Sunday, March 6, 2011

U.K. and U.S.A. vCJD, CJD, TSE screen (a) the blood supply and (b) blood donors Commons Hansard Written Answers and FDA March 2011

vCJD screen (a) the UK blood supply and (b) blood donors for vCJD. [43356] Commons Hansard Written Answers March 1-3 2011

3 Mar 2011 : Column 535W—continued

vCJD Simon Kirby: To ask the Secretary of State for Health if he will take steps to screen (a) the UK blood supply and (b) blood donors for vCJD. [43356]

Anne Milton: No such screening can yet take place as at present as there are no validated blood screening tests for variant Creutzfeldt-Jakob disease available. The Department, together with the United Kingdom Blood Services, continues to monitor scientific research and development in this area.

Simon Kirby: To ask the Secretary of State for Health (1) if he will assess the merits of removing the warning Risk of Adverse Reaction Infection Including 3 Mar 2011 : Column 559W vCJD from blood bags; and if he will make a statement; [43357]

(2) for what reasons his Department places the warning Risk of Adverse Reaction Infection Including vCJD on blood bags. [43358]

Anne Milton: To comply with the requirements of Good Manufacturing Practice the United Kingdom Blood Services place warnings on blood bags as a final alert to clinical staff that blood components, being of human origin, always carry a potential risk of transmission of infection. Transfusions can also cause other unpredictable side effects, such as allergic reactions. Though fortunately any such events are rare, there is no intention to remove warnings from blood bags.

Variant Creutzfeldt-Jakob disease (vCJD) is mentioned specifically on blood pack labels because it is a relatively new and rare infection. There have been three cases where blood has been the presumed route of vCJD transmission, all from donations in 1999 or before, from donations where the donor later went on to develop clinical vCJD to a recipient who themselves later went on to develop clinical vCJD.

Simon Kirby: To ask the Secretary of State for Health if he will ensure the provision of advice to people who are about to receive blood or blood components on the risk of infection of vCJD. [43359]

Anne Milton: Guidance from the Department places responsibility on Hospital Transfusion Committees to ensure that patients who are likely to receive a blood transfusion are given timely information, informing them of the indication for transfusion, the risks and benefits of transfusion, and any available alternatives to transfusion.

NHS Blood and Transplant (NHSBT) provides a patient information leaflet for hospital staff to give to patients who may receive a transfusion. It indicates that patients should be told that transfusions should only be given if the benefits outweigh the risks, and they should be informed of alternatives to transfusion if these are appropriate and available. The infective risks of blood transfusion are clearly stated. The section on variant Creutzfeldt-Jakob disease (vCJD) specifically states:

"Although the risk of getting variant CJD is probably low from a single transfusion, the risk of any infection will increase with additional blood transfusions. Each year approximately 2 million units of blood are transfused in England, and there have just been a handful of cases where patients are known to have become infected with vCJD from a blood transfusion."

The leaflet is publicly available on the NHSBT website at:

http://hospital.blood.co.uk/library/pdf/INF_PCS_HL_001_05_will_i_need_leaflet_ENGLISH.pdf


http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110303/text/110303w0002.htm#11030356000121



1 Mar 2011 : Column 368W—continued

CJD Frank Dobson: To ask the Secretary of State for Health what estimate he has made of the cost to the public purse of measures taken by the (a) blood service and (b) NHS, excluding the blood service, to reduce the risk of transmission of Creutzfeldt-Jakob disease by blood or blood products since 1998. [41549]

Anne Milton: Since 1998 a number of measures have been introduced by the United Kingdom blood services to reduce the risk of transfusion transmitted variant Creutzfeldt-Jakob disease (vGJD). These measures include the introduction of leucodepletion (the removal of white blood cells), the importation of fresh frozen plasma for children and the deferral from donation of transfusion recipients. In addition, the use of plasma from UK donors for fractionation purposes has ceased.

For national health service blood and transplant the highest costs associated with these measures are the estimated loss of income from the sale of plasma from UK blood donors (£325 million) and the introduction of leucodepletion (£182 million). Further measures bring the estimated total cost to £540 million since 1998, with an estimated current annual cost of approximately £40 million.

