Saturday, May 09, 2015

Psychiatric Symptoms in Patients With Sporadic Creutzfeldt-Jakob Disease in Germany

Psychiatric Symptoms in Patients With Sporadic Creutzfeldt-Jakob Disease in Germany

 

Anna Krasnianski, MD; Geeske T. Bohling; Markus Harden; and Inga Zerr, MD

 

J Clin Psychiatry 2015 10.4088/JCP.13m08915 © Copyright 2015 Physicians Postgraduate Press, Inc. Background: Psychiatric symptoms in sporadic Creutzfeldt-Jakob disease (sCJD) are still not sufficiently evaluated.

 

Aim: To describe psychiatric symptoms in sCJD with respect to molecular subtype.

 

Method: Patients in this retrospective study were classified according to established diagnostic criteria. 248 sCJD patients with known molecular subtype were recruited from January 1993 to December 2004 and investigated. Psychiatric symptoms were defined according to Möller and colleagues and the AMDP system (Study Group for Methods and Documentation in Psychiatry) and were collected by direct examination by study physicians or extracted from medical documentation. Our data were compared with published data on variant CJD (vCJD).

 

Results: Psychiatric symptoms were common in sCJD patients (90%) and mostly found already at the disease onset (agitation in 64% of the patients, hallucinations in 45%, anxiety in 50%, depression in 37%). All psychiatric symptoms but illusions were found early in the disease course. Psychiatric symptoms in sCJD were less frequent than in vCJD.

 

Conclusions: We provide the first detailed analysis of psychiatric symptoms in a large group of patients with sCJD with respect to differences concerning frequency and time point of occurrence of psychiatric symptoms between molecular subtypes. These data suggest that psychiatric symptoms occurring early in the disease course are common not only in vCJD but also in other CJD types.

 


 

 

Sunday, May 03, 2015

 

Unusual Case of Sporadic Creutzfeldt–Jakob Disease Subtype VV1

 


 

 Wednesday, April 08, 2015

 

Sporadic Creutzfeldt-Jakob Disease MM1+2C and MM1 Are Identical in Transmission Properties

 


 

 Wednesday, February 04, 2009

 

Creutzfeldt-Jacob disease presenting as severe depression: a case report

 


 

Sunday, August 09, 2009

 

*** CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 


 

Tuesday, August 18, 2009

 

*** BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009

 


 

I said this over a decade ago, and I believe it still holds true today ;

 

just speaking of human TSE's; "different strains (of same disease) in different species (of the same disease), different routes of infection (of same disease), different infectivity levels (dose rate) of the (same disease), different parts of the brain affected (of the same disease), different genetic make-up of humans (with same disease) = different symptoms, different lengths of illness from 1st onset of illness to death, (of the same disease) + different cultures = different geographical locations = different strains (of same disease)...TSS"

 

PRION2015 FORT COLLINS

 


 


 


 

Wednesday May 27

 

14:45 Jean-Phillipe Deslys Atomic Energy Commission, France,

 

Transmission of prions to primates after extended silent incubation periods: * IMPLICATIONS FOR BSE AND SCRAPIE RISK ASSESSMENT IN HUMAN POPULATIONS.

 

16:45

 

Quingzhong Kong Case Western Reserve University

 

Zoonotic Potential of CWD Prions

 


 

 *** Kuru Video ***

 

Kuru: The Science and The Sorcery

 


 

*** Scrapie Video

 


 

*** Human Mad Cow Video

 


 

*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video

 


 

2014

 

***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.

 

***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.

 

*** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].

 

snip...

 


 

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...

 


 

*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO

 


 


 


 


 

Tuesday, December 16, 2014

 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

why do we not want to do TSE transmission studies on chimpanzees $

 

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

snip...

 

R. BRADLEY

 


 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01 Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...

 

2001

 

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.

