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Canada Fraser Health Statement on Creutzfeldt-Jakob Disease outbreak

Posted Jun 15 2013 1:48pm
 
 

Fraser Health Statement on Creutzfeldt-Jakob Disease
 
 
June 14, 2013
 
 
Dr. Paul Van Buynder, Chief Medical Health Officer has released the following statement to clarify reports about suspect cases of “human mad cow disease” in the Lower Mainland:
“I am concerned to see reports this evening in social and traditional media related to our investigation into a small number of possible cases of Creutzfeldt-Jakob disease (CJD). Media have reported that these cases are connected to Bovine Spongiform Encephalopathy – more commonly known as mad cow disease.
Fraser Health has investigated six possible cases of CJD over the past year. After a case review today we can say that one person has CJD and two others are very likely to have it. The other three cases are very unlikely to have CJD.
I want to be clear there is absolutely no evidence that these three confirmed or probable cases are linked to food consumption.
CJD is a neurological disorder reported an average of about 30 times a year in Canada. There are a handful of cases reported in B.C. each year and we expect around 2 cases in the Fraser region. While three in this time frame is one or two more than I expect, it is within statistical likelihood.
There is no outbreak and I want to reassure residents of the lower mainland that there is no risk to the public or to residents in our facilities.
These are classical cases of CJD. Tests conducted on these patients have ruled out variant CJD associated with disease in cattle. There has never been a home grown case of variant CJD in Canada so this is not surprising.
We have a strong public health surveillance system in B.C. and a review of the cases has not revealed any links between them which would suggest a common source of any kind. The patients investigated come from a number of different cities and settings.
Our sympathies are with the families of these cases of severe progressive disease."
Dr. Paul Van Buynder
Learn more about Creutzfeldt-Jakob Disease.
Greetings Dr. Paul Van Buynder et al @ FraserHealth,
 
 
 
Sadly, in the year 2013, we are still going by science that is 3 decades old, to manage risk factors from the many different strains of the TSE prion disease.
 
 
Dr. Paul Van Buynder et al state ;
 
 
> I want to be clear there is absolutely no evidence that these three confirmed or probable cases are linked to food consumption.
 
 
 
when in reality, you have no clue Sir.
 
 
sporadic CJD is not a single strain of the TSE prion sporadic phenotypes (there are many, and they are mounting).
 
 
sporadic CJD has now been linked to atypical BSE, and atypical Scrapie, and many reputable scientist around the globe are especially concerned with the CWD of cervids, and it’s different strains, which we now know there are more strains.
 
 
the UKBSEnvCJD only theory is a false myth, and proven to be so.
 
 
also, all iatrogenic CJD is, is sporadic CJD until route and source of the TSE agent is confirmed.
 
 
what fuels this madness, and the spread of this disease, are Doctors and officials that continue to spread this junk science.
 
 
you are part of the problem, in my opinion, and I mean no disrespect Sir.
 
if I still sound angry, I am, 15+ years later.
 
 
I have wasted 15 years daily following the science as it emerges with the TSE prion disease, and documenting it. I hope you take the time to read some of it.
 
 
no need to reply, most never do, but I urge you to educate yourself on this topic of the TSE prion disease, and cease spreading the false science that continues to fuel the spread of this TSE prion disease. ...
 
 
thank you, kind regards,
terry
 
 
layperson ...lost my mom to the hvCJD ‘confirmed’, and I just made a promise. ...
 
 
Monday, October 10, 2011
 
EFSA Journal 2011 The European Response to BSE: A Success Story
 
 
snip...
 
 
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011).
 
 
*** This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded.
 
Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

 
snip...
 
 
 
 
 
 
 
Thursday, August 12, 2010
 
 
Seven main threats for the future linked to prions
 
 
First threat
 
 
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
 
 
 
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

 
Second threat
 
 
snip...
 
 
 
 
 
 
Rural and Regional Affairs and Transport References Committee
 
 
The possible impacts and consequences for public health, trade and agriculture of the Government's decision to relax import restrictions on beef Final report June 2010
 
 
2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49
 
 
2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. *** Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo-has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50
 
 
 
 
 
Wednesday, March 31, 2010
 
 
Atypical BSE in Cattle
 
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE.
 
When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. 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.
 
This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

 
 
 
 
*** 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.

 
 
 
 
The chances of a person or domestic animal contracting CWD are “extremely remote,” Richards said. The possibility can’t be ruled out, however. “One could look at it like a game of chance,” he explained. “The odds (of infection) increase over time because of repeated exposure. That’s one of the downsides of having CWD in free-ranging herds: We’ve got this infectious agent out there that we can never say never to in terms of (infecting) people and domestic livestock.”
 