There is no separate assessment of such costs for the NHS outside the blood service. However, synthetic (recombinant) clotting factor for the treatment of bleeding disorders, such as haemophilia, has been provided to all patients for whom it is suitable since 2005, and to those under the age of 16 since 1998, at a current annual cost of approximately £200 million.

Commons Hansard Written Answers Text for 1 March 2011

http://www.publications.parliament.uk/pa/cm201011/cmhansrd/cm110301/text/110301w0003.htm#1103022000031



Wednesday, February 2, 2011

Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay

http://transmissiblespongiformencephalopathy.blogspot.com/2011/02/detection-of-prion-infection-in-variant.html



vCJD, CJD, TSE screen (a) the USA blood supply and (b) blood donors for vCJD, CJD, TSE 2011



Posted: 3/2/2011

October 28, 2010

Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011

http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244061.htm



October 29, 2010

Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011

http://www.fda.gov/AdvisoryCommittees/CommitteesMeetingMaterials/BloodVaccinesandOtherBiologics/TransmissibleSpongiformEncephalopathiesAdvisoryCommittee/ucm244062.htm



Tuesday, September 14, 2010

Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)

http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html



Monday, February 7, 2011

FDA's Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html



Sunday, May 10, 2009

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

TO : william.freas@fda.hhs.gov

May 8, 2009

Greetings again Dr. Freas, TSEAC et al,

I would kindly, once again, wish to comment at this meeting about the urgent actions that need to be taken asap, to the Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability from my neck injury, I will not be attending this meeting either, however I hope for my submission to be read and submitted. ...

IN reply to ;

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


Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture's Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).


Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:



http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf


From: Terry S. Singeltary Sr.

To: FREAS@CBER.FDA.GOV

Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov

Sent: Friday, December 01, 2006 2:59 PM

Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION

snip...

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)

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 blood 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. ...

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

snip... 48 pages...



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8


PDF]Freas, William TSS SUBMISSION

File Format: PDF/Adobe Acrobat -

Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary

Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...


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


Tuesday, February 8, 2011

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

http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html


Thursday, February 24, 2011

The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products

http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.html


Friday, February 11, 2011

Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD

http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html



Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html



Wednesday, December 29, 2010

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY PRION END OF YEAR REPORT DECEMBER 29, 2010

http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/transmissible-spongiform-encephalopathy.html


Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html


Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html


Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html



Monday, February 7, 2011

FDA's Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html



Thursday, February 24, 2011

The risk of variant Creutzfeldt-Jakob disease among UK patients with bleeding disorders, known to have received potentially contaminated plasma products

http://vcjdtransfusion.blogspot.com/2011/02/risk-of-variant-creutzfeldt-jakob.html


Wednesday, March 2, 2011 Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011

October 28, 2010

http://tseac.blogspot.com/2011/03/transmissible-spongiform.html


Tuesday, September 28, 2010

Variant CJD: where has it gone, or has it?

Pract Neurol 2010; 10: 250-251

http://vcjdtransfusion.blogspot.com/2010/09/variant-cjd-where-has-it-gone-or-has-it.html


Wednesday, September 08, 2010

Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010

http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html


Saturday, July 17, 2010

Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.

2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE

http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html


Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html


Friday, February 18, 2011

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

http://bse-atypical.blogspot.com/2011/02/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


i wonder if CFIA Canada uses the same OBEX ONLY diagnostic criteria as the USDA ?

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


Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.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



USA Blood products, collected from a donor who was at risk for vCJD, were distributed



Enforcement Report for October 20, 2010



October 20, 2010

PRODUCT

1) Cryoprecipitated AHF. Recall # B-2523-10;

2) Plasma. Recall # B-2524-10;

3) Red Blood Cells. Recall # B-2525-10;

4) Fresh Frozen Plasma. Recall # B-2526-10

CODE

1) Unit: W038508310277;

2) Units: 3127765, W038508310277, 3129157, 4121927;

3) Units: W038508310277, 3129157, 3127765, 4025397, 4121927, 4018030;

4) Units: 4025397, 4018030

RECALLING FIRM/MANUFACTURER

Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on July 22, 2010 and July 28, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

13 units

DISTRIBUTION

GA, MD, SC, Austria, Israel, South Korea, Switzerland

___________________________________

PRODUCT

1) Fresh Frozen Plasma. Recall # B-2531-10;

2) Recovered Plasma. Recall # B-2532-10;

