DOI: 10.3201/eid1509.090253
Suggested citation for this article: Race B, Meade-White KD, Miller MW, Barbian KD, Rubenstein R, LaFauci G, et al. Susceptibilities of nonhuman primates to chronic wasting disease. Emerg Infect Dis. 2009 Sep; [Epub ahead of print]
Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
Brent Race,1 Kimberly D. Meade-White,1 Michael W. Miller, Kent D. Barbian, Richard Rubenstein, Giuseppe LaFauci, Larisa Cervenakova, Cynthia Favara, Donald Gardner, Dan Long, Michael Parnell, James Striebel, Suzette A. Priola, Anne Ward, Elizabeth S. Williams,2 Richard Race,3 and Bruce Chesebro3
Author affiliations: Rocky Mountain Laboratories, Hamilton, Montana, USA (B. Race, K.D. Meade-White, K.D. Barbian, C. Favara, D. Gardner, D. Long, M. Parnell, J. Striebel, S.A. Priola, A. Ward, R. Race, B. Chesebro); Colorado Division of Wildlife, Fort Collins, Colorado, USA (M.W. Miller); State University of New York Downstate Medical Center, Brooklyn, New York, USA (R. Rubenstein); New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA (G. LaFauci); American Red Cross, Rockville, Maryland, USA (L. Cervenakova); and University of Wyoming, Laramie, Wyoming, USA (E.S. Williams)
1These authors contributed equally to this article. 2Deceased. 3Co-senior authors.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy, or prion disease, that affects deer, elk, and moose. Human susceptibility to CWD remains unproven despite likely exposure to CWD-infected cervids. We used 2 nonhuman primate species, cynomolgus macaques and squirrel monkeys, as human models for CWD susceptibility. CWD was inoculated into these 2 species by intracerebral and oral routes. After intracerebral inoculation of squirrel monkeys, 7 of 8 CWD isolates induced a clinical wasting syndrome within 33–53 months. The monkeys’ brains showed spongiform encephalopathy and protease-resistant prion protein (PrPres) diagnostic of prion disease. After oral exposure, 2 squirrel monkeys had PrPres in brain, spleen, and lymph nodes at 69 months postinfection. In contrast, cynomolgus macaques have not shown evidence of clinical disease as of 70 months postinfection. Thus, these 2 species differed in susceptibility to CWD. Because humans are evolutionarily closer to macaques than to squirrel monkeys, they may also be resistant to CWD.
http://www.cdc.gov/eid/content/15/9/pdfs/09-0253.pdfFor Immediate Release Wednesday, July 29, 2009
Species Barrier May Protect Macaques from Chronic Wasting Disease
Data from an ongoing multi-year study suggest that people who consume deer and elk with chronic wasting disease (CWD) may be protected from infection by an inability of the CWD infectious agent to spread to people. The results to date show that 14 cynomolgus macaques exposed orally or intracerebrally to CWD remain healthy and symptom free after more than six years of observation, though the direct relevance to people is not definitive and remains under study. Cynomolgus macaques often are used as research models of human disease because they are very close genetically to humans and are susceptible to several forms of human brain-damaging disease. Thus, it was decided to see whether exposure to CWD could induce disease in the macaques. The study appears online in the journal Emerging Infectious Diseases.
CWD is a type of brain-damaging disease known as a transmissible spongiform encephalopathy (TSE) or prion disease. CWD primarily affects deer, elk, and moose. Other TSE diseases include mad cow disease, or bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep, and sporadic Creutzfeldt-Jakob disease (CJD) in humans. Humans are not susceptible to sheep scrapie, but BSE appears to have infected about 200 people, primarily in Europe in the 1990s. Those findings provided the rationale for the present CWD-macaque study, which began in 2003.
"We plan to continue this study for at least several more years because, although the risk to macaques so far appears to be low, we know that these diseases can take more than 10 years to develop," says Bruce Chesebro, M.D., chief of the Laboratory of Persistent Viral Diseases at Rocky Mountain Laboratories (RML) in Hamilton, Mont. RML is part of the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH). The RML group is leading the study with collaborators from the Colorado Division of Wildlife; State University of New York Downstate Medical Center; New York State Institute for Basic Research in Developmental Disabilities; American Red Cross; and the University of Wyoming.
