Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom

Commentary

Alimentary prion infections: Touch-down in the intestine

Volume 5, Issue 1 January/February/March 2011 Bianca Da Costa Dias, Katarina Jovanovic and Stefan F.T. Weiss View affiliations Hide affiliations Bianca Da Costa DiasSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Katarina JovanovicSchool of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa Stefan F.T. WeissCorresponding author: stefan.weiss@wits.ac.za School of Molecular and Cell Biology; University of the Witwatersrand; Johannesburg, Republic of South Africa

Neurodegenerative diseases are caused by proteinaceous aggregates, usually consisting of misfolded proteins which are often typified by a high proportion of ß-sheets, which accumulate in the Central Nervous System. These diseases, including Morbus Alzheimer, Parkinson disease and Transmissible Spongiform Encephalopathies (TSEs) also termed prion disorders, afflict a substantial proportion of the human population and as such the etiology and pathogenesis of these diseases has been the focus of mounting research. Although many of these diseases arise from genetic mutations or are sporadic in nature, the possible horizontal transmissibility of neurodegenerative diseases poses a great threat to population health. In this article we discuss recent studies which suggest that the “non-transmissible” status bestowed upon Alzheimer and Parkinson diseases may need to be revised as these diseases have been successfully induced through tissue transplants. Furthermore, we highlight the importance of investigating the “natural” mechanism of prion transmission including peroral and perenteral transmission, proposed routes of gastrointestinal uptake and neuroinvasion of ingested infectious prion proteins. We examine the multitude of factors which may influence oral transmissibility and discuss the zoonotic threats which Chronic Wasting Disease (CWD), Bovine Spongiform Encephalopathy (BSE) and Scrapie may pose resulting in vCJD or related disorders. In addition, we suggest that the 37 kDa/67 kDa laminin receptor on the cell surface of enterocytes, a major cell population in the intestine, may play an important role in the intestinal pathophysiology of alimentary prion infections.

http://www.landesbioscience.com/journals/prion/article/14283



Commentary ß-amyloid oligomers and prion protein: Fatal attraction?

Volume 5, Issue 1 January/February/March 2011 Gianluigi Forloni and Claudia Balducci

Gianluigi Forloni Corresponding author: forloni@marionegri.it

Claudia Balducci Biology of Neurodegenerative Diseases Lab; Department of Neuroscience; “Mario Negri” Institute for Pharmacological Research; Milano, Italy

The relationship between Alzheimer disease (AD) and prion-related encephalopathies (TSE) has been proposed by different points of view. Recently, the scientific attention has been attracted by the results proposing the possibility that PrPc, the protein whose pathologic form is responsible of TSE, can mediated the toxic effect of ß amyloid (Aß) oligomers. The oligomers are considered the culprit of the neurodegenerative process associated to AD, although the pathogenic mechanism activated by these small aggregates remain to be elucidated. In the initial study based on the binding screening PrPc was identified as ligand /receptor of Aß oligomers, while long term potentiation (LTP) analysis in vitro and behavioural studies in vivo, demonstrated that the absence of PrPc abolished the damage induced by Aß oligomers. The high affinity binding Aß oligomers-PrPc has been confirmed, whereas a functional role of this association has been excluded by three different studies. We approached this issue by the direct application of Aß oligomers in the brain followed by the behavioural examination of memory deficits. Our data using PrP knock-out mice suggest that Aß 1-42 oligomers are responsible for cognitive impairment in AD but PrPc is not required for their effect. Similarly, in two other studies the LTP alterations induced by Aß 1-42 oligomers was not influenced by the absence of PrP. Possible explanations of these contradictory results are discussed.



http://www.landesbioscience.com/journals/prion/article/14367/



http://www.landesbioscience.com/journals/prion/toc/volume/5/issue/1/




BSE101/1 0136

IN CONFIDENCE

CMO

From: Dr J S Metters DCMO

4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES



http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf



CJD1/9 0185

Ref: 1M51A

IN STRICT CONFIDENCE

From: Dr. A Wight

Date: 5 January 1993

Copies:

Dr Metters

Dr Skinner

Dr Pickles

Dr Morris

Mr Murray


TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES


http://collections.europarchive.org/tna/20080102191246/http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf


Friday, October 22, 2010


Peripherally Applied Aß-Containing Inoculates Induce Cerebral ß-Amyloidosis


http://betaamyloidcjd.blogspot.com/2010/10/peripherally-applied-containing.html




Friday, September 3, 2010

Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids, Prionpathy, Prionopathy, TSE


http://betaamyloidcjd.blogspot.com/2010/09/alzheimers-autism-amyotrophic-lateral.html




http://betaamyloidcjd.blogspot.com/




Posted On December 20, 2003 AFTER THE FIRST CASE OF MAD COW DISEASE IN THE USA WAS DOCUMENTED


" Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. "


http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers




SO, just who are The Center for Consumer Freedom ;

http://www.consumerfreedom.com/index.cfm



let's take a closer look shall we ;

The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"

CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.

http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom


http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom



What Is the Center for Consumer Freedom, and Why Is It Attacking PETA?

The Center for Consumer Freedom is a nonprofit corporation run by lobbyist Richard Berman through his Washington, D.C.-based for-profit public relations company, Berman & Co. The Center for Consumer Freedom, formerly known as the Guest Choice Network, was set up by Berman with a $600,000 “donation” from tobacco company Philip Morris.

Berman arranges for large sums of corporate money to find its way into nonprofit societies of which he is the executive director. He then hires his own company as a consultant to these nonprofit groups. Of the millions of dollars “donated” by Philip Morris between the years 1995 and 1998, 49 percent to 79 percent went directly to Berman or Berman & Co.

Richard Berman is an influence peddler. He has worked out a scheme to funnel charitable donations from wealthy corporations into his own pocket. In exchange, he provides a flurry of disinformation, flawed studies, op-ed pieces, letters to the editor, and trade-industry articles, as well as access to his high-level government contacts, who are servants of the industries he represents.

Berman’s name might sound familiar. In 1995, Berman and Norm Brinker, his former boss at Steak and Ale Restaurants, were identified as the special-interest lobbyists who donated the $25,000 that disgraced then-House Speaker Newt Gingrich, who was hauled before the House Ethics Committee for influence-peddling over the money. Berman and Brinker were lobbying against raising the minimum wage.

Richard Berman is a spin doctor. For example, he has argued against a Mothers Against Drunk Driving (MADD) initiative to lower the blood alcohol content (BAC) limit for drivers by claiming that the stricter limits would punish responsible social drinkers. He has claimed that U.S. Centers for Disease Control and Prevention (CDC) warnings about salmonella-related food poisoning are just “whipping up fear over food.”

Here’s how an internal Philip Morris memo described Berman’s spin: “His proposed solution would broaden the focus of the ‘smoking issue,’ and expand into the bigger picture of over-regulation.” Smoking won’t kill you; over-regulation will.

Berman is “a one-man wrecking crew on important issues.” His approach has been described as “misleading” and “despicable.” Berman has been called “a tobacco company whore,” but he’s branched out since then.

Using “freedom of choice” as his battle cry, Berman has now taken on PETA and a number of other groups and organizations whose points of view could have an impact on the profits of his clients by waking consumers up. Berman’s Guest Choice Network has an “advisory panel” whose members in 1998 included officials representing companies ranging from Cargill Processed Meat Products and Outback Steakhouse to Minnesota Licensed Beverage Association and Sutter Home Winery. Berman’s clients are companies with vested interests in low employee wages; cheap, unhealthy restaurant-chain food, particularly meat; and tobacco, soft drink, and alcohol consumption—companies like Ruth’s Chris Steakhouse, Armour Swift, and Philip Morris, whose product line includes Kraft Foods and everything from Marlboro cigarettes to Oscar Meyer wieners and which is a major shareholder in its former subsidiary Miller Brewing, now known as SABMiller.

PETA’s recent successes in gaining fast-food industry concessions for more humane conditions for farm animals have sent ripples of fear through the food and beverage service industry. About the same time that McDonald’s buckled to PETA’s demands, Richard Berman changed his front group’s name and stepped up his attacks.