3) Red Blood Cells Leukocytes Reduced. Recall # B-2533-10

CODE

1) Unit: W115910041730;

2) Units: W115910080008, W115910081199;

3) Units: W115910080008, W115910041730, W115910081199

RECALLING FIRM/MANUFACTURER

Central California Blood Center, Fresno, CA, by e-mail on July 19, 2010 and July 23, 2010 and by facsimile on July 23, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

6 units

DISTRIBUTION

Austria, CA

END OF ENFORCEMENT REPORT FOR OCTOBER 20, 2010

#

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm230357.htm

Enforcement Report for October 13, 2010

October 13, 2010

PRODUCT

1) Red Blood Cells Leukocytes Reduced. Recall # B-2275-10;

2) Recovered Plasma. Recall # B-2276-10;

3) Cryoprecipitated AHF, Pooled. Recall # B-2277-10

CODE

1), 2) and 3) Unit: 6400811

RECALLING FIRM/MANUFACTURER

South Texas Blood & Tissue Center, San Antonio, TX, by fax on April 7, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

3 units

DISTRIBUTION

FL, TX

___________________________________

PRODUCT

Fresh Frozen Plasma. Recall # B-2283-10

CODE

Units: W001606004574; W001606003405

RECALLING FIRM/MANUFACTURER

Department of the Air Force 88th Medical Group SGQC WPAFB, Wright Patterson, AFB, OH, by letter dated April 17, 2008. Firm initiated recall is complete.

REASON

Blood products, collected from a donor who may have warranted deferral for residency in an area at risk for variant Creutzfeldt-Jakob Disease, were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

NJ

___________________________________

PRODUCT

1) Red Blood Cells Leukocytes Reduced. Recall # B-2322-10

2) Fresh Frozen Plasma. Recall # B-2323-10

CODE

1) and 2) Unit: W280310400336

RECALLING FIRM/MANUFACTURER

Upstate New York Transplant Services, Inc., Buffalo, NY, by telephone and fax on June 21, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

NY

___________________________________

PRODUCT

Red Blood Cells. Recall # B-2324-10

CODE

Unit: W121610120511

RECALLING FIRM/MANUFACTURER

The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

NY

___________________________________

PRODUCT

Recovered Plasma. Recall # B-2325-10

CODE

Unit: W121610120511

RECALLING FIRM/MANUFACTURER

The Blood Connection, Inc., Piedmont, SC, by fax and computerized notification system on June 17, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

Switzerland

___________________________________

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm229271.htm



TSS

----- Original Message -----
From: Terry S. Singeltary Sr.
To: BLOODCJD@YAHOOGROUPS.COM
Sent: Thursday, October 07, 2010 12:58 PM
Subject: [BLOODCJD] USA Blood products, collected from a donor who was at risk for vCJD, were distributed END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010

PRODUCT

1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;

2) Red Blood Cells. Recall # B-2449-10;

3) Cryoprecipitated AHF. Recall # B-2450-10;

4) Plasma. Recall # B-2451-10

CODE

1) Units: W038509802210, W038509800965;

2) Units: W038509802210, W038509800965, W038508801111, W038508330725;

3) Unit: W03850830725;

4) Units: W038509801111, W038508330725

RECALLING FIRM/MANUFACTURER

Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

9 units

DISTRIBUTION

Korea, SC, GA

___________________________________

PRODUCT

Recovered Plasma. Recall # B-2306-10

CODE

Unit: W137508110097

RECALLING FIRM/MANUFACTURER

Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

KY

___________________________________

PRODUCT

Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10

CODE

Units: W041609075327D (part a and b), 3922801 (part a and b)

RECALLING FIRM/MANUFACTURER

Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

4 units

DISTRIBUTION

MS

___________________________________

PRODUCT

1) Recovered Plasma. Recall # B-2363-10;

2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;

3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10

CODE

1) and 3) Units: 2613522, 2578779;

2) Unit: 2578779

RECALLING FIRM/MANUFACTURER

South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

5 units

DISTRIBUTION

TX

___________________________________

END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010

#

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm



PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan

___________________________________

PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY

___________________________________

PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm



PRODUCT

1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;

2) Recovered Plasma. Recall # B-2156-10

CODE

1) Unit: W036309907231;