The findings by the RML group support published field studies done by others in regions of Colorado and Wyoming where CWD is endemic. Between 1979 and 2001, there were no significant increases in human TSE diseases despite the likelihood that hunters in those areas were exposed to CWD through contact with infected animal tissue and contaminated hunting tools such as knives and saws. Extensive laboratory data also supports a human species barrier against CWD.
Notably, the RML study also included identical testing in squirrel monkeys, which are genetically less similar to humans than macaques. Of 15 squirrel monkeys exposed orally to CWD, two displayed disease symptoms 69 months after infection. Of 13 squirrel monkeys exposed intracerebrally to CWD, 11 displayed symptoms between 33 and 53 months after infection. In symptomatic animals, the presence of the CWD agent was confirmed in brain, spleen and lymph nodes.
The results in squirrel monkeys were not surprising because a study elsewhere in two squirrel monkeys yielded similar results. The study by the RML group was different, however, in that it tested oral exposure to CWD and also studied eight CWD samples from different areas of the country. The results in squirrel monkeys confirmed that disease progression in that species appears consistent with disease progression in deer and elk, where severe weight loss is nearly always present.
"The fact that the squirrel monkeys, like the deer and elk, suffered severe weight loss suggests that chronic wasting disease might affect a common region of the brain in different species," notes Dr. Chesebro.
NIAID conducts and supports research - at NIH, throughout the United States, and worldwide-to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID Web site at http://www.niaid.nih.gov.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov. -------------------------------------------------------------------------------- Reference: Race B et al. Susceptibilities of nonhuman primates to chronic wasting disease. Emerging Infectious Diseases. DOI: 10.3201/eid1509.090253.
http://www.nih.gov/news/health/jul2009/niaid-29.htmGreetings,
let's compare PRNP differences from this animal, Macaca fascicularis, to human, elk and deer.
what this means is human, deer, and elk have serine s and asparagine n and arginine at these positions whereas the macaque seq -- at least the seq deposited at GenBank -- has tryptophan, proline and lysine at these positions.
at positions where human, deer, and elk agree but macaque disagrees, the species barrier deer/elk to human cannot be tested with macaque.
see below if everything lines up alright ?
note the region S..N.......N and later R where this monkey is inappropriate model for testing species barrier cervid to human.
macFas MANLGCWMLVLFVATWSDLGLCKKRPKPGG-WNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQGGGTHNQWHKPSKPKTSMKHMAGAAAAGAVVGGL
homSap ..............................-..................................................................S..N.......N.................
odoHem MVKSHI.S.I......M...V...........G..........................................................GWGQ....S..N.......N...V.............
cerEla MVKSHI.S.I......M...V...........G..........................................................GWGQ....S..N.......N...V.............
Consensus ..manl.c.m......t...l......................................................................wgqg....S..N.......N...m.............
129 256
macFas GGYMLGSAMSRPLIHFGNDYEDRYYRENMYRYPNQVYYRPVDQYSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQYEKESQAYYQRGSSMVLFSSPPVILLISFLIFLIVG
homSap ............I....S...........H..........M.E...................................................R.................................
odoHem ............................................N...T.........V..................I...............QR.........A.VI....................
cerEla ............................................N...T.........V..................I...............QR..E......A.VI....................
Consensus ............................................s...n.........!..................!...............#R.........s.m!....................
>macFas Macaca fascicularis (Cynomolgus macaque)
MANLGCWMLVLFVATWSDLGLCKKRPKPGGWNTGGSRYPGQGSP
GGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQGGGTHNQWHKP
SKPKTSMKHMAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGNDYEDRYYRENMYRYPNQ
VYYRPVDQYSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQY
EKESQAYYQRGSSMVLFSSPPVILLISFLIFLIVG
>odoHem Odocoileus hemionus (mule deer)
MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQ
GSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGTHSQW
NKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGNDYEDRYYRENMYRY
PNQVYYRPVDQYNNQNTFVHDCVNITVKQHTVTTTTKGENFTETDIKMMERVVEQMCI
TQYQRESQAYYQRGASVILFSSPPVILLISFLIFLIVG
>cerEla Cervus elaphus nelsoni (American elk)
MVKSHIGSWILVLFVAMWSDVGLCKKRPKPGGGWNTGGSRYPGQ
GSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGTHSQW
NKPSKPKTNMKHVAGAAAAGAVVGGLGGYMLGSAMSRPLIHFGNDYEDRYYRENMYRY
PNQVYYRPVDQYNNQNTFVHDCVNITVKQHTVTTTTKGENFTETDIKMMERVVEQMCI
TQYQRESEAYYQRGASVILFSSPPVILLISFLIFLIVG
>homSap Homo sapiens
MANLGCWMLVLFVATWSDLGLCKKRPKPGGWNTGGSRYPGQGSP
GGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQGGGTHSQWNKP
SKPKTNMKHMAGAAAAGAVVGGLGGYMLGSAMSRPIIHFGSDYEDRYYRENMHRYPNQ
VYYRPMDEYSNQNNFVHDCVNITIKQHTVTTTTKGENFTETDVKMMERVVEQMCITQY
ERESQAYYQRGSSMVLFSSPPVILLISFLIFLIVG
http://www.mad-cow.org/I wonder also which strain of CWD was used in this experiment ?
