Saturday, December 18, 2010

First probable human case of mad cow disease in Taiwan was listed posthumously 2010/12/18 21:14:28

1st case of probable mad cow disease listed posthumously in Taiwan 2010/12/18 21:14:28

Taipei, Dec. 18 (CNA) The first probable human case of mad cow disease in Taiwan was listed posthumously Saturday, following the death in May of a man who had symptoms of the fatal brain-wasting illness.

The listing was made after officials and experts on a Department of Health (DOH) panel on Creutzfeldt-Jakob Disease (CJD) held a meeting to determine whether the man had died from the disease as result of eating infected beef.

"We believe it is very likely that the man who died in May this year contracted the disease during his stay in the United Kingdom, " the DOH said in a press statement. "We cannot rule out the possibility that he ate infected beef during that time."

Scientists believe that many years after eating cattle infected with bovine spongiform encephalopathy (BSE) , commonly known as mad cow disease, humans can develop symptoms of new variant CJD (vCJD) , also known as human mad cow disease.

The 36-year-old man had lived in the U.K. between 1989 and 1997, when mad cow disease was at its peak in that country. He began to show vCJD symptoms, including memory loss and hypersomnia, in 2008. Doctors reported the case to the DOH's Centers for Disease Control in March 2009.

As his family refused to give doctors permission to perform an autopsy, the DOH said, it could not list the patient as a confirmed case of vCJD. His body has since been cremated.

Though the cause of death could not be determined by means of an autopsy, it was an extremely likely case of vCJD, based on the man's symptoms, travel history and the results of magnetic resonance imaging and electroencephalograms, the DOH said.

According to the DOH's CJD advisory panel, it was unlikely that the patient contracted the disease in Taiwan.

"His death could be counted as an imported case of vCJD and unlikely to pose any threat to Taiwan's disease control network," the DOH statement said.

Citing its tracking records, the DOH said the man had donated blood to two patients 10 years ago.

"Neither of them has contracted the disease," the statement said, adding that precautionary measures had been taken to prevent any spread of the disease during the time the man was hospitalized in Taiwan.

According to the World Health Organization, CJD is a fatal human degenerative condition characterized by progressive brain dysfunction and is categorized into four forms -- sporadic, familial, iatrogenic and variant.

The UK Department of Health has said vCJD differs from CJD in that the former is more likely to strike younger people.

Since 1997 when the DOH set up a CJD reporting and monitoring system, 436 suspected CJD or vCJD have been reported in Taiwan, DOH figures show. Of that number, 246 were listed as possible or extremely possible cases of sporadic or familial forms of CJD, five were confirmed as traditional forms of CJD and one was listed as probable vCJD, according to the DOH tallies.

The others were ruled out as possible cases of CJD.

(By Chen ching-fang and Sofia Wu) enditem /pc

http://focustaiwan.tw/ShowNews/WebNews_Detail.aspx?ID=201012180020&Type=aLIV


Thursday, November 25, 2010

Probable variant Creutzfeldt-Jakob disease in Asia: A case report from Taiwan and review of two prior cases

http://creutzfeldt-jakob-disease.blogspot.com/2010/11/probable-variant-creutzfeldtjakob.html


Sunday, October 24, 2010

Australia Mad cow assessments come to a standstill, USDA hasn't a clue $

http://usdameatexport.blogspot.com/2010/10/australia-mad-cow-assessments-come-to.html


2010

Rural and Regional Affairs and Transport References Committee The possible impacts and consequences for public health, trade and agriculture of the Government’s decision to relax import restrictions on beef Final report June 2010

2.65 At its hearing on 14 May 2010, the committee heard evidence from Dr Alan Fahey who has recently submitted a thesis on the clinical neuropsychiatric, epidemiological and diagnostic features of Creutzfeldt-Jakob disease.48 Dr Fahey told the committee of his concerns regarding the lengthy incubation period for transmissible spongiform encephalopathies, the inadequacy of current tests and the limited nature of our current understanding of this group of diseases.49

2.66 Dr Fahey also told the committee that in the last two years a link has been established between forms of atypical CJD and atypical BSE. Dr Fahey said that: They now believe that those atypical BSEs overseas are in fact causing sporadic Creutzfeldt-Jakob disease. They were not sure if it was due to mad sheep disease or a different form. If you look in the textbooks it looks like this is just arising by itself. But in my research I have a summary of a document which states that there has never been any proof that sporadic Creutzfeldt-Jakob disease has arisen de novo—has arisen of itself. There is no proof of that. The recent research is that in fact it is due to atypical forms of mad cow disease which have been found across Europe, have been found in America and have been found in Asia. These atypical forms of mad cow disease typically have even longer incubation periods than the classical mad cow disease.50

http://www.aph.gov.au/senate/committee/rrat_ctte/mad_cows/report/report.pdf


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:

The BSC policy was set up for one purpose only, trade—the illegal trading of all strains of TSE globally throughout North America, which is home to CBSC, IBSC and HBSC, many scrapie strains and two strains of CJD to date. (please note typo error, those should have read cBSE, lBSE, and hBSE...tss)

I would also like, while I have the opportunity, to explain the beef-off-the-shelves myth. At the first Senate hearing on 14 December, it was explained that the reason why they allowed BSC beef into Australia was the beef-off-the-shelves policy, whereby if we found a case of BSC in Australia they would have to recall all—

Friday, 5 February 2010 Senate RRA&T 3

RURAL AND REGIONAL AFFAIRS AND TRANSPORT

Senator HEFFERNAN—Which of course is total BS.