2) Unit: W036309616077

RECALLING FIRM/MANUFACTURER

BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

TX, Switzerland

___________________________________

PRODUCT

Red Blood Cells Leukocytes Reduced. Recall # B-2157-10

CODE

Unit: 6371718

RECALLING FIRM/MANUFACTURER

South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

TX

___________________________________

PRODUCT

Source Plasma. Recall # B-2212-10

CODE

Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599

RECALLING FIRM/MANUFACTURER

BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

10 units

DISTRIBUTION

CA

___________________________________

PRODUCT

1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;

2) Recovered Plasma. Recall # B-2214

CODE

1) and 2) Unit: 6325245

RECALLING FIRM/MANUFACTURER

South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

FL, TX

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm



PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm



PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC

___________________________________

PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN

___________________________________

PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm



PRODUCT

1) Plasma Frozen within 24 hours (FP24). Recall # B-2448-10;

2) Red Blood Cells. Recall # B-2449-10;

3) Cryoprecipitated AHF. Recall # B-2450-10;

4) Plasma. Recall # B-2451-10

CODE

1) Units: W038509802210, W038509800965;

2) Units: W038509802210, W038509800965, W038508801111, W038508330725;

3) Unit: W03850830725;

4) Units: W038509801111, W038508330725

RECALLING FIRM/MANUFACTURER

Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on July 9 and 21, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

9 units

DISTRIBUTION

Korea, SC, GA

___________________________________

PRODUCT

Recovered Plasma. Recall # B-2306-10

CODE

Unit: W137508110097

RECALLING FIRM/MANUFACTURER

Lane Memorial Blood Bank, Eugene, OR, by fax on June 10, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

KY

___________________________________

PRODUCT

Red Blood Cells (Apheresis) Leukocytes Reduced. Recall # B-2348-10

CODE

Units: W041609075327D (part a and b), 3922801 (part a and b)

RECALLING FIRM/MANUFACTURER

Blood Systems Inc/dba United Blood Services, Meridian, MS, by telephone and fax on May 26, 2010 and May 28, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

4 units

DISTRIBUTION

MS

___________________________________

PRODUCT

1) Recovered Plasma. Recall # B-2363-10;

2) Cryoprecipitated AHF, Pooled. Recall # B-2364-10;

3) Red Blood Cells Leukocytes Reduced. Recall # B-2365-10

CODE

1) and 3) Units: 2613522, 2578779;

2) Unit: 2578779

RECALLING FIRM/MANUFACTURER

South Texas Blood and Tissue Center, San Antonio, TX, by fax and e-mail on May 5, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

5 units

DISTRIBUTION

TX

___________________________________

END OF ENFORCEMENT REPORT FOR OCTOBER 6, 2010

#

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm228605.htm



PRODUCT Red Blood Cells. Recall # B-2300-10 CODE Unit: W001607702825 RECALLING FIRM/MANUFACTURER Recalling Firm: Department of the Air Force, Wright Patterson AFB, OH, by letter dated April 8, 2008. Manufacturer: Depart of Air Force 88th Medical Group SGQC WPAFB, Wright Patterson AFB, OH. Firm initiated recall is complete. REASON Blood product, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION Japan

___________________________________

PRODUCT Recovered Plasma. Recall # B-2302-10 CODE Units: R08951; P90041; P90041 RECALLING FIRM/MANUFACTURER Blood Center of Northcentral Wisconsin, Inc., Wausau, WI, by fax on January 2, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION NY

___________________________________

PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-2338-10; 2) Plasma Frozen. Recall # B-2339-10 CODE 1) and 2) Unit: 5039861 RECALLING FIRM/MANUFACTURER Community Blood Center, Inc., Appleton, WI, by letter dated September 21, 2007 or by electronic notification on September 21, 2007. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION WI, Switzerland

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 22, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm227078.htm



PRODUCT

1) Cryoprecipitated AHF, Pooled. Recall # B-2155-10;

2) Recovered Plasma. Recall # B-2156-10

CODE

1) Unit: W036309907231;

2) Unit: W036309616077

RECALLING FIRM/MANUFACTURER

BloodCenter of Wisconsin, Inc., Milwaukee, WI, by fax and internet on May 5, 2010 and May 13, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

TX, Switzerland

___________________________________

PRODUCT

Red Blood Cells Leukocytes Reduced. Recall # B-2157-10

CODE

Unit: 6371718

RECALLING FIRM/MANUFACTURER

South Texas Blood & Tissue Center, San Antonio, TX, by telephone on January 23, 2010 and by fax on January 25, 2010. Firm initiated recall is complete.