0C7.04
North American Cervids Harbor Two Distinct CWD Strains
Authors
Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.
Content
Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.
see page 29, and see other CWD studies ;
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdfSunday, November 23, 2008
PRION October 8th - 10th 2008 Book of Abstracts
http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.htmlP35
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.
http://www.istitutoveneto.it/prion_09/Abstracts_09.pdfWHAT will these strains look like passed via iatrogenically, 1st, 2nd, 3rd passage ???
WHAT will different strains of CWD in humans look like pathologically ???
like some sub-types of sporadic CJD ???
i always remember this ;
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
snip...
http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdfIt seems that both DY and HY TME strains are already present as a mixture in the original Stetsonville inoculum and during subsequent passages undergo selection during interspecies transmission [3]. For instance, one of the 4 clones passaged into Syrian golden hamsters bifurcated into a strain characterized by an incubation period ranging from 219 to 522 days and the PrP banding pattern typical of the DY strain of mink, and a second strain with an incubation period of 219 days and PrP pattern that of the DY strain. Upon further passages into hamsters, the incubation periods decreased, the emerging “strain” presented a mixture of HY and DY strains only on subsequent passages, distinct DY strain emerged, and from that, the HY TME strain was selected.
http://transmissible-mink-encephalopathy.blogspot.com/2009/07/transmissible-mink-encephalopathy.htmlThe atypical scrapie (SC-PS152) agent appeared to undergo a strain phenotype shift upon transmission to porcine PrP transgenic mice. Surprisingly, this novel strain phenotype was similar to that of sheep BSE propagated in the same mice in terms of several features: 1) survival times observed after stabilization in PoPrP-Tg001 mice (second passages) were similar (Table); 2) PrPresmolecular profiles of the 2 agents in porcine PrP mice were indistinguishable (Figure 3); and 3) vacuolation profiles observed in second passages largely overlapped (Figure 4). These findings could reflect the evolutionary potential of prion agents upon transmission to a foreign host able to promote strain shift and emergence of new properties (38,39).
http://www.cdc.gov/eid/content/15/8/pdfs/08-1218.pdf38. Scott MR, Groth D, Tatzelt J, Torchia M, Tremblay P, DeArmond SJ, et al. Propagation of prion strains through specific conformers of the prion protein. J Virol. 1997;71:9032–44. PubMed
39. Bartz JC, Bessen RA, McKenzie D, Marsh RF, Aiken JM. Adaptation and selection of prion protein strain conformations following interspecies transmission of transmissible mink encephalopathy. J Virol. 2000;74:5542–7. PubMed DOI: 10.1128/JVI.74.12.5542-5547.2000
12. L-type BSE has been transmitted to wild-type, bovinised, ovinised and humanised mice as well as to cattle and a cynomolgus macaque by intracerebral inoculation. Incubation periods, clinical signs, neuropathology as well as the neurological distribution of PrPsc were distinct from classical BSE13,12. With the exception of transmissions to wild-type mice, primary transmissions resulted in clinical disease. Although primary transmission to wild-type mice did not result in clinical disease,secondary transmissions from some of these animals resulted in clinical disease. Sub-passage of L-type BSE in wild-type12 and ovinised mice13 suggests that L-type BSE may be converted to an infection of a similar phenotype to classical BSE. However, further experiments using serial sub-passages of infections in a range of species are required to more fully investigate whether L-type BSE may convert to a disease with a classical BSE phenotype.