Mr Bellinger—Correct. This is written in the FSANZ document—Food Standards Australia New Zealand. Why isn’t this same policy in New Zealand? It is not—it is only in Australia. We are the only country in the world to have this idiotic policy. So we again call for the tabling of the WTO obligations paperwork. We do not believe that exists.

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


Friday, October 15, 2010 U.S.

Beef Talks May Progress as Japan Gathers Mad-Cow Disease Risk Data about U.S.A.

http://docket-aphis-2006-0041.blogspot.com/2010/10/us-beef-talks-may-progress-as-japan.html


Tuesday, December 29, 2009

Taiwan to resume USA beef ban over mad cow disease threat

http://usdavskorea.blogspot.com/2009/12/taiwan-to-resume-usa-beef-ban-over-mad.html


Monday, November 30, 2009

Taiwan, USDA, and USA beef, what the consumer does not know, could kill them

http://usdavskorea.blogspot.com/2009/11/taiwan-usda-and-usa-beef-what-consumer.html


Tuesday, November 10, 2009

Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan and USA

http://usdavskorea.blogspot.com/2009/11/surveillance-on-bovine-spongiform.html


Name: Terry S. Singeltary Sr. Date: Jan 26, 2007

Dear Terry S. Singeltary Sr.

My name in Seoungwon Lee and I work for National Assemblywoman (MP) Sang-Jeong Sim, in South Korea. Below is a message from Mr. Kwon. Please get back to us regarding the letter.

Thank you.

Seoungwon Lee Legislative Assistant National Assembly Republic of Korea

Dear Terry S. Singeltary Sr.

Greetings from Korea.

I have learned about what you and your family have been through a internet. Being the father of a small family, I can only imagine the sense of loss that you and your family still must feel regarding your mother.

Through the internet, many people here in Korea have learnt about the story of your family and it has created a great deal of concern. Your experience had particular relevance for the citizens here, for the Korean government, in connection to the free trade agreement it is negotiating with the United States, is about to restart the sale of the unsafe American beef to the general public.

The Korean government has already imported the first load American beef and is currently going through the inspection period. There has been a great deal of controversy regarding the safety of these products, and a precipitous increase in public interest regarding the causes and symptoms of vCJD.

It is in this context that we are preparing a session together with National Assembly members and relevant NGOs to hear from those who have had direct experience with the human variant of BSE. We are very interested in hearing about the symptoms that your mother showed, your views on the response from the US government to the many deaths that resulted from this disease, the reaction from the general public, and any other area that you would wish to speak about. There would also be experts and academics in the area to speak at the session as well. We believe that it would greatly contribute to raising awareness about the issue, as well as help politicians and civic activists to consider the repercussions of the beef import issue.

We would like to request your help in this regard. We are planning for the session to be held in Seoul on the 23rd of this November. We would very much like to have you present in order to help prevent such tragic incidents from happening in Korea. We would, of course, pay for the trip and accommodations for the duration of your stay. If you were to participate, we could also meet with members from the agricultural committee of the National Assembly and from other related organizations to urge more interest to the issue.

Please do not hesitate to offer suggestions or ask us any questions that you might have. We look forward to a positive response and to meeting you in Seoul.

Thank you.

Sincerely, Sim Sang-Jeong

Head of the Democratic Labor Party Parliamentary Committee on the Korea-US FTA Member of the National Assembly Republic of Korea

http://www.fpif.org/fpiftxt/3940


http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html


June 11, 2008, 10:14PM

U.S. slams door on revising S. Korea beef

import pact Pressed at home, Seoul had wanted 30-month limit on age of the cattle

http://www.chron.com/disp/story.mpl/nation/5832282.html


http://usdavskorea.blogspot.com/2008/06/us-slams-door-on-revising-s-korea-beef.html


BSE YOUNGEST AGE STATISTICS UNDER 30 MONTHS

http://bseyoungestage.blogspot.com/


Tuesday, May 13, 2008

Concerned Americans against Mad Cow Disease STATEMENT OF SOLIDARITY with Koreans May 13, 2008

http://usdavskorea.blogspot.com/2008/05/concerned-americans-against-mad-cow.html


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


Subject: Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION


Date: August 24, 2005 at 2:47 pm PST

August 24, 2005

Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION

Greetings APHIS ET AL,

My name is Terry S. Singeltary Sr.