 
 
 
 
 
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
 
 
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
 
 
 
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
 
 
 
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
 
 
 
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
 
 
 
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
 
 
 
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
 
 
 
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
 
 
 
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
 
 
 
 
 
 
Wednesday, March 28, 2012
 
 
 
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $

 
 
 
 
 
CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
 
 
 
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.

 
please see ;
 
 
 
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
 
 
 
 
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2 1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44 2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34 0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.
CJD Deaths Reported by CJDSS1, 1994-20122
 
 
 
As of May 31, 2012
 
 
 
 
 
 
 
 
 
SEE DECEMBER 2012 CANADA
 
 
 
 
 
USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss
 
 
National Prion Disease Pathology Surveillance Center
Cases Examined1
(May 18, 2012)
Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 50 32 28 4 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 123 74 65 8 1 0
2000 145 103 89 14 0 0
2001 210 120 110 10 0 0
2002 248 149 125 22 2 0
2003 266 168 137 31 0 0
2004 326 187 164 22 0 13
2005 344 194 157 36 1 0
2006 382 196 166 28 0 24
2007 377 213 185 28 0 0
2008 396 232 206 26 0 0
2009 423 256 212 43 1 0
2010 413 257 216 41 0 0
2011 410 257 213 43 0 0
2012 153 82 51 15 0 0
TOTAL 44685 26406 2227 387 6 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 14 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
Rev 5/18/2012
 
 
 
 
 
 
 
> 6 Includes
 
 
 
> 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 
> The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).
 
 
 
 
WELL, it seems the USA mad cow strains in humans classified as type determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased over the years, and the same old song and dance continues with sporadic CJD cases $$$

 
 
 
 
CJD CANADA WINTER 2012

 
 
 
 
 
 
 
 
 
 
Tuesday, March 05, 2013
 
 
A closer look at prion strains Characterization and important implications Prion
 
 
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
 
 
 
 
Tuesday, July 31, 2012
 
 
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital
 
 
 
 
 
Thursday, August 02, 2012
 
CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients
 
 
 
 
Sunday, March 31, 2013
 
 
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years old, shall we pray
 
 
 
 
 
Tuesday, May 21, 2013
 
CJD, TSE, PRION, BLOOD Abstracts of the 23rd Regional Congress of the International Society of Blood Transfusion, Amsterdam, The Netherlands, June 2-5, 2013
 
 
 
 
 
Friday, June 29, 2012
 
Highly Efficient Prion Transmission by Blood Transfusion
 
 
 
 
 
Monday, May 6, 2013
 
Warning of mad cow disease threat to blood transfusions
 
 
 
 
Tuesday, April 30, 2013
 
Mad cow infected blood 'to kill 1,000’
 
 
 
 
Wednesday, August 24, 2011
 
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
 
 
 
 
Thursday, January 17, 2013
 
 
TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)
 
 
 
 
 
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, November 26, 2012
 
Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer
 
 
 
 
Thursday, December 29, 2011
 
 
Aerosols An underestimated vehicle for transmission of prion diseases?
 
 
 
 
please see more on Aerosols and TSE prion disease here ;
 
 
 
 
Saturday, February 12, 2011
 
Another Pathologists dies from CJD, another potential occupational death ?
 
 
another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ??
 
 
 
 
 
Tuesday, December 14, 2010
 
 
Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J,
 
UPDATE DECEMBER 2010
 
 
 
 
 
 
 
Tuesday, September 14, 2010
 
 
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
 
 
 
 
Thursday, September 02, 2010
 
NEUROSURGERY AND CREUTZFELDT-JAKOB DISEASE Health Law, Ethics, and Human Rights The Disclosure Dilemma
 
 
 
 
Thursday, August 12, 2010
 
 
USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010
 
 
 
 
Sunday, August 01, 2010
 
 
Blood product, collected from a donors possibly at increased risk for vCJD only, was distributed USA JULY 2010
 
 
 
 
 
 
Thursday, July 08, 2010
 
Nosocomial transmission of sporadic Creutzfeldt–Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010
 
 
 
 
 
Thursday, July 08, 2010
 
GLOBAL CLUSTERS OF CREUTZFELDT JAKOB DISEASE - A REVIEW 2010
 
 
 
 
 
Wednesday, June 02, 2010
 
 
CJD Annex H UPDATE AFTER DEATH PRECAUTIONS Published: 2 June 2003 Updated: May 2010
 
 
 
 
 
Tuesday, May 11, 2010
 
 
Current risk of iatrogenic Creutzfeld–Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments
 
 
 
 
 
Tuesday, May 04, 2010
 
 
Review of the Human Pituitary Trust Account and CJD Issue 20 January 2010
 
 
 
 
 
Tuesday, March 16, 2010
 
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010
 
 
 
 
Monday, August 17, 2009
 
Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009
 
 
 
 
Monday, July 20, 2009
 
Pre-surgical risk assessment for variant Creutzfeldt-Jakob disease (vCJD) risk in neurosurgery and eye surgery units
 
 
 
 
Friday, July 17, 2009
 
Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009
 
 
 
 
Sunday, May 10, 2009
 
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
 
 
 
 
Thursday, January 29, 2009
 
Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999-2008 (WARNING TO Neurosurgeons and Ophthalmologists) Volume 15, Number 2-February 2009 Research
 
 
 
 
 
Wednesday, August 20, 2008
 
 
Tonometer disinfection practice in the United Kingdom: A national survey
 
 
 
 
 
Tuesday, August 12, 2008
 
Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)
 
 
 
 
Monday, December 31, 2007
 
 
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation
 
 
 
 
Subject: CJD: update for dental staff
 
 
Date: November 12, 2006 at 3:25 pm PST
 
1: Dent Update. 2006 Oct;33(8):454-6, 458-60.