http://www.seac.gov.uk/statements/newforms-bse.htmGreetings again,
This study is good news, but do NOT let this study fool anyone. It proves nothing for humans. well, at least that is what the officials have been telling us for decades when they transmit all these other TSEs to all these other species, ''oh, that they DID transmit to mouse, to vole, to hamsters, to primate, to squirrel monkeys, to Cynomolgus macaques, etc. etc. i could go on, but these are NOT humans, so the study means little toward human transmission'' etc.
i saw this headline the other day in the newspaper that some fool wrote ;
News Canada
Humans likely resistant to disease found in deer:
study By BOB WEBER, THE CANADIAN PRESS
Last Updated: 4th August 2009, 1:43am
http://www.edmontonsun.com/news/canada/2009/08/04/10353111-sun.htmlThen this fool writes ;
U.S. study: deer infected with chronic wasting disease safe to eat By Bob Weber, THE CANADIAN PRESS
http://www.edmontonsun.com/news/edmonton/2009/08/03/10349946.htmlwho ever wrote this story with the headlines will needlessly expose many to this disease, through nothing more than sensationalized media hype. and what about second hand transmission via friendly fire? have any of you ever looked at the real threat here from second, third, fourth passage etc. from TSE's. i keep trying to tell people that the consumption of cwd infected deer or elk might kill some, but it is the 'friendly fire', that is the bigger threat in my opinion. as the TSEs mutate, and or as they are passaged 1, 2, 3, times, they become more virulent. By changing what this study really showed, and sensationalizing the subject title with fiction, you saw what happened next, every other five and dime reporter picked up on the sensationalized subject, that was completely fabricated. I could care less who eats CWD tainted meat, but it's the after affects, the exposing millions, when they don't even know it, to possibly suffer the horrible consequences years, decades later, is not acceptable, and these five and dime news reporters are just as responsible for senselessly and needlessly exposing others with lazy reporting of sensationalized media reporting. then the other five and dimers pick up on it, and it spreads, just like CWD and BSe do, and you have every hunter out there now that will say that it's now o.k. to eat CWD infected deer and elk, because this study said that.
THAT'S NOT WHAT THIS STUDY SAID DAMN'T !!!
Science Daily (press release) - 22 hours ago 3, 2009) - Data from an ongoing multi-year study suggest that people who consume deer and elk with chronic wasting disease (CWD) may be protected from ...
http://www.sciencedaily.com/releases/2009/07/090730111152.htmUS study suggests deer infected with chronic wasting disease safe ... Bridge River Lillooet News - 21 hours ago A new study has added to evidence that meat from deer infected with chronic wasting disease - an infection similar to mad cow disease - is safe for humans ...
People Who Eat Deer And Elk With Chronic Wasting Disease May Avoid ...
Science Daily (press release) - 22 hours ago 3, 2009) - Data from an ongoing multi-year study suggest that people who consume deer and elk with chronic wasting disease (CWD) may be protected from ...
US study suggests deer infected with chronic wasting disease safe ...
Medicine Hat News - 22 hours ago EDMONTON - A new study has added to evidence that meat from deer infected with chronic wasting disease - an infection similar to mad cow disease - is safe ...
US study suggests deer infected with chronic wasting disease safe ...
Winnipeg Free Press - Bob Weber - Aug 3, 2009 EDMONTON - A new study has added to evidence that meat from deer infected with chronic wasting disease - an infection similar to mad cow disease - is safe ...
US study suggests deer infected with chronic wasting disease safe ...
CanadaEast.com - Aug 3, 2009 EDMONTON - A new study has added to evidence that meat from deer infected with chronic wasting disease - an infection similar to mad cow disease - is safe ...
The Canadian Press US study suggests deer infected with chronic wasting disease safe ... The Canadian Press - ?Aug 3, 2009? EDMONTON - A new study has added to evidence that meat from deer infected with chronic wasting disease - an infection similar to mad cow disease - is safe ...
http://news.google.com/news?um=1&ned=us&hl=en&q=chronic+wasting+disease&cf=all&scoring=d&start=10NOW, lets look at the rest of the science ;
Program ID: Innovation Anthology #214 Program Date: 04/07/2009 Program Category: Health and Medicine, Prions, Social Sciences, Wildlife
CWD Potential Risk to Human Health Chronic wasting disease is an emerging epidemic among deer and elk on the prairies.
CWD is the cervid equivalent of mad cow disease. And according to Dr. Daniel Krewski, an expert in population health risk assessment, prion researchers are very worried about the impact of CWD on human health.