 

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 20, 2014

 

CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR HUMAN TRANSMISSION THEREFROM 2014

 


 

Tuesday, July 01, 2014

 

*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM ***

 


 

Thursday, July 03, 2014

 

*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets? ***

 


 

Thursday

 

CWD TO HUMANS, AND RISK FACTORS THERE FROM (see latest science)

 

Tuesday, November 04, 2014

 

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

 


 

Thursday, April 30, 2015

 

Immediate and ongoing detection of prions in the blood of hamsters and deer following oral, nasal, or blood inoculations

 


 

Friday, January 30, 2015

 

*** Scrapie: a particularly persistent pathogen ***

 


 

Sunday, April 12, 2015

 

*** Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies 2014 Annual Report ***

 


 

Saturday, April 11, 2015

 

*** ISU veterinary researchers study retinal scans as early detection method for mad cow disease

 


 

Sunday, November 23, 2014

 

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

 


 

Monday, November 3, 2014

 

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

 

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

 

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

 

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

 

***The sporadic cases include 2660 cases of sporadic Creutzfeldt-Jakob disease (sCJD),

 

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

 

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

 


 

Thursday, January 15, 2015

 

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

 


 

Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

 

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

 

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

 

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

 

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

 

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

 

Saturday, January 17, 2015

 

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

 


 

*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report ***

 


 

Tuesday, November 04, 2014

 

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

 


 

Thursday, January 22, 2015

 

Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to disease etiology?

 


 


 

Sunday, July 06, 2014

 

Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study

 

Conclusions—The a priori hypotheses were supported.

 

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

 


 

PLEASE REMEMBER ;

 

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

 

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

 

if not, why not...

 

Friday, November 30, 2007

 

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

 


 


 

Friday, January 10, 2014

 

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

 


 


 

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014

 


 

Singeltary comment ;

 


 

Saturday, December 13, 2014

 

Terry S. Singeltary Sr. Publications TSE prion disease

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

snip...

 


 

Tuesday, April 14, 2015

 

Transmissible Spongiform Encephalopthy TSE Prion Disease

 


 

Wednesday, April 15, 2015

 

KURU Transmissible Spongiform Encephalopthy TSE Prion Disease

 


 

Sunday, May 3, 2015

 

PRION2015 FORT COLLINS

 


 

 Thursday, July 10, 2008

 

A New Prionopathy update July 10, 2008

 

snip...

 

DOES ANYONE BESIDES ME SEE A PATTERN YET ???

 

Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.

 

SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.

 

Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.

 

snip...

 

Sporadic creutzfeldt-jakob disease in two adolescents

 


 

see full text sporadic CJD the big lie;

 

snip...

 

IT seems we have come full circle from the 'ORIGINAL 10' i.e. the 1st 10 adolescents in the UKBSEnvCJD only theory. and now we find us at the 1st 10 in USA, or is it the first 10, or the tip of the iceburg, many that went undocumented ???

 

lets look at the full circle, to date ;

 


 

Sunday, August 10, 2008

 

*** A New Prionopathy OR more of the same old BSe and sporadic CJD

 


 

full text ;

 


 

 

Wednesday, October 09, 2013

 

WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation

 


 

 

 

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

 

Saturday, July, 18, 2009

 

Greetings,

 

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. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.

 

The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.

 

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. 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. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

 

please see history, and the ever evolving TSE science to date ;

 

Saturday, June 13, 2009

 

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

 


 

 

 

DEEP THROAT TO TSS 2000-2001

 

(take these old snips of emails with how ever many grains of salt you wish. ...tss)

 

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

 

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

 

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

 

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

 

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

 

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)

 


 

 

U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001

 


 

 

Tuesday, April 21, 2015

 

Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING SCHEDULED FOR June 1, 2015

 


 

 

 

Comment from Terry Singeltary This is a Comment on the Food and Drug Administration (FDA) Notice: Draft Guidance for Industry on Ensuring Safety of Animal Feed Maintained and Fed On-Farm; Availability

 

For related information, Open Docket Folder Docket folder icon

 

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Show agency attachment(s) Attachments View All (0)

 

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Comment View document:

 


 


 

 

Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 Singeltary Comment

 

Greetings FDA et al,

 

I wish to comment on Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180.

