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Location: BACLIFF, Texas, United States

My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth. There is a route, and there is a source. There are many here in the USA. WE must make CJD and all human TSE, of all age groups 'reportable' Nationally and Internationally, with a written CJD questionnaire asking real questions pertaining to route and source of this agent. Friendly fire has the potential to play a huge role in the continued transmission of this agent via the medical, dental, and surgical arena. We must not flounder any longer. ...TSS

Saturday, February 01, 2014

vCJD With Extremely Low Lymphoreticular Deposition of Prion Protein MAY NOT HAVE BEEN DETECTABLE

 Case Report/Case Series | January 20, 2014

 

Variant Creutzfeldt-Jakob Disease With Extremely Low Lymphoreticular Deposition of Prion Protein

 

ONLINE FIRST

 

 Simon Mead, PhD1,2; Jonathan D. F. Wadsworth, PhD2; Marie-Claire Porter, MRCP1; Jacqueline M. Linehan, BSc2; Wojciech Pietkiewicz, MD3; Graham S. Jackson, PhD2; Sebastian Brandner, MD, FRCPath4; John Collinge, MD, FRCP, FRS1,2

 

[+] Author Affiliations

 

JAMA Neurol. Published online January 20, 2014. doi:10.1001/jamaneurol.2013.5378

 

 ABSTRACT

 

Importance Human transmission of bovine spongiform encephalopathy causes the fatal neurodegenerative condition variant Creutzfeldt-Jakob disease (vCJD) and, based on recent human prevalence studies, significant subclinical prion infection of the UK population. To date, all clinical cases have been fatal, totaling 228 mostly young adults residing in the United Kingdom.

 

Observations Here we describe the investigation and case history of a patient recently diagnosed as having vCJD in the United Kingdom. Although his presentation, imaging findings, cerebrospinal fluid investigation results, and clinical progression were typical of other cases, tonsillar biopsy and subsequent examination of multiple tissues at autopsy showed minimal deposition of disease-associated prion protein in peripheral lymphoreticular tissue. The result of a blood test for vCJD, the Direct Detection Assay for vCJD, was negative.

 

Conclusions and Relevance These findings suggest that some patients with vCJD have very low peripheral prion colonization and therefore may not have detectable prion deposition in diagnostic tonsillar biopsy or markers of prion infection in blood. These results have implications for accurate interpretation of diagnostic tests and prevalence studies based on lymphoreticular tissue or blood.

 


 

<<>>

 

not good, this is not good. makes one wonder about the final figures on the previous estimates from tonsils tissue samples and results there from ??? ...tss

 

An earlier study of appendix and some tonsil tissue, from operations conducted between 1995 and 1999, found three positive samples out of 12,674 screened for abnormal prion protein using the IHC method [5]. The prevalence estimate calculated from this study was 237 per million overall (95% CI: 49-692 per million) – or 380 per million (95% CI=80-1120 per million) in those born between 1961 and 1985. This prevalence estimate equals to one infection per 4,000 of the population in the 1961 to 1985 birth cohort, the cohort in which most vCJD cases have arisen.

 

In 2008, the Spongiform Encephalopathy Advisory Committee (SEAC) considered the available NATA data [6]. At that time no abnormal prion protein positive samples had been found in nearly 55,000 samples, analysed by the high throughput dual EIA screening technique, including about 11,000 samples from the 1961 to 1985 birth cohort [7]. This translated to a prevalence estimate of zero per million (95% CI=0-324 per million) in this birth cohort. Statistical analysis of the data from the previous appendix survey and NATA showed the prevalence rates were consistent with each other.

 

To further investigate the prevalence of abnormal prion protein in the NATA samples from patients in the 1961 to 1985 birth cohort, the IHC technique was applied to screen 9,160 samples within that cohort; these samples which had already been shown to be negative when screened by the dual EIA technique [8]. One specimen showed a single strongly positive follicle. The specimen was negative when further investigated by EIA, IHC, and immunoblotting. This finding of 1 in 9,160 gives a prevalence estimate of 109 infections per million (95% CI: 3-608 per million) in those born between 1961 and 1985 which is not statistically different from the prevalence estimate based on the previous appendix study (exact p =0.64).

 

The results of NATA and the “IHC screening” sub-study were considered by SEAC in 2010 [9]. The committee agreed that “even though the positive sample suggested a possible prevalence of 1:10,000, the result from the Hilton data of 1:4,000 would still remain the most precautionary figure for risk management purposes”.

 

The Health Protection Agency is also coordinating a second Appendix Survey in order to test for abnormal prion protein in archived appendix tissues in two birth cohorts of individuals[10]. The study is an unlinked anonymous survey testing approximately 20,000 samples from individuals born between 1961 and 1985 and 10,000 from those born between 1941 and 1960. The study is continuing but the interim data shows that four out of 13,878 suitable samples across both birth cohorts have tested positive for disease associated prion protein (PrP CJD ). This translates to a prevalence estimate of 288 per million (95% CI=79-738 per million). Two of the four positive samples were from the 1941-1960 birth cohort resulting in a prevalence estimate of 641 per million (95% CI=78-2314 per million) compared to 186 per million (95% CI=23-671 per million) in the younger cohort of individuals. The interim data has been reviewed by the ACDP TSE Risk Assessment Sub-Group [11].

 

snip...see ;

 

Friday, February 10, 2012

 

Creutzfeldt-Jakob disease (CJD) biannual update (2012/1) potential iatrogenic (healthcare-acquired) exposure to CJD, and on the National Anonymous Tonsil Archive

 


 

Monday, August 13, 2012

 

Summary results of the second national survey of abnormal prion prevalence in archived appendix specimens August 2012

 


 

Tuesday, October 05, 2010

 

Large-scale immunohistochemical examination for lymphoreticular prion protein in tonsil specimens collected in Britain

 

05 Oct 2010 14:46

 


 

Monday, October 14, 2013

 

Researchers estimate one in 2,000 people in the UK carry variant CJD proteins

 


 

WHAT about the sporadic CJD TSE proteins ?

 

WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$

 

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

 


 

Monday, December 02, 2013

 

*** A parliamentary inquiry has been launched today into the safety of blood, tissue and organ screening following fears that vCJD – the human form of ‘mad cow’ disease – may be being spread by medical procedures

 


 

Wednesday, December 11, 2013

 

Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease

 


 


 

Thursday, January 2, 2014

 

*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ???

 


 

 Friday, January 10, 2014

 

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

 


 

 Monday, January 13, 2014

 

*** Prions in Variably Protease-Sensitive Prionopathy: An Update Pathogens 2013

 

Pathogens 2013, 2, 457-471; doi:10.3390/pathogens2030457

 


 

Wednesday, January 15, 2014

 

*** INFECTION PREVENTION AND CONTROL OF CJD, VCJD AND OTHER HUMAN PRION DISEASES IN HEALTHCARE AND COMMUNITY SETTINGS Variably Protease-Sensitive Prionopathy (VPSPr) January 15, 2014

 


 

Sunday, January 19, 2014

 

*** National Prion Disease Pathology Surveillance Center Cases Examined1 as of January 8, 2014 ***

 


 

Thursday, January 23, 2014

 

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

 


 
 
kind regards,
terry
 

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