 
CJD: update for dental staff.

 
 
 
 
Saturday, January 16, 2010
 
Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al
 
 
Evidence For CJD/TSE Transmission Via Endoscopes
 
From Terry S. Singletary, Sr flounder@wt.net 1-24-3

 
 
 
 
Thursday, October 25, 2012
 
Current limitations about the cleaning of luminal endoscopes and TSE prion risk factors there from
 
 
Article in Press

 
 
 
 
2011 TO 2012 UPDATE
 
Saturday, December 3, 2011
 
Candidate Cell Substrates, Vaccine Production, and Transmissible Spongiform Encephalopathies
 
 
Volume 17, Number 12—December 2011

 
 
 
 
Sunday, June 26, 2011
 
 
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
 
 
 
 
 
Monday, February 7, 2011
 
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ??
 
 
 
 
Volume 33, Issue 3, Article first published online: 20 JAN 2013
Special Lecture
Human prion diseases: Molecular, cellular and population biology
Mark W. Head
National CJD Research & Surveillance Unit, Centre for Clinical Brain Sciences, School of Clinical Sciences,
The University of Edinburgh, Edinburgh, UK

 
snip...
 
 
 
Potential future zoonoses
 
 
 
Scrapie is endemic in many countries around the world, yet there is no evidence to suggest that it is pathogenic for humans. The intense investigations of ruminant TSEs that followed the BSE epidemic have resulted in the identification of several distinct animal prion diseases, atypical or Nor98 scrapie in sheep and H-type and L-type BSE in cattle.32 Moreover, BSE is experimentally transmissible to sheep and there are concerns that if BSE were to have infected the national flock in the UK its presence might be masked by endemic scrapie, but it might retain its pathogenicity for humans.33,34 Another concern, particularly for the North American countries, is the spread of chronic wasting disease in farmed and free-ranging deer and elk.35 There is no known epidemiological link between any of these animal prion diseases and human disease, but there are active efforts to try to quantify strain-related species barriers between the diseases known to be a risk (BSE/ vCJD), those thought not to represent a risk (scrapie) and those for which data is lacking (atypical scrapie, H- and L-type BSE and BSE in sheep).36 In assessing whether or not human prion diseases might have an animal origin, it is important to have a proper understanding of the clinicopathological heterogeneity of the sporadic human prion diseases, because it is against this backdrop that any new acquired forms of the disease will be seen and from which it will need to be distinguished.
 
 
 
Sporadic CJD and variably protease-sensitive prionopathy
 
 
 
Sporadic CJD is the most commonly occurring human prion disease; it occurs world-wide and it has long been known to be clinically and pathologically heterogeneous. The molecular basis for this heterogeneity is currently thought to reside in a combination of the PRNP codon 129 polymorphic status of the patient (MM, MV, or VV) and the type (type 1 or type 2) of the protease-resistant component of PrPSc determined by protease K digestion and Western blotting (termed PrPres).37,38 The original sCJD sub-classification system of Parchi et al. that recognized six sCJD subtypes (MM1/MV1, MM2c, MM2t, MV2,VV2 and VV1) has had to be modified to accommodate the growing number of cases recognized to contain both type 1 and type 2 PrPres in different or sometimes the same regions of the brain.39,40 Moreover, intensive surveillance and investigation of forms of human prion disease that lack PRNP mutation and known risk factors has identified another sporadic human prion disease, termed protease-sensitive prionopathy (VPSPr).41While intensively investigated, the etiology and diversity of the sporadic human prion diseases remain poorly understood.
 
 
 
snip...
 
 
 
There is also a potentially important practical corollary to the idea of prion-like spread, which may affect future stem cell therapies for neurodegenerative diseases. Presumably therapeutic stem cell-derived neurons would be equally susceptible to “infection” (with misfolded protein aggregates) as the patient’s own cells, unless steps were taken to prevent this,55 the most obvious of which would be to prevent expression of the gene product that can be converted to a pathological prion-like isoform.The suggestion that a prion-like mechanism of spread of molecular pathology underlies diseases as diverse as Alzheimer’s disease and Parkinson’s disease has led some researchers to explore whether the molecular pathology of these diseases is transmissible in an experimental setting56–58 and to suggest that perhaps some cases of these more common neurodegenerative illnesses might, like CJD, be acquired.58,59
 
 
 
snip...
 