 

Once again, I wish to kindly bring up the failed attempt of the FDA and the ruminant to ruminant mad cow feed ban of August 4, 1997. This feed ban is still failing today, as we speak. Even more worrisome, is the fact it is still legal to feed cervids to cervids in the USA, in fact, the FDA only _recommends_ that deer and elk considered to be of _high_ risk for CWD do not enter the animal food chain, but there is NO law, its only voluntary, a recipe for a TSE prion disaster, as we have seen with the ruminant to ruminant feed ban for cattle, where in 2007, one decade post August 1997 mad cow feed ban, where in 2007 10,000,000 POUNDS OF BANNED BLOOD LACED MEAT AND BONE MEAL WHEN OUT INTO COMMERCE, TO BE FED OUT. Since 2007, these BSE feed ban rules have been breached time and time again. tons and tons of mad cow feed went out in Alabama as well, where one of the mad cows were documented, just the year before in 2006, and in 2013 and 2014, breaches so bad (OAI) Official Action Indicated were issued. those are like the one issued where 10 million pounds of banned blood laced meat and bone meal were fed out.

 

What is the use of having a Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180, if it cannot be enforced, as we have seen with a mandatory ruminant to ruminant feed ban?

 

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

 

======

 

In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

*** Ruminant feed ban for cervids in the United States? ***

 

31 Jan 2015 at 20:14 GMT

 


 

19 May 2010 at 21:21 GMT

 

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

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

2013

 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE

 


 

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 0500 EMC 1 Terry S. Singeltary Sr. Vol #: 1

 


 


 

PLEASE SEE FULL TEXT SUBMISSION ;

 


 

10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

 

Date: March 21, 2007 at 2:27 pm PST

 

REASON

 

Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

42,090 lbs.

 

DISTRIBUTION

 

WI

 

REASON

 

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

 

VOLUME OF PRODUCT IN COMMERCE

 

9,997,976 lbs.

 

DISTRIBUTION

 

ID and NV

 

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

Terry S. Singeltary Sr.

 

*** See attached file(s) No documents available. Attachments View All (1) Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Terry Singeltary Comment View Attachment:

 


 

Sunday, April 5, 2015

 

*** Guidance for Industry Ensuring Safety of Animal Feed Maintained and Fed On-Farm Draft Guidance FDA-2014-D-1180 ***

 


 

Sunday, November 23, 2014

 

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

 


 

 

>>> Up until about 6 years ago, the pt worked at Tyson foods where she worked on the assembly line, slaughtering cattle and preparing them for packaging. She was exposed to brain and spinal cord matter when she would euthanize the cattle. <<<

 

 SEE MORE HERE ;

 

 CJD TEXAS 38 YEAR OLD FEMALE WORKED SLAUGHTERING CATTLE EXPOSED TO BRAIN AND SPINAL CORD MATTER

 


 

 

snip...

 

 see ;

 

 Sunday, February 12, 2012

 

 National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

 


 

 

Wednesday, November 09, 2011

 

 Case report Sporadic fatal insomnia in a young woman: A diagnostic challenge: Case Report TEXAS

 

 HOW TO TURN A POTENTIAL MAD COW VICTIM IN THE USA, INTO A HAPPENSTANCE OF BAD LUCK, A SPONTANEOUS MUTATION FROM NOTHING.