REASON

Blood product, collected from a donor who failed to answer questions regarding risk for vCJD, was distributed.

VOLUME OF PRODUCT IN COMMERCE

1 unit

DISTRIBUTION

TX

___________________________________

PRODUCT

Source Plasma. Recall # B-2212-10

CODE

Units: 09FMOG6851; 09FMOG3410; 09FMOG2756; 09FMOG1418; 09FMOF6640; 09FMOF2642; 09FMOF1554; 09FMOD7746; 09FMOF0063; 09FMOF7599

RECALLING FIRM/MANUFACTURER

BioLife Plasma Service LP, Springfield, MO, by fax on April 1, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

10 units

DISTRIBUTION

CA

___________________________________

PRODUCT

1) Red Blood Cells Leukocytes Reduced. Recall # B-2213-10;

2) Recovered Plasma. Recall # B-2214

CODE

1) and 2) Unit: 6325245

RECALLING FIRM/MANUFACTURER

South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on February 8, 2010. Firm initiated recall is complete.

REASON

Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.

VOLUME OF PRODUCT IN COMMERCE

2 units

DISTRIBUTION

FL, TX

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 15, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225990.htm



PRODUCT Source Plasma. Recall # B-2056-10 CODE Units: FD0500537, FD0502880, FD0503259, FD0509894, FD0515518, FD0516063, FD0517957, FD0518606, FD0522255, FD0523346, FD0523544, FD0524204, FD0524698, FD0525142, FD0525845, FD0526653, FD0526878, FD0527579, FD0527845, FD0528519, FD0528827, FD0529544, FD0529761, FD0530471, FD0530712, FD0531425, FD0531801, FD0532483, FD0532869, FD0537501, FD0537687, FD0538370, FD0543210, FD0546250, FD0546632, FD0547328, FD0547832, FD0548286, FD0548743, FD0549325, FD0549840, FD0550427, FD0551448, FD0551572, FD0552307, FD0553173, FD0553418, FD0554063, FD0554834, FD0555041, FD0559685, FD0560235, FD0560592, FD0561168, FD0561786, FD0562212, FD0562883, FD0563248, FD0564435, FD0564723, FD0565467, FD0565880, FD0566540, FD0567053, FD0567723, FD0567965, FD0568941, FD0569180, FD0570057, FD0571177, FD0571477, FD0572411, FD0572818, FD0573582, FD0573871, FD0574531, FD0576955, FD0577140, FD0579983, FD0580403, FD0581156, FD0581623, FD0582680, FD0583090, FD0584073, FD0584500, FD0585410, FD0586089, FD0586790, FD0587500, FD0588791, FD0589023, FD0590248, FD0590600, FD0591592, FD0592445, FD0593277, FD0593712, FD0594626, FD0595049, FD0596132, FD0596519, FD0597701, FD0598681, FD0599198, FD0600210, FD0600690, FD0601755, FD0602401, FD0603415, FD0603985, FD0605122, FD0608608, FD0609074, FD0609979, FD0610508, FD0611469, FD0612006, FD0612905 RECALLING FIRM/MANUFACTURER DCI Biologicals LLC, Farmington, NM, by facsimile on September 26, 2009 and electronic mail dated January 15, 2010. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 119 units DISTRIBUTION NY, UK

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 8, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm225223.htm



PRODUCT Source Plasma. Recall # B-2134-10 CODE Units: 3910020431, 3910019695, 3910018715, 3910018227, 3910017100, 3910016675, 3910015596, 3910015120, 3910014175, 3910013575, 3910012934, 3910012281, 3910010102, 3910009899, 3910007715, 3910007430 RECALLING FIRM/MANUFACTURER Talecris Plasma Resources, Inc., N Las Vegas, NV, by fax on July 17, 2009. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 16 units DISTRIBUTION NC

___________________________________

PRODUCT 1) Red Blood Cells. Recall # B-2215-10; 2) Fresh Frozen Plasma. Recall # B-2216-10 CODE 1) and 2) Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION MN