 
 
MOLECULAR BASIS OF HUMAN PRION DISEASES
 
 
 
Molecular strain typing Molecular strain typing in the form of classifying the mobility and glycoform ratio of protease-resistant prion protein byWestern blotting is a remarkably useful adjunct to neuropathological assessment during the post-mortem diagnosis of human prion diseases (Fig. 1). The glycoform ratio difference between vCJD and all forms of sCJD is a remarkably robust phenomenon, although the mechanism underlying it remains obscure. All cases of vCJD examined show type 2B PrPres, irrespective of brain region assayed and the PrPres type is also found in lymphoreticular tissues, albeit with presumably tissue-specific minor modification of mobility and an accentuation of the glycoform ratio. Similarly sCJD cases are characterized by a narrow range of glycoform ratios, distinct from vCJD, and the presence of either type 1 or type 2 PrPres (type 1A and type 2A).The PrPres types found in the brain in iCJD and kuru resemble those found in sCJD (type 1A and type 2A), from which they were presumably derived. Individual cases of gCJD, GSS and FFI usually have type 1 or type 2 PrPres, but with a glycoform ratio in which the non-glycosylated component is under-represented (which we have termed A/B). However, this is not always true and a broad spectrum of glycoform ratios can be found in genetic prion diseases. Moreover, some cases of GSS are characterized by an approximately 8 kDa (N- and C-terminally truncated) PrPres fragment, and some cases of FFI have little detectable PrPres at all. Despite the diagnostic utility, a simple one-to-one correspondence between PrPres type and disease phenotype (and by implication to agent strain) seems unlikely in principle and is complicated by the facts. First, the choice of analyzing only that fraction of PrPSc which survives a particular concentration of protease may seem arbitrary. Second, the interpretation of a molecular population variable, such as glycosylation site occupancy, as conforming to two or three discrete types, could be seen as simplistic. Lastly, protease digestion may be considered to be a somewhat blunt instrument to distinguish secondary and higherorder conformational differences in PrPSc. Even when genotype (mutations and polymorphisms) is taken into account, three major types (1, 2, 8 kDa) and three wild-type genotypes (MM,MV and VV) provide insufficient molecular variation to account for all the phenotypic variations observed. For example, two forms of sCJD share methione homozygosity and type 2A PrPres but one form closely resembles FFI (without the causative mutation) and the other is CJD-like.8 Two more substantial problems, which may point toward a more subtle and perhaps informative approach to PrPSc analysis, are discussed below. The co-occurrence of PrPres types 1 and 2 Once controversial, the idea that PrPSc in individual cases might be composed of mixtures (or different types co-occurring) is now well recognized and accepted.40,70 There are probably two phenomena at play here. One is the finding of different predominant types in individual samples from different parts of the brain or more rarely approximately equal amounts of type 1A and type 2A in the same sCJD brain samples.The other is the observation made using antibodies that specifically recognize type 1 or type 2 PrPres, that a minority type always accompanies a majority type in sCJD and vCJD, albeit at sub-detectable levels when conventional antibodies are used.71–75 The former issue is more tractable and a consensus is beginning to emerge that when multiple brain sampling and sensitive co-detection is performed on cohorts of sCJD cases, a plateau is reached at between 30–40% of cases showing co-occurrence. Our own data examining four regions (temporal cortex, parietal cortex, occipital cortex and thalamus) instead of frontal cortex only, shows a rise in detected co-occurrence from 3% to 24% of cases.76 Interestingly, only very rarely did this re-analysis involve a change in the predominant type found in the brain overall. Parchi et al. have offered a revised version of their 1999 sporadic CJD classification system that adds mixed type to the original “pure” types and have shown that the most common of these 12 sCJD subtypes can be recognized on histological grounds, without reference to biochemical analysis.39,40,77 It will be interesting to see in the fullness of time whether this additional complexity reflects a more refined series of discrete clinicopathological phenotypes or whether it is indicative of a spectrum of phenotypes depending on the spacio-temporal accumulation of PrPSc types set against the patient genotype.78
 
 
 