 

 OR WAS IT $$$

 


 

 

Creutzfeldt-Jakob Disease Surveillance in Texas

 


 

 

Sunday, July 11, 2010

 

 CJD or prion disease 2 CASES McLennan County Texas population 230,213 both cases in their 40s

 


 

 


 

 

 see the continuing rise of sporadic CJD in Texas here ;

 


 

 

 

[PDF]2015 comment singeltary.pdf - RegInfo.gov


www.reginfo.gov/public/do/DownloadDocument?documentID...0
Mar 2, 2015 - Regulations. gov - Comment regulationsgov ... Regulationsgov - Comment Page 2 of2 ... snip...please see attached pdf file, with references of breaches in the .... The purpose ofthis notice is to solicit comments from the public {as ..... science based. they should do everyone a favor and dissolve there.

 

 

 

Mar 2, 2015 - the atypical Nor-98 Scrapie, which has been linked to sporadic CJD. ... the rise. with different strains mounting. victims becoming younger. with.

 

WHO issues best practices for naming new human infectious diseases Note for the media

 

8 May 2015 | GENEVA - WHO today called on scientists, national authorities and the media to follow best practices in naming new human infectious diseases to minimize unnecessary negative effects on nations, economies and people.

 

Terms that should be avoided in disease names include geographic locations (e.g. Middle East Respiratory Syndrome, Spanish Flu, Rift Valley fever), people’s names (e.g. Creutzfeldt-Jakob disease, Chagas disease), species of animal or food (e.g. swine flu, bird flu, monkey pox), cultural, population, industry or occupational references (e.g. legionnaires), and terms that incite undue fear (e.g. unknown, fatal, epidemic).

 


 

 

Greetings WHO,

 

I kindly submit the following, and I will continue to call it what it is, aka mad cow disease, and not only linked to the bovine and nvCJD to humans. mad cow disease has now been linked to sporadic cjd, and scrapie has now been linked to sporadic cjd, with great concern for chronic wasting disease in cerevids i.e. cwd. or just call it what it is, Transmissible Spongiform Encephalopathy TSE Prion disease. but I will call it for what it is, mad cow type disease, simply because of what the stigma brings, and as long as USDA INC are still feeding cows to cows, the OIE, and WHO continues to disregard the safety of humans there from mad cow type disease, through the continued denial and blatant disregard for the science to date, I refuse to play the game of denial. it is what it is, and trying to protect the industries involved, by changing the name, it will NOT stop the disease, only help the industry from the stigma. it is what it is, the mad cow has been out of the barn, and there is no putting it back now. it is what it is $$$...

 

 

kindest regards, terry

 

 

Saturday, December 13, 2014

 

Terry S. Singeltary Sr. Publications TSE prion disease

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

snip...

 


 

 

Terry S. Singeltary Sr. Bacliff, Texas USA 77518 flounder9@verizon.net

Sunday, May 03, 2015

Unusual Case of Sporadic Creutzfeldt–Jakob Disease Subtype VV1

Unusual Case of Sporadic Creutzfeldt–Jakob Disease Subtype VV1

 

 

To the Editor: Creutzfeldt-Jakob disease is characterized by a variety of symptoms, including rapidly progressive dementia, ataxia, and myoclonus.

 

Sporadic Creutzfeldt-Jakob disease (sCJD) has a median disease duration of 6 months.1

 

Seven different molecular subtypes of sCJD hae been identified (MM1, MM2-C, MM2T, MV1, MV2, VV1, and VV2), based on prion protein gene (PRNP) codon 129 polymorphism and the prion protein type 2.

 

VV1 is the rarest molecular subtype of sCJD (only about 1% of cases). To date, reported cases of sCJD VV1 have been characterized by young age at disease onset, long duration, and progressive dementia.

 

We describe a unique case of sCJD VV1 with older age at disease onset and shorter illness duration.

 
 

CASE REPORT

 

snip...

