except it is not linked to any genetic make up of that family), another nvcjd victim back in 2005 in Texas, apparently another UK victim that had moved to Texas, and never ate anything. these are the facts as I have come to know them (official documents), since hvcjd took my mom in December of 1997. just made a promise to mom, never forget, and never let them forget, the rest of the story, the truth you don’t hear about. ...our fine federal friends and the USDA inc, has lied to all of us...
 
CONFIRMED HUMAN BSE AKA MAD COW DISEASE vCJD TEXAS USA
 
Monday, June 02, 2014 Confirmed Variant CJD Case in Texas
 
 
kind regards, terry