Variably protease-sensitive prionopathy The phenotypic complexity of the sporadic forms of human prion disease has increased with the report of a new sporadic human prion disease, termed variably proteasesensitive prionopathy (VPSPr) that is distinct from previously recognized sub-types of sCJD.41,79 There are no mutations in the open reading frame of PRNP. The patients have no known risk factors for the disease, but the disease is most common in theVV genotype, as opposed to sCJD, which is most common in the MM genotype. The neuropathology involves medium-sized vacuolation and characteristic microplaques. Durations of illness can be very long and this coupled with symptoms that do not conform well to CJD have prompted speculation that the condition may be under-ascertained. The most interesting aspect of the disease from a biochemical perspective is that although PrPSc is abundantly present in the brain, PrPres is difficult to detect because of its sensitivity to proteolysis and because what remains after proteinase K (PK) digestion is both C- and N-terminally cleaved by PK digestion and seen as a faint 8 kDa band on Western blots (Fig. 2). The degree of protease resistance is reported to reflect the codon 129 genotype, withVV being least resistant andMM being most resistant, despite having the same 8 kDa PrPres fragment predominating.79We have identified two cases of VPSPr prospectively in the UK80,81 and recently completed a retrospective review for such cases confirming many of the original observations by Gambetti and colleagues.41,79 Our work has shown that some areas of the VPSPr brain contain PrPres similar in appearance to that found in sCJD and conversely that some cases of sCJD have a very minor PrPres band similar to the 8 kDa PrPres band that typifies VPSPr.82
 
 
 
snip...
 
 
 
The biochemical basis of the strain phenomenon The results of transmission of individual samples from single examples of the six different Parchi et al.39 sCJD subtypes (MM1/MV1, VV1, MM2c, MV2, VV2) into humanized transgenic mice suggest the existence of four distinct sCJD agents, termed M1, M2, V1 and V2, and a fifth strain corresponding to MM2t or sporadic fatal insomnia.99,100 Interestingly, when we performed formally analogous experiments in the cell-free PMCA reaction, similar results were obtained: The PrPres type of the seed was conserved in the PMCA product and the efficiency of conversion appeared to be determined by compatibility at codon 129 of PRNP.101 The behavior of the seeds from heterozygous patients were particularly interesting, in that MV1 sCJD seeds selectively amplified in MM substrate producing type 1 PrPres and MV2 sCJD seeds selectively amplified in VV substrate producing type 2 PrPres (Fig. 6). These results reinforce the association between methionine at codon 129 and the production of type 1 PrPres and valine at codon 129 and the production of type 2 PrPres.
 
 
 
EMERGING RISKS
 
 
 
Zoonotic disease BSE is the only animal prion strain with demonstrated pathogenicity for humans.While it is tempting to suggest that scrapie might represent the animal reservoir that results in some cases of sCJD, there is no epidemiological evidence to support this hypothesis. The pathogenicity of new or newly described animal prion diseases for humans is unclear and this is particularly true for H- and L-type BSE, atypical scrapie and for chronic wasting disease (CWD), all of which are probably consumed. Human susceptibility has been modeled by attempted transmission to (humanized) transgenic mice with sometimes conflicting results, depending on the transgenic model used and depending upon whether central or peripheral tissues are examined.102–106 We have attempted to establish whether PMCA can model the molecular component of these hypothetical cross-species transmission events.107 The existing data correspond well with the established facts. First, PrPSc in vCJD brain samples amplifies most efficiently in humanized mouse MM substrate, less efficiently in MV substrate and not at all in VV. Cattle BSE PrPres is less efficient than vCJD, but shows the same substrate genotypic preference. Sheep scrapie fails to amplify detectably in any of the three substrates; however, sheep BSE PrPres does amplify, again with a codon 129 preference for methionine (Fig. 7). We are currently extending this approach to encompass atypical scrapie, H- and L-type BSE and CWD using human rather than humanized PMCA substrates.
 
 
 
Secondary infection
 
 
 
In the same way that animal reservoirs cannot be completely excluded as causes of individual sCJD cases, neither can other environmental sources, such as medical procedures. The known routes of iatrogenic CJD acquisition are historically growth hormone therapy, dura mater grafting, corneal grafting and certain highly specialized neurosurgical procedures. The secondary transmission of vCJD by blood transfusion and experimental evidence showing the efficiency of the transfusion of viable blood cells between scrapie and BSE-infected and naive sheep have prompted a reappraisal of transfusion-transmitted CJD, including consideration being given to the possibility of prion blood testing or filtration.25,26,108,109
 
 
 
Blood transfusion is the original and most extensively used cellular therapy, but we may be on the threshold of a new era of cellular therapies based on embryonic stem cell and induced pluripotent stem cell technologies. Although the potential for stem cell therapy-mediated prion transmission might be judged remote, this was also considered to be the case for transfusion transmission of CJD before 2004.
 
 
 
snip...
 
 
 
SUMMARY AND PERSPECTIVE
 
 
 
While the prospect of a major epidemic of vCJD in the UK and elsewhere seems to be receding, there remain a series of uncertainties surrounding the eventual numbers of individuals that will suffer from this devastating condition.The issues include the effects of genotype on susceptibility and the possible existence of substantial numbers of asymptomatic infected individuals that may pose risks of onward transmission. sCJD remains the most frequently occurring human prion disease and arguably the least well understood. Other idiopathic forms of human prion disease (such as VPSPr), characterized by protease-sensitive forms of the prion protein, also exist and their true prevalence may be hard to ascertain. The possible risks from newly described animal prion diseases and from emerging cellular therapies are currently poorly quantified. On a more theoretic level the prion hypothesis has provided a unifying conceptual framework for TSE research and provided a paradigm to interrogate the similarities and differences between the diverse neurodegenerative conditions involving prion-like mechanisms of molecular pathology.
 