 
 
 


Free first page
 
 
 
 
 

Wednesday, April 08, 2015

Sporadic Creutzfeldt-Jakob Disease MM1+2C and MM1 Are Identical in Transmission Properties
http://creutzfeldt-jakob-disease.blogspot.com/2015/04/sporadic-creutzfeldt-jakob-disease.html
 
Saturday, April 04, 2009
 
An unusually presenting case of sCJD—The VV1 subtype Volume 111, Issue 3, Pages 282-291 (April 2009)
 
An unusually presenting case of sCJD—The VV1 subtype
 
Kaloyan S. Taneva, Mimi Yilmab
 
Received 16 November 2007; received in revised form 4 September 2008; accepted 12 September 2008.
 
Abstract
 
Creutzfeldt–Jakob disease (CJD) is a rapidly progressive neurodegenerative disease caused by prions. Typically CJD presents with a triad of rapidly progressive dementia, abnormal movements (e.g., myoclonus) and electroencephalographic (EEG) changes. Recently, CJD has been subdivided into subtypes based on host genetic polymorphisms and the characteristics of the pathological prion protein. Different subtypes likely have different clinical and laboratory presentations. We describe a case of sporadic CJD of the VV1 subtype. We describe our patient's clinical symptoms, time course, laboratory workup, structural and functional neuroimaging data, EEG data and CJD biomarkers. Our patient presented with clinical symptoms atypical for CJD. Because of that, her clinical symptoms were initially attributed to psychiatric reasons. After extensive clinical and laboratory investigation, we concluded that the patient probably had CJD. Postmortem neuropathological results confirmed this clinical hypothesis. We compare our patient's clinical, laboratory and neuroimaging data to the data on typical CJD as well as the data on the few CJD VV1 cases described in the literature. We discuss our case's relevance to the diagnosis of CJD.
 
Keywords: Creutzfeldt–Jakob disease, Dementia, Neuroimaging, Magnetic resonance imaging, Electroencephalography, Biomarkers, Prion diseases a Department of Psychiatry, Massachusetts General Hospital, 55 Fruit Street, Warren 1220/Blake 11, Boston, MA 02114, United States
 
b University of Connecticut Health Center, Farmington, CT, United States
 
Corresponding author. Tel.: +1 617 726 7511; fax: +1 617 724 9155.
 
PII: S0303-8467(08)00320-X
 
doi:10.1016/j.clineuro.2008.09.017
 
© 2008 Elsevier B.V. All rights reserved.
 
 
 
rare atypical strain of sporadic cjd ??? seems these rare strains are increasing ???
 
Wednesday, February 04, 2009
 
Creutzfeldt-Jacob disease presenting as severe depression: a case report
 
 
 
A case-control study of sporadic Creutzfeldt-Jakob disease in Switzerland: analysis of potential risk factors with regard to an increased CJD incidence in the years 2001-2004
 
 
 
Thursday, July 10, 2008
 
A New Prionopathy update July 10, 2008
 
snip...
 
DOES ANYONE BESIDES ME SEE A PATTERN YET ???
 
Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.
 
SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.
 
Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.
 
snip...
 
Sporadic creutzfeldt-jakob disease in two adolescents
 
 
 
see full text sporadic CJD the big lie;
 
snip...
 
IT seems we have come full circle from the 'ORIGINAL 10' i.e. the 1st 10 adolescents in the UKBSEnvCJD only theory. and now we find us at the 1st 10 in USA, or is it the first 10, or the tip of the iceburg, many that went undocumented ???
 
lets look at the full circle, to date ;
 
 
 
Sunday, August 10, 2008
 
A New Prionopathy OR more of the same old BSe and sporadic CJD
 
 
 
HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008
 
snip...
 
Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
 
snip...
 
 
 
Elsevier Editorial System(tm) for The Lancet Infectious Diseases Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary
 
Abstract:
 
TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007. snip...
 
see full text 31 pages ;
 
 
 
Friday, November 30, 2007
 
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
 
 
 
Saturday, April 04, 2009
 
An unusually presenting case of sCJD—The VV1 subtype
 
 
 
Tuesday, April 21, 2015
 
Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING SCHEDULED FOR June 1, 2015
 
 


 
tss