I would kindly like to comment on [Docket No. 05-004-1] RIN 0579-AB93 ;

PROPOSED RULES

Exportation and importation of animals and animal products:

Whole cuts of boneless beef from-

Japan,

48494-48500 [05-16422]

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=0900006480086ebc&disposition=attachment&contentType=msw6


Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA

https://web01.aphis.usda.gov/BSEcom.nsf/0/b78ba677e2b0c12185256dd300649f9d?OpenDocument&AutoFramed


PLEASE SEE FULL TEXT HERE ;

Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA

http://madcowfeed.blogspot.com/2008/07/docket-no-03-080-1-usda-issues-proposed.html


Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028 Public Submission Title Comment from Terry S Singletary

Comment 2006-2007 USA AND OIE POISONING GLOBE WITH BSE MRR POLICY

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted products from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone. These are the facts as I have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species.

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did...

http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801f8151


Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;

BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f8152&disposition=attachment&contentType=msw8


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


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


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


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/



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, 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


Friday, December 17, 2010

PRION DISEASE Action Plan National Program 103 Animal Health 2012-2017

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/prion-disease-action-plan-national.html


P.9.21

Molecular characterization of BSE in Canada

Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada

Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.

Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.

Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.

http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf


Wednesday, August 11, 2010

REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html


Thursday, August 19, 2010

REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html


Thursday, August 19, 2010

SCRAPIE CANADA UPDATE Current as of 2010-07-31 The following table lists sheep flocks and/or goat herds confirmed to be infected with scrapie in Canada in 2010.

Current as of: 2010-07-31

http://nor-98.blogspot.com/2010/08/scrapie-canada-update-current-as-of.html


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.

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


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


PEACE !

TSS

Labels: ,

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

Infection control of CJD, vCJD and other human prion diseases in healthcare and community settings

Part 4 has been redrafted (February 2010) to clarify how best to manage patients in healthcare and community settings. A number of recent policy decisions have been incorporated into this guidance including:

• Standard infection control precautions should be used to clear up spillages as quickly as possible of all material from patients with, or "at increased risk" of, CJD/vCJD in a healthcare setting. 10,000ppm rather than 20,000ppm sodium hypochlorite is recommended for practical purposes.

• High or medium risk tissues from patients with, or "at increased risk" of, CJD or vCJD, should be incinerated, and low risk tissues or body fluids should follow normal clinical waste disposal.

• Instruments used in high or medium risk procedures on patients with, or "at increased risk" of, CJD/vCJD can be quarantined and re-used exclusively on the same patient, subject to tracking of instruments throughout the decontamination cycle, and ensuring that under no circumstances should quarantined instrument sets be reprocessed for use on other patients unless the diagnosis of CJD or vCJD has been positively excluded.

• Individuals who have been identified prior to high risk surgery as having received blood or blood components from 80 or more donors since January 1980 are now designated as "at increased risk" of vCJD and have been added to Table 4a.

• The anterior eye has been reclassified as low risk with regards to tissue infectivity.

In addition, updated information on other guidance, including dentistry, anaesthesia and intensive care, has been incorporated.

Published: 2 June 2003 Revised and updated: 13 December 2010

CONTENTS

• Introduction

• Other relevant guidance

Caring for patients with, or "at increased risk" of, CJD or vCJD

Management arrangements for infection control

• Tissue infectivity

• Iatrogenic transmission

CJD

vCJD

• Patient categorisation

Patients "at increased risk" of CJD or vCJD

• Hospital care of patients

Taking samples and other invasive medical procedures

Spillages

Clinical waste

Childbirth

Bed linen

Occupational exposure

Surgical procedures and instrument management

Single use instruments

Handling of instruments that are not designated as single-use

Quarantining instruments

Decontamination of instruments

Storage of instruments for research purposes

Incineration of instruments

Complex instruments

Use of laser for tonsillectomy – smoke plumes

Anaesthesia and intensive care

Endoscopy

Ophthalmology

• Community healthcare

Caring for symptomatic patients at home

Spillages

Clinical waste

Published: 2 June 2003

Revised and updated: 13 December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4

Bed linen

• Pregnancy

• Dentistry

• After death

PLEASE SEE FULL TEXT 24 PAGES ;

http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_122647.pdf


Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1 ANNEX A1

Distribution of TSE infectivity in human tissues and body fluids

A1.1 There is evidence that the distribution of the disease-specific partially protease-resistant form of prion protein (PrPTSE) in tissues is more widespread in the body in variant CJD (vCJD) patients than in patients affected by sporadic CJD (1, 2, 3). In sporadic CJD, the presence of abnormal prion protein in patients with clinical disease appears to be restricted to the central nervous system (CNS). However, abnormal prion protein has been detected in various lymphoid tissues, including tonsils, spleen, gastrointestinal lymphoid tissue (appendix and rectum), lymph nodes, thymus and adrenal gland of patients with clinical vCJD. Abnormal prion protein has also been detected in lymphoid tissues within the appendix removed from 2 patients some 8 and 24 months before they developed vCJD (4, 5) suggesting that abnormal prion protein could be present in the lymphoid tissue of people incubating vCJD for some time before the onset of clinical disease. In similar tests, abnormal prion protein has not been detected in these tissues from sporadic CJD patients. Infectivity has been demonstrated in tonsil and spleen in vCJD by experimental transmission (6).