 
 
 
 
 
 
SNIP...see more here ;
 
 
 
Tuesday, June 4, 2013
 
 
INTERPRETING RESULTS OF FSIS VERIFICATION SAMPLING OF DOMESTIC BEEF PRODUCT DERIVED FROM ADVANCED MEAT RECOVERY SYSTEMS (AMR01/FAMR01) FSIS Notice 38-12
 
 
 
 
 
 
 
Thursday, February 21, 2013
 
 
National Prion Disease Pathology Surveillance Center Cases Examined January 16, 2013
 
 
 
 
 
 
16 YEAR OLD SPORADIC FFI ?
 
 
 
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe
 
 
 
 
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012
 
 
 
 
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25, 2012
 
 
 
 
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA
 
 
 
 
Wednesday, June 13, 2012
MEXICO IS UNDER or MIS DIAGNOSING CREUTZFELDT JAKOB DISEASE AND OTHER PRION DISEASE SOME WITH POSSIBLE nvCJD
 
 
 
 
Tuesday, May 21, 2013
Canada, USA, Bad feed, mad cows: Why we know three BSE cases had a common origin and why the SSS policy is in full force $$$
 
 
 
 
Sunday, June 9, 2013
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory Committee Meeting Webcast
 
 
 
 
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a methodological outline for evidence-based guidance
 
 
 
 
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease
 
 
 
 
 
 
 
 
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens comment period due to new studies
 
 
 
 
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
 
 
 
Wednesday, March 20, 2013
GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to Expand Its Use of Reported Health Problems to Oversee Product
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 19, 2013 2:46 PM
To: gomezj@gao.gov
Cc: siggerudk@gao.gov ; youngc1@gao.gov ; oighotline@gao.gov
 
 
 
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease
 
 
 
 
 
 
 
UPDATED DATA ON 2ND CWD STRAIN
 
 
 
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
 
 
 
 
Tuesday, May 21, 2013
IS ALZHEIMER’S DISEASE A PRION DISEASE? the possible secondary transmission by blood transfusion are posed
 
 
 
 
 
 
Tuesday, May 7, 2013
Proteinopathies, a core concept for understanding and ultimately treating degenerative disorders?
 
 
 
 
 
 
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
 
 
 
 
 
 
 
 
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in Amyotrophic Lateral Sclerosis (ALS)
 
 
 
Sunday, February 10, 2013
Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder?
 
 
 
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
 
 
 
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
 
 
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
 
 
 
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
 
 
 
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
 
 
 
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
 
 
 
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE
 
 
 
SCENARIO 3: ‘THE THIN STEMMED GLASS’

 
... a TSE is found that is linked to Alzheimer’s disease.
 
 
 
Thursday, January 17, 2013
TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)
 
 
 
Published online before print May 20, 2013, doi: 10.1073/pnas.1301175110
PNAS May 20, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse brain
Florence Clavagueraa, Hiroyasu Akatsub, Graham Fraserc, R. Anthony Crowtherc, Stephan Franka, Jürgen Hencha, Alphonse Probsta, David T. Winklera,d, Julia Reichwalde, Matthias Staufenbiele, Bernardino Ghettif, Michel Goedertc,1,2, and Markus Tolnaya,1,2
aDepartment of Neuropathology, Institute of Pathology, University Hospital, 4031 Basel, Switzerland; bChoju Medical Institute, Fukushimura Hospital, Toyohashi City 441-8124, Japan; cMedical Research Council Laboratory of Molecular Biology, Cambridge CB2 0QH, United Kingdom; dDepartment of Neurology, University Hospital, 4031 Basel, Switzerland; eNovartis Institutes for Biomedical Research, 4056 Basel, Switzerland; and fIndiana Alzheimer Disease Center and Department of Pathology and Laboratory Medicine, Indiana University, Indianapolis, IN 46202
Edited by Anders Bjorklund, Lund University, Lund, Sweden, and approved April 25, 2013 (received for review January 18, 2013)
Filamentous inclusions made of hyperphosphorylated tau are characteristic of numerous human neurodegenerative diseases, including Alzheimer’s disease, tangle-only dementia, Pick disease, argyrophilic grain disease (AGD), progressive supranuclear palsy, and corticobasal degeneration. In Alzheimer’s disease and AGD, it has been shown that filamentous tau appears to spread in a stereotypic manner as the disease progresses. We previously demonstrated that the injection of brain extracts from human mutant P301S tau-expressing transgenic mice into the brains of mice transgenic for wild-type human tau (line ALZ17) resulted in the assembly of wild-type human tau into filaments and the spreading of tau inclusions from the injection sites to anatomically connected brain regions. Here we injected brain extracts from humans who had died with various tauopathies into the hippocampus and cerebral cortex of ALZ17 mice. Argyrophilic tau inclusions formed in all cases and following the injection of the corresponding brain extracts, we recapitulated the hallmark lesions of AGD, PSP and CBD. Similar inclusions also formed after intracerebral injection of brain homogenates from human tauopathies into nontransgenic mice. Moreover, the induced formation of tau aggregates could be propagated between mouse brains. These findings suggest that once tau aggregates have formed in discrete brain areas, they become self-propagating and spread in a prion-like manner.
snip...
The present work indicates that once small numbers of tau inclusions have formed in the brain, they may become selfpropagating and spread in a prion-like manner, independently of other pathogenic mechanisms. What is true of aggregated human tau may also be the case of other aggregation-prone proteins that cause human neurodegenerative diseases, including α-synuclein, superoxide dismutase 1, huntingtin, trans-activator regulatory (TAR) DNA-binding protein 43 (TDP-43), and Aβ (47). The inhibition of cell-to-cell transmission of pathological aggregates, for instance by passive immunotherapy, may constitute an effective mechanism-based therapeutic strategy for most human neurodegenerative diseases.
 