DR. DANIEL KREWSKI: And what would happen if that disease were to jump the species barrier. Hunters who consume deer and elk who may have CWD What we would like to do is get out ahead of the risk curve and try to anticipate and prevent the next transmission of a disease of this type to humans. So we are focusing on is it possible that CWD could transmit to humans? We will be hosting an expert group meeting in Ottawa where we are bringing over 10 international experts in this area to ask that question. Are there things that we can do to try to prevent that from happening as was the case with BSE turning into vCJD (variant Creutzfeld-Jacob disease) from the consumption of beef contaminated with the BSE (bovine spongiform encephalopathy) agent?
Dr. Krewski emphasizes the importance of investing now in preventive action to contain chronic wasting disease.
Thanks today to Canadian Institutes for Health Research.
http://www.innovationanthology.com/programs.php?id=229Sunday, April 12, 2009
CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains
http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.htmlThursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip...
full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.htmlFrom: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay,
Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was
attached to your email), we did not say CWD in humans will present like
variant CJD.
That assumption would be wrong. I encourage you to read the whole
article and call me if you have questions or need more clarification
(phone: 404-639-3091). Also, we do not claim that "no-one has ever been
infected with prion disease from eating venison." Our conclusion stating
that we found no strong evidence of CWD transmission to humans in the
article you quoted or in any other forum is limited to the patients we
investigated.
Ermias Belay, M.D.
Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG
HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
also,
A. Aguzzi - Chronic Wasting Disease (CWD) also needs to be addressed. Most
serious because of rapid horizontal spread and higher prevalence than BSE in
UK, up to 15% in some populations. Also may be a risk to humans - evidence
that it is not dangerous to humans is thin.
http://www.tseandfoodsafety.org/activities/bse_conference_basel_april_02/2summarSNIP...END...TSS
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,? Michael W. Miller,? Pierluigi Gambetti,§ and Lawrence B. Schonberger*
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; ?University of Wyoming, Laramie, Wyoming, USA; ?Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htmChronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
snip...full text ;
http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htmVolume 12, Number 10-October 2006
Research
Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Samantha MaWhinney,* W. John Pape,? Jeri E. Forster,* C. Alan Anderson,?§ Patrick Bosque,?¶ and Michael W. Miller#
*University of Colorado at Denver and Health Sciences Center, Denver, Colorado, USA; ?Colorado Department of Public Health and Environment, Denver, Colorado, USA; ?University of Colorado School of Medicine, Denver, Colorado, USA; §Denver Veteran's Affairs Medical Center, Denver, Colorado, USA; ¶Denver Health Medical Center, Denver, Colorado, USA; and #Colorado Division of Wildlife, Fort Collins, Colorado, USA
Suggested citation for this article
The transmission of the prion disease bovine spongiform encephalopathy (BSE) to humans raises concern about chronic wasting disease (CWD), a prion disease of deer and elk. In 7 Colorado counties with high CWD prevalence, 75% of state hunting licenses are issued locally, which suggests that residents consume most regionally harvested game. We used Colorado death certificate data from 1979 through 2001 to evaluate rates of death from the human prion disease Creutzfeldt-Jakob disease (CJD). The relative risk (RR) of CJD for CWD-endemic county residents was not significantly increased (RR 0.81, 95% confidence interval [CI] 0.40-1.63), and the rate of CJD did not increase over time (5-year RR 0.92, 95% CI 0.73-1.16). In Colorado, human prion disease resulting from CWD exposure is rare or nonexistent. However, given uncertainties about the incubation period, exposure, and clinical presentation, the possibility that the CWD agent might cause human disease cannot be eliminated.