A1.2 PrPTSE has been identified in posterior spinal nerve roots in only an occasional case of sporadic CJD and GSS (7), but not in peripheral nerve in vCJD (3, 8). Transmission studies on peripheral nerve samples from cases of sporadic CJD by intracerebral inoculation into primates have shown no evidence of infectivity (9). PrPTSE has been detected in spinal dorsal root ganglia and trigeminal ganglia in vCJD (8), and in trigeminal ganglia in sporadic CJD (10). PrPTSE has also been detected in olfactory epithelium in sporadic CJD patients at post mortem (11), and in the olfactory tract in vCJD (12). Infectivity and PrPTSE have not been detected in dental pulp in a series of sporadic CJD cases (13), and PrPTSE was not detected in the alveolar nerve, dental pulp, gingiva, salivary gland, tongue in a small series of vCJD cases (14).

A1.3 Table A1 presents current information on the distribution of infectivity in tissues and body fluids in CJD other than vCJD, and in vCJD, based on data from experimental studies, where available, and on information from other studies of natural TSE disease in humans and animals. It also shows where PrPTSE has been detected in tissues. Published: 2 June 2003 1

Updated: December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1

A1.4 The precise relationship between the presence of PrPTSE and infectivity is not certain – for example, the absence of detectable PrPTSE does not necessarily mean absence of infectivity. Conversely, detection of small amounts of PrPTSE in a tissue does not necessarily mean that it will transmit disease in all circumstances. This guidance has been formulated on the basis of likelihood of the presence of infectivity using the identification of PrPTSE as a specific marker. In general terms, there is thought to be a broad correlation between PrPTSE load in a given tissue and the likelihood that the given tissue might present a risk of infection. The relative levels of PrPTSE in different tissues provide useful information for the assessment of relative risks of different procedures.

A1.5 In Table A1, tissue infectivity is classified as high, medium or low, on the basis of infectivity assays in experimental animals. Although such studies are limited in CJD and vCJD tissues, the preliminary data that are available support the findings in tissues from other natural and experimental TSE models. Therefore the relative levels of PrPTSE in different tissues provide useful information for the assessment of relative risks of different surgical and endoscopic procedures.

A1.6 The information given in this Annex describes the position at the time of publication. This will be kept under review and is subject to change as further information becomes available.

Table A1 – Distribution of TSE infectivity in human tissues and body fluids

Key: +ve = tested positive -ve = tested negative

NT = not tested P = infectivity proven in experimental transmission studies

SNIP...

1Spinal ganglia have a high assumed level of infectivity in the WHO Guidelines. However, unpublished results on the infectivity of spinal ganglia indicate that this tissue is of medium infectivity.

Published: 2 June 2003 3 Updated: December 2010 Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex A1 2Dura mater is designated low infectivity as virtually no detectable abnormal prion protein has been found in cases of CJD; however, as grafts of these tissues are associated with CJD transmission, probably as a result of contamination by brain and because of the lengthy period of implantation in the CNS, procedures conducted on intradural tissues (i.e. brain , spinal cord and intracranial sections of cranial nerves) or procedures in which human dura mater was implanted in a patient prior to 1992, remain high risk.

3Although PrPTSE has not been detected in the CSF in either sporadic or variant CJD (15), experimental transmission of infectivity has been achieved from CSF in sporadic CJD in 4 of 27 primates by intracerebral inoculation (9) indicating that levels of infectivity are likely to be much lower than in the central nervous system.

4PrPTSE has been detected in dura mater, skin, kidney, liver, pancreas, ovary and uterus in a case of vCJD in USA with a lengthy duration of illness (16). Earlier studies of these tissues in UK vCJD cases gave negative results (2,8,17).

References

SNIP... SEE FULL TEXT 5 PAGES ;

http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_122645.pdf


Summary of advice (revised January 2010)

Annex J provides a clear and pragmatic way of assessing CJD and vCJD risk prior to surgery or endoscopy. Growing numbers of patients have been informed that they are at increased risk of CJD or vCJD. Therefore it is recommended that all patients about to undergo any surgery or endoscopy should be asked if they have ever been notified as at increased risk of CJD or vCJD. This recommendation is outlined in paragraphs J1 and J2.