 
 
Saturday, May 25, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse brain
 
 
 
Tuesday, May 21, 2013
IS ALZHEIMER’S DISEASE A PRION DISEASE? the possible secondary transmission by blood transfusion are posed
 
 
 
Tuesday, May 7, 2013
Proteinopathies, a core concept for understanding and ultimately treating degenerative disorders?
 
 
 
Sunday, February 10, 2013
Parkinson's Disease and Alpha Synuclein: Is Parkinson's Disease a Prion-Like Disorder?
 
 
 
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
 
 
 
 
Thursday, January 17, 2013
TSE guidance, surgical, dental, blood risk factors, Part 4 Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings (updated January 2013)
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS, gCJD, hvCJD, sCJD, TSE, PRION, update 2011
 
 
 
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
 
 
 
CJD1/9 0185 Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;
ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1
 
 
 
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?
3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.
92/11.4/1-1 BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2
 
 
 
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
 
 
 
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
 
 
 
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
 
 
 
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
(see video at bottom)
 
 
 
Sunday, September 6, 2009
MAD COW USA 1997
(SEE SECRET VIDEO)
 
 
 
Creutzfeldt-Jakob Disease Public Health Crisis
 
 
 
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.
 
 
 
Published March 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
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?
Published March 26, 2003
 
 
 
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
CHAPTER 14
Laying Odds
Are prion diseases more prevalent than we thought?
Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?
Revisiting Sporadic CJD
It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.
Singeltary has similar inclinations. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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.
 
 
 
CJD Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
 
 
 
 
 
 
 
 
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
 
 
 
Volume 3, Number 8 01 August 2003
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.
 
 
 
Greetings,
> > > 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. < < <
actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article.
Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.
snip...end...tss
Re: vCJD in the USA * BSE in U.S.
15 November 1999 Terry S Singeltary, NA
In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.
Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.
My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.
The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?
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. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.
No BSE in the U.S.A. I would not be so sure of that considering that since 1990;
Since 1990 the U.S. has raised 1,250,880,700 cattle;
Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;
There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;
Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;
Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. 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. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.
I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.
Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.
It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........
The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.
Terry S. Singeltary Sr.
P.O. Box 42, Bacliff, Texas 77518 USA
Competing interests:None declared
 
 
 
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
2 January 2000
Terry S Singeltary
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
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
 
 
 
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:
 
 
 
"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.
Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...
 
 
 
 
 
 
 
 
 
 
 
 
 
STILL IS FULL OF HOLES 2013 ;
 
 
 
Thursday, June 6, 2013

 
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013
 
 
 
Greetings,

 
since our fine federal friends have decided not to give out any more reports on the USA breaches of the feed ban and surveillance etc. for the BSE TSE prion mad cow type disease in the USDA livestock, I thought I might attempt it. I swear, I just don’t understand the logic of the SSS policy, and that includes all of it. I assure you, it would be much easier, and probably better for the FDA and the USDA INC., if they would simply put some kind of report out for Pete’s sake, instead of me doing it after I get mad, because I am going to put it all out there. the truth.
 
 
 
PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI, RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to the eventual suspect tainted feed reaching livestock. please, if any USDA official out there disputes this, please explain then how they could not. paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow feed ban reaching livestock, or contamination and exposure there from, as well.
 
 
 
I would sure like to see the full reports of just these ;

 
4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y

 
9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N
 
 
 
9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
 
 
 
9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N

 
see full list of the fda mad cow bse feed follies, toward the bottom, after a short brief update on the mad cow bse follies, and our good friend Lester Crawford that was at the FDA.
 