The key to Berman’s aggressive strategy is, in his own words, “to shoot the messenger ... we’ve got to attack their credibility as spokespersons,”—an interesting remark from someone whose background and funding so severely challenge his own credibility.

http://www.consumerdeception.com/index.asp



NOW, what about that Journal of Neurology article published by Singeltary ;


JOURNAL OF NEUROLOGY

MARCH 26, 2003

Send Post-Publication Peer Review to journal:

Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

flounder@wt.net flounder9@verizon.net


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

http://www.neurology.org/cgi/eletters/60/2/176#535



about sporadic CJD and BSE ;

CJD RISING SWITZERLAND

CJD is a predominantly sporadic disorder but can also occur as a dominantly inherited or infective condition. Only one of the 26 most recent confirmed cases was identified as carrying a disease related mutation of the PRNP gene, none had identifiable iatrogenic exposure, and none resembled variant CJD. Thus 25 of the 26 cases appear to be sporadic cases. Sporadic CJD is distributed worldwide with a reported incidence of about one in a million per year. Raised awareness of the disease in recent years could account for an increase in reported cases of CJD, although neither an increase in the average age of patients nor more frequent recognition of CJD amongst residents of nursing homes (where dementing illness is prevalent and misdiagnosis might be expected) were seen in the Swiss cases. Moreover, improved ascertainment as an explanation for the observed increase would imply levels of under-reporting in countries other than Switzerland, which appear implausible. The authors of the Lancet report suggest that the rise in cases might be due to some form of unidentified iatrogenic transmission or to exposure to a zoonotic source of infection, though cases do not resemble variant Creutzfeldt-Jakob disease (vCJD). The ongoing surveillance of CJD in Switzerland and the rest of Europe is essential to monitor the situation to see if this rise is sustained in Switzerland, and if a similar rise occurs in other countries (see http://www.eurocjd.ed.ac.uk).

http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=1921



Prion data suggest BSE link to sporadic CJD Declan Butler

Predicting the number of cases of Creutzfeldt-Jakob disease (CJD) in people as a result of transmission of bovine spongiform encephalopathy (BSE) has just got more difficult.Whereas it was thought that BSE only caused a new form of the disease called variant CJD (vCJD), a study in mice from a team led by John Collinge at University College London suggests that it may also cause a disease indistinguishable from the commonest form of classical, or 'sporadic', CJD...

http://www.nature.com/nature/journal/v420/n6915/full/420450a.html




Sent: Saturday, December 11, 2010 3:17 PM

Subject: Species-barrier-independent prion replication in apparently resistant species

Species-barrier-independent prion replication in apparently resistant species

Pertenece a: UCL University College London Eprints

Descripción: Transmission of prions between mammalian species is thought to be limited by a "species barrier," which depends on differences in the primary structure of prion proteins in the infecting inoculum and the host, Here we demonstrate that a strain of hamster prions thought to be nonpathogenic for conventional mice leads to prion replication to high levels in such mice but without causing clinical disease. Prions pathogenic in both mice and hamsters are produced. These results demonstrate the existence of subclinical forms of prion infection with important public health implications, both with respect to iatrogenic transmission from apparently healthy humans and dietary exposure to cattle and other species exposed to bovine spongiform encephalopathy prions, Current definitions of the species barrier, which have been based on clinical endpoints, need to be fundamentally reassessed.


Autor(es): Hill, AF - Joiner, S - Linehan, J - Desbruslais, M - Lantos, PL - Collinge, J -

Id.: 52395313

Versión: 1.0

Estado: Final

Palabras clave: TRANSMISSIBLE MINK ENCEPHALOPATHY, CREUTZFELDT - JAKOB - DISEASE, FATAL FAMILIAL INSOMNIA, STRAIN VARIATION, TRANSGENIC MICE, SCRAPIE INFECTIVITY, HAMSTER SCRAPIE, VARIANT CJD, BSE AGENT, PROTEIN -

Tipo de recurso: Article -

Tipo de Interactividad: Expositivo

Nivel de Interactividad: muy bajo

Audiencia: Estudiante - Profesor - Autor -

Estructura: Atomic

Coste: no

Copyright: sí

Requerimientos técnicos: Browser: Any -

Fecha de contribución: 10-dic-2010

Contacto:

http://biblioteca.universia.net/html_bura/ficha/params/id/52395313.html



for those interested, see more here with comments........


Saturday, December 11, 2010

Species-barrier-independent prion replication in apparently resistant species

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/species-barrier-independent-prion.html



Thursday, November 18, 2010

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html




Wednesday, December 22, 2010

Manitoba veterinarian has been fined $10,000 for falsifying certification documents for U.S. bound cattle and what about mad cow disease ?

http://usdameatexport.blogspot.com/2010/12/manitoba-veterinarian-has-been-fined.html




Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html




Monday, November 22, 2010

Atypical transmissible spongiform encephalopathies in ruminants: a challenge for disease surveillance and control

REVIEW ARTICLES

http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/atypical-transmissible-spongiform.html



Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html



Seven main threats for the future linked to prions

The NeuroPrion network has identified 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.


http://www.neuroprion.org/en/np-neuroprion.html



Thursday, August 12, 2010

Seven main threats for the future linked to prions


http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html



http://prionpathy.blogspot.com/



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://collections.europarchive.org/tna/20080102185948/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



Sunday, November 28, 2010

Variably protease-sensitive prionopathy in a PRNP codon 129 heterozygous UK patient with co-existing tau, a synuclein and AB pathology


http://prionopathy.blogspot.com/2010/11/variably-protease-sensitive-prionopathy.html



what about that sheep scrapie, and how the feds so freely said that sheep scrapie has and would never transmit to humans......well, think again. ...terry

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

http://bse-atypical.blogspot.com/2010/11/increased-susceptibility-of-human-prp.html



Sunday, December 12, 2010

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/efsa-reviews-bsetse-infectivity-in.html



Tuesday, March 16, 2010

COMMONWEALTH OF AUSTRALIA Hansard Import restrictions on beef FRIDAY, 5 FEBRUARY 2010 AUSTRALIA

COMMONWEALTH OF AUSTRALIA

Proof Committee Hansard

RRA&T 2 Senate Friday, 5 February 2010

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

[9.03 am]

BELLINGER, Mr Brad, Chairman, Australian Beef Association

CARTER, Mr John Edward, Director, Australian Beef Association

CHAIR—Welcome. Would you like to make an opening statement?

Mr Bellinger—Thank you. The ABA stands by its submission, which we made on 14 December last year, that the decision made by the government to allow the importation of beef from BSE affected countries is politically based, not science based. During this hearing we will bring forward compelling new evidence to back up this statement. When I returned to my property after the December hearing I received a note from an American citizen. I will read a small excerpt from the mail he sent me in order to reinforce the dangers of allowing the importation of beef from BSE affected countries. I have done a number of press releases on this topic, and this fellow has obviously picked my details up from the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He states, and rightfully so:

You should be worried. Please let me explain. I’ve kept up with the mad cow saga for 12 years today, on December 14th 1997, some four months post voluntary and partial mad cow feed ban in the USA, I lost my mother to the Heidenhain variant Creutzfeldt-Jakob disease (CJD). I know this is just another phenotype of the infamous sporadic CJDs. Here in the USA, when USA sheep scrapie was transmitted to USA bovine, the agent was not UK BSE—it was a different strain. So why then would human TSE from USA cattle look like UK CJD from UK BSE? It would not. So this accentuates that the science is inconclusive still on this devastating disease. He goes on to state:

The OIE— the International Organisation of Epizootics, the arm of the WTO— is a failed global agent that in my opinion is bought off via bogus regulations for global trade and industry reps. I have done this all these years for nothing but the truth. I am a consumer, I eat meat, but I do not have to sit idly by and see the ignorance and greed of it all while countless numbers of humans and animals are being exposed to the TSE agents. All the USA is interested in is trade, nothing else matters.

Even Dr Stanley Prusiner, who incidentally won the Nobel Health Prize in 1997 for his work on the prion—he invented the word ‘prion’, or it came from him—states:

snip...see full text 110 pages ;

http://www.aph.gov.au/hansard/senate/commttee/S12742.pdf



for those interested, please see much more here ;


http://docket-aphis-2006-0041.blogspot.com/2010/03/commonwealth-of-australia-hansard.html



http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html



Tuesday, July 13, 2010


(SEE BEEF PRODUCTS EXPORTED TO AUSTRALIA FROM USA...TSS)


AUSTRALIAN QUESTIONNAIRE TO ASSESS BSE RISK (OIE) Terrestrial Animal Health Code, 2009 and USA export risk factor for BSE to Australia

http://usdameatexport.blogspot.com/2010/07/australian-questionnaire-to-assess-bse.html



Saturday, August 14, 2010

USA NON-SPECIES CODING SYSTEM (BEEF IMPORT EXPORT BSE RISK THERE FROM)

US denies it's illegally sending beef to Australia ?