snip... full text ;
http://0-www.cdc.gov.mill1.sjlibrary.org/ncidod/EID/vol12no10/06-0019.htmfull text ;
http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.htmlSaturday, May 16, 2009
Chronic Wasting Disease Herd Certification Program Document ID APHIS-2006-0118-0096
http://chronic-wasting-disease.blogspot.com/2009/05/chronic-wasting-disease-herd.htmlSunday, April 12, 2009
CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains
http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.htmlMonday, July 06, 2009
Prion infectivity in fat of deer with Chronic Wasting Disease
http://chronic-wasting-disease.blogspot.com/2009/07/prion-infectivity-in-fat-of-deer-with.htmlWednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.htmlThursday, March 19, 2009
Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)
http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.htmlWednesday, March 18, 2009
Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay
http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.htmlCHRONIC WASTING DISEASE BLOG
http://chronic-wasting-disease.blogspot.com/Thursday, July 23, 2009
UW Hospital warning 53 patients about possible exposure to rare brain disease
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/uw-hospital-warning-53-patients-about.htmlFinally, the way the CJD surveillance is in the USA, the way the diagnostic criteria is set up for differentiating between the TSE's in different species, and strains and or phenotypes there of, you would never know when a documented case of CWD to human occurred. ...TSS
Further characterisation of the prion protein molecular types detectable in the NIBSC CreutzfeldteJakob disease brain reference materials
Helen M. Yull, James W. Ironside, Mark W. Head* National CJD Surveillance Unit, School of Molecular & Clinical Medicine (Pathology), University of Edinburgh, Edinburgh, United Kingdom
Received 17 November 2008; revised 29 December 2008; accepted 23 January 2009
Abstract
Sporadic and variant CreutzfeldteJakob disease brain reference materials available from the UK National Institute for Biological Standards and Control have been subjected to further characterisation by Western blot analysis, with particular reference to the co-occurrence of different abnormal disease-associated prion protein (PrPSc) types. The results confirm the presence of genuine type 1 and type 2 protease-resistant PrP (PrPres) in each of the three sporadic CreutzfeldteJakob disease reagents, and provide evidence supporting the lower level presence of type 1 PrPres in the variant CreutzfeldteJakob disease reagents. We conclude that these reagents provide a valuable resource for future research and development.
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1.4. Mixed PrP types The co-occurrence of types 1 and 2 in cases of sCJD is now a well recognised phenomenon [5,10,11,12] and several independent studies have each concluded that when an extensive brain sampling protocol is employed 20-50% of sCJD cases can be seen to contain both type 1 and type 2 PrPres [7,10,13,14,15].
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On a superficial level the presence of more than one PrPSc type in individual CJD brains may seem at variance with the molecular strain typing hypothesis, which proposes that individual prion strains are enciphered by unique and self-perpetuating conformations and glycosylation states. However, this is not necessarily the case. It has long been known that multiple strains may be derived in mice from individual scrapie isolates, and cross-species transmission can, on occasion lead to an abrupt change in apparent strain characteristics.
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2009 The International Association for Biologicals. Published by Elsevier Ltd. All rights reserved. Keywords: CreutzfeldteJakob disease; Standards; Prion protein; Molecular typing; Co-occurrence
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WBS-4VRWNKF-3&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=5a0c2f13b5476b0ddfea5bf9882300dfBeyond PrPres Type 1/Type 2 Dichotomy in Creutzfeldt-Jakob Disease
ArticleRelated ContentComments: 0.Formal Correction: This article has been formally corrected to address the following errors.
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Abstract Author Summary Introduction Materials and Methods Results Discussion Author Contributions References Emmanuelle Uro-Coste1#, Hervé Cassard2#, Stéphanie Simon3, Séverine Lugan2, Jean-Marc Bilheude4, Armand Perret-Liaudet5, James W. Ironside6, Stéphane Haik7,8, Christelle Basset-Leobon1, Caroline Lacroux2, Katell Peoch'9, Nathalie Streichenberger5, Jan Langeveld10, Mark W. Head6, Jacques Grassi3, Jean-Jacques Hauw8, Francois Schelcher2, Marie Bernadette Delisle1, Olivier Andréoletti2*