 
 
ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$
 
 
 
NAI = NO ACTION INDICATED

 
 
OAI = OFFICIAL ACTION INDICATED

 
VAI = VOLUNTARY ACTION INDICATED

 
RTS = REFERRED TO STATE


 
Inspections conducted by State and FDA investigators are classified to reflect the compliance status at the time of the inspection, based upon whether objectionable conditions were documented. Based on the conditions found, inspection results are recorded in one of three classifications:
 
 
 
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
 
 
 
VAI (Voluntary Action Indicated) when inspectors find objectionable conditions or practices that do not meet the threshold of regulatory significance, but warrant an advisory to inform the establishment that inspectors found conditions or practices that should be voluntarily corrected. VAI violations are typically technical violations of the 1997 BSE Feed Rule. These violations include minor recordkeeping lapses or conditions involving non-ruminant feeds.
 
 
 
NAI (No Action Indicated) when inspectors find no objectionable conditions or practices or, if they find objectionable conditions, those conditions are of a minor nature and do not justify further actions.
 
 
 
 
 
 
 
when sound science was bought off by junk science, in regards to the BSE TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$
 
 
 
when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was taken away that infamous day in December of 2003, all cards were off the table, it was time to change the science, and change they did. ...tss
 
 
 
snip. ...please see full text ;
 
 
 
Thursday, June 6, 2013
 
 
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013
 
 
 
 
 
 
Suspect symptoms

 
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
28 Mar 01
Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
 
 
 
 
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
 
 
 
 
***SCRAPIE GOATS CALIFORNIA 13 CASES TO DATE ! ***
 
 
***SCRAPIE GOATS MICHIGAN 8 CASES TO DATE ! ***
 
 
(an unusually high amount of scrapie documented in goats for a happenstance of bad luck, or spontaneous event, THAT DOES NOT HAPPEN IN OTHER STATES ?? )
 
 
 
Sunday, June 2, 2013
Characterisation of an Unusual TSE in a Goat by Transmission in Knock-in Transgenic Mice
 
 
 
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
 
 
 
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
 
 
 
Wednesday, January 18, 2012
Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie
Journal of Neuropathology & Experimental Neurology: February 2012 - Volume 71 - Issue 2 - p 140–147
 
 
 
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
 
 
 
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
 
 
 
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
 
 
 
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
 
 
 
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
 
 
 
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
 
 
 
why do we not want to do TSE transmission studies on chimpanzees $
 
 
 
snip...

 
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
 
 
 
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011 However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40).
 
 
 
 
***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
 
 
 
 
 
 
*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
 
 
 
 
 
*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
 
 
 
 
 
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
 
 
 
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.

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

 
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
 
 
 
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
 
 
 
 
 
 
 
 
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
 
 
 
 
 
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
 
 
 
 
 
I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS
 
 
 
 
A kind greetings from Bacliff, Texas !
I have often pondered if the whole damn mad cow follies started over here in the USA, and somehow, the USA shipped it over to the UK ?
It happened with S. Korea and CWD, via Canada. see ;
 
 
 
The disease was confirmed only in elk in the Republic of Korea in 2001, 2004 and 2005. Epidemiological investigations showed that CWD was introduced via importation of infected elk from Canada between 1994 and 1997.
 
 
 
 
 
 
 
but I still am not so sure that the mad cow follies did not start long ago right here in the USA i.e. Richard Marsh and deadstock downer cattle to those mink, and then the USA shipped it to hell and back. just pondering out loud here. ...tss
 
 
 
Monday, June 3, 2013
Unsuccessful oral transmission of scrapie from British sheep to cattle
 
 
 
 
 
 
Friday, April 19, 2013
APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION
 
 
 
 
 
 
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease
 
 
 
 
 
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
 
 
 
 
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease
 
 
 
 
 
2012 atypical L-type BSE BASE California reports

 
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California BSE Case - July 2012
 
 
atypical L-type BASE BSE California
 
 
SUMMARY REPORT CALIFORNIA BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012
 
Summary Report BSE 2012
 
Executive Summary

 
 
 
 
Saturday, August 4, 2012
 
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
 
 
 
 
 
 
 
 
 
Singeltary submission ;
Wednesday, May 16, 2012
 
 
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
 
Proposal ID: 29403

 
 
 
 
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
Subject: Re: Hello Dr. Gibbs...........
Date: Wed, 29 Nov 2000 14:14:18 –0500
From: "Clarence J. Gibbs, Jr., Ph.D."
To: "Terry S. Singeltary Sr." References: 3a254430.9fb97284@wt.net
Hi Terry:
326 E Stret N.E., Washington, D. C. 20002.
Better shrimp and oysters than cards!!!!
Have a happy holiday and thanks for all the information you bring to the screen.
Joe Gibbs
==========
 
 
 
Sunday, June 09, 2013
 
 
Missouri House forms 13-member Interim Committee on the Cause and Spread of Chronic Wasting Disease CWD
 
 
 
 
 
layperson,
Terry S. Singeltary SR.
P.O. Box 42
Bacliff, Texas USA 77518
 
 
 
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