Friday, 13/08/2010

http://usdameatexport.blogspot.com/2010/08/usa-non-species-coding-system-beef.html



Saturday, June 19, 2010

U.S. DENIED UPGRADED BSE STATUS FROM OIE

http://usdameatexport.blogspot.com/2010/06/us-denied-upgraded-bse-status-from-oie.html



Sunday, August 15, 2010

ATYPICAL BSE NOW LINKED TO CAUSING SPORADIC CJD OVERSEAS Commonwealth of Australia

http://bse-atypical.blogspot.com/2010/08/atypical-bse-now-linked-to-causing.html



Tuesday, January 5, 2010

JOINT STATEMENT FROM USTR, USDA ON TAIWAN'S ACTIONS TO UNJUSTIFIABLY RESTRICT U.S. BEEF IMPORTS IN VIOLATION OF OUR BILATERAL AGREEMENT Release No. 0002.10 Contact: USTR, Nefeterius McPherson (202) 395-3230 USDA, Caleb Weaver (202) 720-4623

http://usdavskorea.blogspot.com/2010/01/joint-statement-from-ustr-usda-on.html


2010


Dear Mr Singeltary,

We would very much like to interview you about the 7 main threats for the future linked to prions for our program series !

is an internet and satellite television station broadcasting globally all news positive and constructive to the world 24 hours/day 7 days /week

It broadcasts in 40+ languages and has a potential viewing audience of 4 billion + world wide

If you are agreeable, would you be available the afternoon of Sunday October 3rd ? We would be driving from Houston. It takes 1 hour for the camera men to set up and then the interview lasts approximately 1 and 1/2 hours.

snip...

"Dear Houston center,

Would you please contact this person for an interview?

Guest : Terry Singeltary

"My mother was murdered by what I call corporate and political homicide i.e. FOR PROFIT! she died from a rare phenotype of CJD i.e. the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. sporadic, simply meaning from unknown route and source. I have simply been trying to validate her death DOD 12/14/97 with the truth."


http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html



http://www.blogger.com/profile/06986622967539963260



So the interview is to raise the awareness of the general public to this very real risk of prion disease.

The interview would be from the angle of your own personal experience /personal research and advocacy.

Wishing you all the very best with your upcoming surgery!

snip...Taiwan...end...TSS



Friday, April 02, 2010 U.S.

beef trade talks to continue but curbs to remain: Japan

http://bse-atypical.blogspot.com/2010/04/us-beef-trade-talks-to-continue-but.html



Even McDonald’s, an international business symbolic of American culture, advertises that it uses only “pure Australian beef” in South Korea. Burger King announced that it only uses beef from Australia and New Zealand. Why? Even famous brands like McDonald’s cannot survive if they are perceived as using unsafe ingredients. They know that Koreans still do not trust the safety of American beef and must distance their brands from American beef.

Therefore the U.S. should aim to export only the best quality beef to Korea and regain the Korean people’s trust. Regaining Koreans’ confidence in U.S. beef will be a long-term gain for many American industries seeking to access the 12th largest economy in the world.

How will we know that U.S. beef has regained trust in South Korea? When McDonald’s in South Korea announces it uses “pure American beef.”

Kwon Seung-woo, a professor at Korea University Business School


http://joongangdaily.joins.com/article/view.asp?aid=2928098



hmmmm, let's see just what the BIG MAC himself had to say ;


Wednesday, November 10, 2010

McDonald's and USA BSE aka mad cow disease McDonald's AND Seriologicals USA NOT PROTECTED FROM MAD COW

http://bse-atypical.blogspot.com/2010/11/mcdonalds-and-usa-bse-aka-mad-cow.html



Atypical BSE in Cattle

BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.

To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

snip...see full text ;

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

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

T. Singeltary

Bacliff, TX, USA

Background:

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

Methods:

12 years independent research of available data

Results:

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

Conclusion:

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

page 114 ;

http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf



To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



Wednesday, March 31, 2010

Atypical BSE in Cattle

http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html



UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html



PRION 2010 Meeting Report International Prion Congress: From agent to disease; September 8–11, 2010; Salzburg, Austria Volume 4, Issue 3 July/August/September 2010

http://www.landesbioscience.com/journals/prion/article/12764/



THIS FDA recall for CWD positive product in commerce, was NOT done for the welfare of the dead CWD postive elk. ...TSS

Wednesday, 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

RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

___________________________________

PRODUCT a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; CODE Elk Meats with production dates of December 29, 30, and 31

RECALLING FIRM/MANUFACTURER

Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009. Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.

REASON

Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).

VOLUME OF PRODUCT IN COMMERCE Unknown

DISTRIBUTION NV, CA, TX, CO, NY, UT, FL, OK

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm154840.htm



Sunday, 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

snip...