1 INSERM U858, Institut de Médecine Moléculaire de Rangueil and Service d'Anatomie Pathologique et Histologie-Cytologie, C.H.U. Rangueil, Toulouse, France, 2 UMR Institut National de la Recherche Agronomique (INRA)/Ecole Nationale Vétérinaire de Toulouse (ENVT) 1225, Interactions Hôtes Agents Pathogènes, ENVT, Toulouse, France, 3 Commissariat à l'Energie Atomique (CEA), Service de Pharmacologie et d'Immunologie, DRM, CEA/Saclay, Gif sur Yvette, France, 4 Bio-Rad, Research and Development Department, Marnes-la-Coquette, France, 5 Hôpital Neurologique, Services de Neurochimie et de Pathologie, Bron, France, 6 National Creutzfeldt-Jakob Disease Surveillance Unit, Division of Pathology, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom, 7 INSERM, Equipe Avenir, Maladies à Prions chez l'Homme, Paris, France, 8 Neuropathology Laboratory, Salpêtrière Hospital, AP-HP, Paris, France, 9 Service de Biochimie et Biologie Moléculaire, Hôpital Lariboisière, Paris (Laboratoire associé au CNR “ATNC”) et EA 3621 Faculté de Pharmacie, Paris, France, 10 Central Institute for Animal Disease Control CIDC-Lelystad, Lelystad, The Netherlands
Abstract Top Sporadic Creutzfeldt-Jakob disease (sCJD) cases are currently subclassified according to the methionine/valine polymorphism at codon 129 of the PRNP gene and the proteinase K (PK) digested abnormal prion protein (PrPres) identified on Western blotting (type 1 or type 2). These biochemically distinct PrPres types have been considered to represent potential distinct prion strains. However, since cases of CJD show co-occurrence of type 1 and type 2 PrPres in the brain, the basis of this classification system and its relationship to agent strain are under discussion. Different brain areas from 41 sCJD and 12 iatrogenic CJD (iCJD) cases were investigated, using Western blotting for PrPres and two other biochemical assays reflecting the behaviour of the disease-associated form of the prion protein (PrPSc) under variable PK digestion conditions. In 30% of cases, both type 1 and type 2 PrPres were identified. Despite this, the other two biochemical assays found that PrPSc from an individual patient demonstrated uniform biochemical properties. Moreover, in sCJD, four distinct biochemical PrPSc subgroups were identified that correlated with the current sCJD clinico-pathological classification. In iCJD, four similar biochemical clusters were observed, but these did not correlate to any particular PRNP 129 polymorphism or western blot PrPres pattern. The identification of four different PrPSc biochemical subgroups in sCJD and iCJD, irrespective of the PRNP polymorphism at codon 129 and the PrPres isoform provides an alternative biochemical definition of PrPSc diversity and new insight in the perception of Human TSE agents variability.
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Discussion Top Coexistence of Different PrPres Types in the Same Subject In this study, detection, by WB, of the coexistence of two PrPres types in about 30% (13/41) of cases is consistent with already published data [12],[14]. This observation could suggest the existence in brain from a single patient of different abnormal PrP species. Although two main PK cleavage sites are associated with PrPres type 1 and type 2 (respectively amino acid 82 and 97), N-terminal sequencing revealed in all investigated cases the presence of a whole spectrum of overlapping cleavage sites. Moreover in a part of investigated cases this technique demonstrated the presence (i) of variable but consistent level of type 1 PrPres in patients classified type 2 using WB and (ii) in some patient classified type 1, of low amount of type 2 PrPres [10]. These observations could suggest that, rather than a pure type 1 or type 2 PrPres, PK digestion of a PrPSc specific conformer generate variable mixture of PrPres fragments (with presence of dominant or sub dominant type 1 or type 2 PrPres), which WB usually failed to reveal accurately because its intrinsic technical limits [14]. Antibodies either harbouring higher affinity to PrP (like Sha31) [18] or probing specifically type 1 PrPres (like 12B2) [20], now allow a better perception of such mixture. However, investigations carried out using artificial mixture of type 1 and type 2 brain homogenate, even using high affinity anti-PrP antibodies, clearly indicate the current limits of WB discriminative power [14]. Together, these data suggest that WB analysis of PrPres on its own could be misleading for adequate discrimination between PrPSc variants in CJD.
Both PrPSc PK resistance ELISA and strain typing ELISA are based on the characterization the N terminal part of the PrPSc PK digestion either by increasing PK amount or modifying detergent conditions. While WB profile could be compared to a snapshot picture of PrPres fragments generated by PK digestion process, these assays reflect the dynamics of the PK cleavage rather than its final result (different forms of PrPres). Consequently they could provide different but also more accurate perception of the PrPSc conformers.
Our findings from the PrPSc capture immunoassays clearly indicate that in a single patient, irrespective of brain area, sCJD associated PrPSc displays uniform biochemical properties, regardless of the regional variation of type 1 and type 2 isoforms determined by WB. Such findings support the idea of the presence of a specific TSE agent in each brain and the accumulation of a single associated PrPSc conformer.
sCJD Classification Because the limited size of our cohort of cases, an in depth comparison between the PrPSc signature (as established in this study) and the Parchi classification system is not possible.