In addition, patients undergoing surgery or neuro-endoscopy which may involve contact with tissues of potentially high level TSE infectivity ("high risk tissues") should, through a set of detailed questions, be assessed for their possible CJD/vCJD risk exposure. These questions are outlined in Table J1 and paragraphs J3 to J6.

Annex J has been revised (July 2009) to include a new question to be asked of all patients about to undergo surgery or neuro-endoscopy on high risk tissues. This new question (question 4 in Table J1) has been added to identify those patients who have received blood or blood components from 80or more blood donors. These patients are now designated as at increased risk of vCJD by the CJD Incidents Panel. Table J1 and paragraph J6 provide guidance on how to identify those patients who have received multiple blood transfusions. An algorithm, included as Appendix A, guides health professionals through the process.

Annex J was further revised (January 2010) to encompass recent evidence that patients who underwent intradural neurosurgery or intradural spinal surgeryand received human-derived dura mater before August 1992 are at increased risk of sCJD, but not vCJD. Table J1 has been modified to reflect this change.

Published: 31 July 2006 Revised and updated: 14 December 2010 1Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J

Recommendation for all surgical and endoscopy patients

SNIP...PLEASE SEE FULL TEXT 10 PAGES ;

http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_122646.pdf


Saturday, December 11, 2010

Species-barrier-independent prion replication in apparently resistant species

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 -

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


PLEASE SEE FULL TEXT AND MORE HERE ;


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



Sunday, December 12, 2010

Predominant Involvement of the Cerebellum in Guinea Pigs Infected with Bovine Spongiform Encephalopathy (BSE)

Journal of Comparative Pathology Article in Press

http://creutzfeldt-jakob-disease.blogspot.com/2010/12/predominant-involvement-of-cerebellum.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



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



Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



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



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, November 30, 2010

Council conclusions on the TSE Road Map 2 A Strategy paper on Transmissible Spongiform Encephalopathies for 2010 - 2015

http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/council-conclusions-on-tse-road-map-2.html



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



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



CHRONIC WASTING DISEASE CWD

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



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)

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



SABTO

Advisory Committee on the Safety of Blood, Tissues and Organs

Summary of 3rd Public Meeting - "Organ transplantation - benefits and risks of higher- risk organs" 10am, 26 October 2010 Coin Street Neighbourhood Centre, London, SE1 9NH

http://www.dh.gov.uk/prod_consum_dh/groups/dh_digitalassets/@dh/@ab/documents/digitalasset/dh_122200.pdf



WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

also in the references at bottom i saw ;

12. A single positive marrow in multiple transmission attempts from cattle orally dosed with BSE-infected brain [Wells et al., 1999; Wells et al., 2005; Sohn et al., 2009].

http://www.who.int/bloodproducts/tablestissueinfectivity.pdf



Thursday, July 08, 2010

Nosocomial transmission of sporadic Creutzfeldt-Jakob disease: results from a risk-based assessment of surgical interventions Public release date: 8-Jul-2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/07/nosocomial-transmission-of-sporadic.html



Sunday, January 17, 2010

Human tissue, recovered from a donor history indicated increased risk factors for Creutzfeldt-Jacob disease Lions Eye Bank

http://creutzfeldt-jakob-disease.blogspot.com/2010/01/human-tissue-recovered-from-donor.html


Saturday, January 16, 2010 Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al

http://creutzfeldt-jakob-disease.blogspot.com/2010/01/evidence-for-cjd-tse-transmission-via.html


Friday, November 20, 2009

SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs Summary of the Eighth Meeting, 27 October 2009

http://vcjdtransfusion.blogspot.com/2009/11/sabto-advisory-committee-on-safety-of.html


Sunday, May 10, 2009

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html


2006

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4271t1.pdf


2004

http://www.fda.gov/ohrms/dockets/ac/04/transcripts/2004-4075T1.DOC


2003

Asante/Collinge et al, 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;


http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm


2001


http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf


Docket Management

Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater

Comment Number: EC -1

Accepted - Volume 1

http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004be11.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfe.html


http://www.fda.gov/ohrms/dockets/dailys/03/Jan03/012403/8004bdfc.html


Daily Dockets - 04/10/03

00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ...

www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003 - Cached


# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)

Docket Management

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm


Monday, August 17, 2009

Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Annex J,K, AND D Published: 2009

http://creutzfeldt-jakob-disease.blogspot.com/2009/08/transmissible-spongiform-encephalopathy.html


Tuesday, March 16, 2010

Transmissible Spongiform Encephalopathy Agents: Safe Working and the Prevention of Infection: Part 4 REVISED FEB. 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/03/transmissible-spongiform-encephalopathy.html


Friday, July 17, 2009

Revision to pre-surgical assessment of risk for vCJD in neurosurgery and eye surgery units Volume 3 No 28; 17 July 2009

http://creutzfeldt-jakob-disease.blogspot.com/2009/07/revision-to-pre-surgical-assessment-of.html