From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

Date: September 30, 2002 at 7:06 am PST

From: "Belay, Ermias"

To:

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

Ermias Belay, M.D. Centers for Disease Control and Prevention

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

From:

Sent: Sunday, September 29, 2002 10:15 AM

To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html



http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html



see full text ;

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html



Tuesday, February 09, 2010

Chronic Wasting Disease: Surveillance Update North America: February 2010



>>> In addition, we documented horizontal transmission of CWD from inoculated mice and to un-inoculated cohabitant cage-mates. <<<



http://ajp.amjpathol.org/cgi/content/abstract/ajpath.2010.090710v1



http://chronic-wasting-disease.blogspot.com/2010/02/chronic-wasting-disease-surveillance.html



There are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;

PPo3-7:

Prion Transmission from Cervids to Humans is Strain-dependent

Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

Key words: CWD, strain, human transmission

Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.



PPo2-27:

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.



PPo2-7:

Biochemical and Biophysical Characterization of Different CWD Isolates

Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany

Key words: CWD, strains, FT-IR, AFM

Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.



http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099



UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


http://chronic-wasting-disease.blogspot.com/




P35

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.pdf



Wednesday, November 17, 2010

CWD Update 98 November 10, 2010


http://chronic-wasting-disease.blogspot.com/2010/11/cwd-update-98-november-10-2010.html



http://chronic-wasting-disease.blogspot.com/



yep, but the SECOND passage was especially a doozy, and remember, oral transmission will take much longer than intracerebral route, and we now have two documented strains of cwd i.e. the regular strain of cwd (whatever the hell that means), and the Wisconsin strain, with probably more in the pipeline. NOW, THE MILLION DOLLAR QUESTION, WAS THE WISCONSIN CWD STRAIN INCLUDED IN THE ORAL TRANSMISSION STUDY ?

also, cwd has been transmitted to deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi).

considering scrapie, over 20 regular strains, with the atypical NOR-98, TWO documented TME strains i.e. hyper and drowsy, c-BSE, h-BSE, l-BSE, all in North America, all of which have been rendered and fed to animals for human and animal food..............terry

Title: Experimental Second Passage of Chronic Wasting Disease (Cwd(mule Deer)) Agent to Cattle

Authors

Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen

Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.

Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.


http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=178318



PLUS, oral transmission between cervids, either infected carcases AND ESPECIALLY FEED THAT HAS ANIMAL PROTEIN, PLEASE SEE ;

PRODUCT Custom deer feed made for a Wisconsin farm. The product was in bags holding about 40 pounds each. Recall # V-122-4. CODE 1-30-04 on the product invoice and mixing record. RECALLING FIRM/MANUFACTURER Crivitz Feed Mill, Crivitz, WI, by telephone on February 20, 2004. Wisconsin State initiated recall is complete. REASON The recalled deer feed contained steamed bone meal which is prohibited material in feed for ruminants.

VOLUME OF PRODUCT IN COMMERCE 515 pounds.

DISTRIBUTION WI.

END OF ENFORCEMENT REPORT FOR APRIL 7, 2004

###

http://www.fda.gov/bbs/topics/enforce/2004/ENF00842.html



Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)

SEE where sporadic cjd in the USA went from 59 cases in 1997, to 216 cases in 2009. a steady increase since 1997. ...TSS

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1997 114 68 59 9 0 0

to

2009 425 259 216 43 0 0

http://www.cjdsurveillance.com/pdf/case-table.pdf



see full text ;

http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html



2010

PLEASE NOTE REFERENCE LINES 5. AND 6. AT BOTTOM ;

Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 88 52 44 7 1 0

1999 120 72 64 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 1(3)

2005 344 194 157 36 1 0

2006 383 197 166 29 0 2(4)

2007 377 214 187 27 0 0

2008 394 231 204 25 0 0

2009 425 259 216 43 0 0

2010 204 124 85 20 0 0

TOTAL 3702(5) 2177(6) 1834 315 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

http://www.cjdsurveillance.com/pdf/case-table.pdf



Tuesday, December 14, 2010

Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings part 4, Annex A1, Annex J, UPDATE DECEMBER 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/12/infection-control-of-cjd-vcjd-and-other.html



Tuesday, December 14, 2010 TAFS1

Position Paper on Relaxation of the Feed Ban in the EU SUMMARY © TAFS, Berne, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/tafs1-position-paper-on-relaxation-of.html



Saturday, December 18, 2010

OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html




Merry Christmas..............PEACE !

kindest regards, terry

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518