However, despite this limitation, two major groups were identified in our panel according to the PrPSc properties. The first major group was constituted with patients harbouring a highly PK resistant PrPSc (MM1 and MV1 patients). The second group included patients harboring a PK labile PrPSc (VV2 and MV2 patients). Using both lesion profile and clinical parameters [2], two major forms of sCJD are commonly recognized. The first sCJD form, named “classical”, is characterized by a “rapid evolution” (usually around 4 months), and affects most of the MM1 and MV1 patients. The second sCJD form, named “atypical”, affects VV2 and MV2 with a longer symptomatic evolution (usually longer than 6 months) and a late dementia. Despite inter-individual variations, sCJD Groups 1 and 2, as we defined them on biochemical criteria were consistent with this classification.
Both VV1 and MM2 sCJD cases are extremely rare; they respectively represent 1% and 4% of the identified sCJD cases. According to the literature, these patients have clinical features and lesion profiles that are very different from other sCJD patients [2]. However, in our study as in previously published studies, WB did not identify any distinct biochemical difference from other type 1 and type 2 cases. In contrast, both the strain typing ELISA and PrPSc resistance assays clearly differentiated these cases from Group 1 and Group 2 cases. This finding, which is consistent with clinico/pathological observations carried out in patients, could indicate that there are indeed differences in PrPSc that distinguish these VV1 and MM2 cases from other sCJD groups.
Prion Strains and PrPSc Phenotype Although prion strains can only be identified definitively by bioassay, molecular in vitro tools to characterize PrPSc are more and more widely used for the rapid identification of particular agents, such as BSE in cattle, sheep, rodent and humans (vCJD) [20],[21]. This has come to be termed “molecular strain typing” and although widely employed, the exact relationship between PrPSc biochemistry and the biological properties of the agents responsible remain to be determined. In sCJD, the presence of four distinct PrPSc biochemical forms apparently correlated to clinico-pathological phenotypes as defined by Parchi et al. [2] could be an indication of the involvement of different TSE agents.
iCJD cases are a consequence of accidental human to human TSE transmission, most likely representing transmission of sCJD. The identification in iCJD cases of the four PrPSc signatures identified in sCJD is consistent with the existence of distinct prions associated with these biochemical forms.
Three examples of human-to-human transmission of variant CJD through blood transfusion have now been identified. While all blood donors were MM at codon 129 PRNP, the recipients had either a MM (n = 2) or a MV genotype (n = 1). Despite this genotype difference there appears to have been conservation of the disease phenotype and PrPres type in all “secondary” vCJD cases [22]–[25]. These observations could suggest that in case of inter-human transmission, difference in donor/recipient genotype could result in un-altered abnormal PrP signature.
Our identification of MM GH iCJD cases harbouring similar PrPSc signature as a VV1 sCJD case or of a VV dura mater iCJD case similar to MM2 sCJD might indicate preservation of a specific PrPSc biochemical signature after human to human transmission between individuals of different codon 129 genotypes.
Treatment with extracts of GH contaminated by CJD has lead to a high number of iCJD cases in France and the UK. The codon 129 genotypes of the affected individuals in the two countries differ, with the French cohort predominantly MM and MV and the British cohort MV and VV [26]. In the absence of any clear explanation for this finding, it was suggested that it might be due to contamination of different batches of GH with different prion strains from individuals of differing PRNP codon 129 genotypes. Our identification of different biochemical forms of PrPSc in GH French patients and in UK patients is consistent with this hypothesis. The variability observed within the French GH cases could signify involvement of different prion strains, consistent with multiple contaminated GH batches in the French epidemic.
Conclusion The identification in this study of different PrPSc species in CJD patients with the same PRNP polymorphism at codon 129 and WB PrPres profile offers a new perspective on our understanding of the relationship between PrP biochemistry, prion disease phenotype and agent strain. We highlight two novel approaches to analysing PrPSc in sCJD and iCJD and offer evidence that these analyses provide potentially-strain associated information, which appears to be lacking from the conventional WB assay.
http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000029Monitoring 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 ;
full text ;
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.htmlSEE THE DAMNING VIDEO NOW AT THE BOTTOM OF THE BLOG BELOW ;
http://creutzfeldt-jakob-disease.blogspot.com/2009/07/usa-hiding-mad-cow-disease-victims-as.htmlTerry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
Labels: CJD, CWD, non-human primate, novel prion strains, USA