Tuesday, August 12, 2008

Biosafety in Microbiological and Biomedical Laboratories Fifth Edition 2007 (occupational exposure to prion diseases)

http://creutzfeldt-jakob-disease.blogspot.com/2008/08/biosafety-in-microbiological-and.html


Tuesday, May 11, 2010

Current risk of iatrogenic Creutzfeld-Jakob disease in the UK: efficacy of available cleaning chemistries and reusability of neurosurgical instruments

http://creutzfeldt-jakob-disease.blogspot.com/2010/05/current-risk-of-iatrogenic.html


Saturday, January 16, 2010

Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al

Evidence For CJD/TSE Transmission Via Endoscopes

http://creutzfeldt-jakob-disease.blogspot.com/2010/01/evidence-for-cjd-tse-transmission-via.html


Tuesday, June 1, 2010

USA cases of dpCJD rising with 24 cases so far in 2010

http://cjdtexas.blogspot.com/2010/06/usa-cases-of-dpcjd-rising-with-24-cases.html


Wednesday, June 16, 2010

Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties

http://creutzfeldt-jakob-disease.blogspot.com/2010/06/defining-sporadic-creutzfeldt-jakob.html


DID EVERYONE FILL OUT THEIR CJD QUESIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???

Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION

http://cjdquestionnaire.blogspot.com/


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

Labels:

Monday, December 13, 2010

NIH Study Suggests That Early Detection is Possible for Prion Diseases

FOR IMMEDIATE RELEASE Thursday, Dec. 2, 2010

Media Contact: Ken Pekoc (301) 402-1663 kpekoc@niaid.nih.gov

NIH Study Suggests That Early Detection is Possible for Prion Diseases

A fast test to diagnose fatal brain conditions such as mad cow disease in cattle and Creutzfeldt-Jakob disease in humans could be on the horizon, according to a new study from National Institutes of Health scientists. Researchers at NIH’s National Institute of Allergy and Infectious Diseases (NIAID) have developed a highly sensitive and rapid new method to detect and measure infectious agents called prions that cause these diseases.

“Although relatively rare in humans and other animals, prion diseases are devastating to those infected and can have huge economic impacts,” says Anthony S. Fauci, M.D., director of NIAID. “Scientists have promising concepts for developing therapies for people infected with prion diseases, but treatments only are helpful if it is known who needs them. This detection model could eventually bridge that gap.”

This image, magnified 100,000 times using a transmission electron microscope, shows thread-like structures of prion protein. View larger image Credit: NIAID/RML Prion diseases are primarily brain-damaging conditions also known as transmissible spongiform encephalopathies. They are difficult to diagnose, untreatable and ultimately fatal. A key physical characteristic of these diseases is dead tissue that leaves sponge-like holes in the brain. Prion diseases include mad cow disease, or bovine spongiform encephalopathy in cattle; scrapie in sheep; Creutzfeldt-Jakob disease in humans; and chronic wasting disease in deer, elk and moose. For more information about NIAID research on prion diseases, visit the NIAID Prion Diseases portal.

Currently available diagnostic tests lack the sensitivity, speed or quantitative capabilities required for many important applications in medicine, agriculture, wildlife biology and research. Because prion infections can be present for decades before disease symptoms appear, a better test might create the possibility for early treatment to stop the spread of disease and prevent death.

Now, a blending of previous test concepts by the NIAID group has led to the development of a new prion detection method, called real time quaking induced conversion assay, or RT-QuIC. This approach is described in a paper now online in the open-access journal PLoS Pathogens. Byron Caughey, Ph.D., led the study at NIAID’s Rocky Mountain Laboratories in Hamilton, Mont.

Scientists believe disease-causing prions are abnormal infectious clusters of prion protein molecules. Normally, prion protein molecules are unclustered, harmless and found in every mammal. In a process not fully understood, abnormal infectious clusters develop and can convert normal prion protein molecules into the infectious prion form; these clusters tend to gather in the brain. Ongoing replication allows the disease to spread and damage the brain.

Infectious prions also are found outside the brain, in saliva, blood, breast milk, urine and the nasal and cerebral spinal fluids used in the study. But the concentrations of infectious prions in these bodily fluids are so low that scientists, clinicians and wildlife biologists have not been able to measure them for routine purposes.

The new assay can detect when miniscule amounts of infectious prions initiate the conversion of large amounts of normal prion protein into an abnormal form in test-tube reactions. By comparing the extent to which different samples can be diluted and still initiate conversion, scientists can estimate the relative infectious concentrations in the original samples. In their study, the NIAID scientists used RT-QuIC to detect prion infections in deer known to have chronic wasting disease and sheep known to have scrapie. In scrapie-infected hamsters, they found surprisingly high levels of prions in nasal fluids, pointing to such fluids as possible sources of contagion in various prion diseases.

Along with optimizing their existing applications in the laboratory, Dr. Caughey and his colleagues are teaming up with a number of other laboratories around the world to extend the practical and scientific applications of RT-QuIC. Related testing approaches might also aid the diagnoses of similar neurodegenerative protein diseases, such as Alzheimer’s, Huntington’s and Parkinson’s diseases. 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 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 http://www.nih.gov.

Reference: J Wilham et al. Rapid end-point quantitation of prion seeding activity with sensitivity comparable to bioassays. PLoS Pathogens 6(12): e1001217. DOI: 10.1371/journal.ppat.1001217 (2010).

--------------------------------------------------------------------------------

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 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.

http://www.niaid.nih.gov/news/newsreleases/2010/Pages/prionCaughey.aspx


http://www.niaid.nih.gov/topics/prion/Pages/default.aspx


Rapid End-Point Quantitation of Prion Seeding Activity with Sensitivity Comparable to Bioassays Prion diseases are deadly infectious neurodegenerative disorders of mammals which involve the misfolding of host prion protein. To better manage these diseases, we need to be able to detect and quantify the infectious particles, or prions, in biological samples. However, current tests lack the sensitivity, speed and/or quantitative capabilities required for many important applications in medicine, agriculture, wildlife biology and research. To address this problem, we have developed a new prion assay that is highly sensitive, rapid, and quantitative. This assay takes advantage of the ability of miniscule amounts of infectious prions to seed the misfolding of large excesses of normal prion protein in test tube reactions. Quantitation is achieved by testing a range of sample dilutions and determining loss of seeding activity, i.e. the end-point dilution. Similar analyses have long been used to quantify prions by inoculation into animals; however, such bioassays take months or years to perform and are both animal-intensive and expensive. Our new method provides a more practical means of detecting and quantifying prions. So far, we have applied this assay to prions from sheep, deer, and hamsters, and have found surprisingly high levels of prions in the nasal and cerebral spinal fluids of infected hamsters.

Article Metrics Related Content Comments: 0 To add a note, highlight some text. Hide notes Make a general comment Jump to

Abstract Author Summary Introduction Materials and Methods Results Discussion Supporting Information Acknowledgments Author Contributions References Jason M. Wilham1, Christina D. Orrú1,2, Richard A. Bessen3, Ryuichiro Atarashi4, Kazunori Sano4, Brent Race1, Kimberly D. Meade-White1, Lara M. Taubner1, Andrew Timmes1, Byron Caughey1*

1 Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Disease, Hamilton, Montana, United States of America, 2 Department of Biomedical Sciences and Technologies, University of Cagliari, Monserrato, Italy, 3 Veterinary Molecular Biology, Montana State University, Bozeman, Montana, United States of America, 4 Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Kyushu, Japan

Abstract Top A major problem for the effective diagnosis and management of prion diseases is the lack of rapid high-throughput assays to measure low levels of prions. Such measurements have typically required prolonged bioassays in animals. Highly sensitive, but generally non-quantitative, prion detection methods have been developed based on prions' ability to seed the conversion of normally soluble protease-sensitive forms of prion protein to protease-resistant and/or amyloid fibrillar forms. Here we describe an approach for estimating the relative amount of prions using a new prion seeding assay called real-time quaking induced conversion assay (RT-QuIC). The underlying reaction blends aspects of the previously described quaking-induced conversion (QuIC) and amyloid seeding assay (ASA) methods and involves prion-seeded conversion of the alpha helix-rich form of bacterially expressed recombinant PrPC to a beta sheet-rich amyloid fibrillar form. The RT-QuIC is as sensitive as the animal bioassay, but can be accomplished in 2 days or less. Analogous to end-point dilution animal bioassays, this approach involves testing of serial dilutions of samples and statistically estimating the seeding dose (SD) giving positive responses in 50% of replicate reactions (SD50). Brain tissue from 263K scrapie-affected hamsters gave SD50 values of 1011-1012/g, making the RT-QuIC similar in sensitivity to end-point dilution bioassays. Analysis of bioassay-positive nasal lavages from hamsters affected with transmissible mink encephalopathy gave SD50 values of 103.5–105.7/ml, showing that nasal cavities release substantial prion infectivity that can be rapidly detected. Cerebral spinal fluid from 263K scrapie-affected hamsters contained prion SD50 values of 102.0–102.9/ml. RT-QuIC assay also discriminated deer chronic wasting disease and sheep scrapie brain samples from normal control samples. In principle, end-point dilution quantitation can be applied to many types of prion and amyloid seeding assays. End point dilution RT-QuIC provides a sensitive, rapid, quantitative, and high throughput assay of prion seeding activity.

Author Summary Top Prion diseases are deadly infectious neurodegenerative disorders of mammals which involve the misfolding of host prion protein. To better manage these diseases, we need to be able to detect and quantify the infectious particles, or prions, in biological samples. However, current tests lack the sensitivity, speed and/or quantitative capabilities required for many important applications in medicine, agriculture, wildlife biology and research. To address this problem, we have developed a new prion assay that is highly sensitive, rapid, and quantitative. This assay takes advantage of the ability of miniscule amounts of infectious prions to seed the misfolding of large excesses of normal prion protein in test tube reactions. Quantitation is achieved by testing a range of sample dilutions and determining loss of seeding activity, i.e. the end-point dilution. Similar analyses have long been used to quantify prions by inoculation into animals; however, such bioassays take months or years to perform and are both animal-intensive and expensive. Our new method provides a more practical means of detecting and quantifying prions. So far, we have applied this assay to prions from sheep, deer, and hamsters, and have found surprisingly high levels of prions in the nasal and cerebral spinal fluids of infected hamsters.

Citation: Wilham JM, Orrú CD, Bessen RA, Atarashi R, Sano K, et al. (2010) Rapid End-Point Quantitation of Prion Seeding Activity with Sensitivity Comparable to Bioassays. PLoS Pathog 6(12): e1001217. doi:10.1371/journal.ppat.1001217

Editor: David Westaway, University of Alberta, Canada

Received: May 4, 2010; Accepted: November 3, 2010; Published: December 2, 2010

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

Funding: This research was funded by the Intramural Research Program of the NIAID, NIH. J.M.W. was supported in part by the Undergraduate Scholarship Program of the NIH and C.D.O. was partially supported by the Master and Back Program of the Regione Sardegna (Italy). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: BCAUGHEY@niaid.nih.gov

SNIP...SEE FULL TEXT ;

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1001217


ONE has to want to find a TSE in order to really find it. I have NOT seen this with the USDA and CDC et al in relations to human and animal TSE i.e. the USA bovine, or any other animal TSE here in North America and and human CJD there from, and all human TSE, not just the 55 and younger. where is it wrote in stone that only the young can only have a CJD related to other species TSE and or iCJD there from, and all the rest, the 55 and older, it is all a happenstance of bad luck, a spontaneous mutation from nothing, a protein that twisted the wrong way, and which by the way is running now at or about 1 in 9,000 in 55 and older, so please, forget this one in a million BSe $$$ i agree with Collinge al recently and have been saying for a long time ;

"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."

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


and for the following reasons, i see little hope for any mass testing of any species for TSE in the USA in the near future, so the good news is in itself good news, it really means nothing in my opinion for the consumer here in the USA. ...TSS


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, November 17, 2010

MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE

http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html


Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html


Detwiler, a former official with USDA’s Animal and Plant Health Inspection Service, said the origin of "atypical" BSE is unknown at this stage. Speculation has focused on whether it is a variation or mutation of classical BSE, or whether it is caused by a different route of exposure, or exposure of the animal at an older age. There is no definitive evidence that "atypical" BSE occurs sporadically, she said. But scientists have shown that tissues – such as brain and spinal cord – infected with "atypical" BSE are infectious. Based upon what currently is known, she advised that cattle surveillance be maintained, and said it may be necessary to "rethink" the target population of animals tested for BSE to include more apparently healthy older cattle. She also said additional

research is needed on the pathogenesis of "atypical" BSE and how it may be transmitted to cattle or other species; and she encouraged countries not to relax BSE-prevention feed restrictions.

October 27, 2006...END...TSS


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

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

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.

REASON

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

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI

___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

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

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm


Saturday, August 14, 2010

BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY

(see mad cow feed in COMMERCE IN ALABAMA...TSS)

http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html


Wednesday, July 28, 2010

re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010

http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html


Wednesday, July 28, 2010

Atypical prion proteins and IBNC in cattle DEFRA project code SE1796 FOIA Final report

http://bse-atypical.blogspot.com/2010/07/atypical-prion-proteins-and-ibnc-in.html


Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?

http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html


Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/pls/apex/f?p=2400:1001:5492868805159684::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,86129



Saturday, December 11, 2010

Species-barrier-independent prion replication in apparently resistant species

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



Sunday, December 12, 2010

Predominant Involvement of the Cerebellum in Guinea Pigs Infected with Bovine Spongiform Encephalopathy (BSE)

Journal of Comparative Pathology Article in Press

http://creutzfeldt-jakob-disease.blogspot.com/2010/12/predominant-involvement-of-cerebellum.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



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.html



Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary

Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007.

http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html


my comments to PLosone here ;


http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd



Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html


Monday, August 9, 2010

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

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


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


HOW many of you recieved a written CJD Questionnaire asking real questions pertaining to route and source (and there are many here in North America) ?

IS every case getting a cjd questionnaire asking real questions ???


Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION USA PRION UNIT

http://cjdquestionnaire.blogspot.com/


TSS

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