___________________________________

PRODUCT Recovered Plasma. Recall # B-2217-10 CODE Unit: 0951592 RECALLING FIRM/MANUFACTURER Memorial Blood Centers, Saint Paul, MN, by letter on November 5, 2008. Firm initiated recall is complete. REASON Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION MN

___________________________________

END OF ENFORCEMENT REPORT FOR SEPTEMBER 1, 2010

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm224723.htm



i have not checked out 2011 recalls of USA blood that has NOT been screened for vCJD. let's just check out the latest and see what's going on ;



PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0812-11; 2) Recovered Plasma. Recall # B-0813-11 CODE 1) and 2) Unit: 0679506 RECALLING FIRM/MANUFACTURER Blood Centers of the Pacific, San Francisco, CA, by telephone and letter on May 22, 2002. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION CA, Switzerland

___________________________________

PRODUCT Source Plasma. Recall # B-0840-11 CODE Units 381070540, 381070350, 381069984, 381069808, 381068965, 381068783, 381068313, 381068151, 381067718, 381067473, 381067140, 381066944, 381066586, 381066289, 381065935, 381064526, 381065364, 381064386, 381064220, 381063426, 381063033, 381062874, 381062488, 381061767, 381061614, 381061260, 381060375, 381060162, 381059688, 381059534, 381059093, 381058859, 381058451, 381058224, 381057903, 381057624, 381057317, 381057103, 381056525, 381055667, 381054442, 381054328, 381053845, 381053686, 381053078, 381052342, 381051924, 381051688, 381048523 and 381048512 RECALLING FIRM/MANUFACTURER Recalling Firm: Talecris Plasma Resources, Research Triangle Park, NC, by facsimile on May 14, 2010. Manufacturer: Talecris Plasma Resources, Peoria, IL. Firm initiated recall is complete. REASON Blood products, collected from a donor who was previously deferred due to a history of Dura Mater Graft, were distributed. VOLUME OF PRODUCT IN COMMERCE 50 units DISTRIBUTION NC

___________________________________

PRODUCT 1) Red Blood Cells Leukocytes Reduced. Recall # B-0848-11; 2) Red Blood Cells Leukocytes Reduced Washed. Recall # B-0849-11; 3) Recovered Plasma. Recall # B-0850-11 CODE 1) Units: 3618494; 2528285; 2) Unit: 3679207; 3) Units: 3679207; 3618494; 2528285 RECALLING FIRM/MANUFACTURER Central California Blood Center, Fresno, CA, by letter dated September 7, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 6 units DISTRIBUTION CA

___________________________________



END OF ENFORCEMENT REPORT FOR MARCH 2, 2011

#

http://www.fda.gov/Safety/Recalls/EnforcementReports/ucm245369.htm



Greetings,


I am sure there are many more in the previous weeks of 2011. I just don't have time now to search them by week. it's pretty much been a weekly event for years and years and years.


I still have not gotten an answer about these type recalls ;


"REASON Blood products, collected from donors in which donor suitability was not adequately determined, were distributed."


DOES this include vCJD ?




i personally think they are missing the bigger picture by not including all human TSE prion disease, especially since we know GSS will transmit by blood, and now that we know that some sporadic CJD cases are caused by atypical BSE. just does not make sense to me. i still say it's a band aid approach to something that needs a tourniquet. ...TSS



Saturday, January 20, 2007



Fourth case of transfusion-associated vCJD infection in the United Kingdom



http://vcjdtransfusion.blogspot.com/2007_01_01_archive.html




P.4.23



Transmission of atypical BSE in humanized mouse models



Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA



Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.



Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice.



Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.



Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time.



The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.



Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.



BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.



Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.



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




P02.35



Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE



Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden



Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass.



Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE.



By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK-resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice.



The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.



O.11.3



Infectivity in skeletal muscle of BASE-infected cattle



Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy



Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.



Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.



Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.



Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.



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




O.2.4



Detection of prions in blood leucocytes



Linda A. Terry, Laurence Howells, Jeremy Hawthorn, Sally Everest, Sarah Jo Moore, Jane C. Edwards Veterinary Laboratories Agency, UK



Background: Infected human blood has been implicated in the iatrogenic transmission of vCJD in four reported cases. Experimental transmission studies have demonstrated that blood from scrapie and BSE infected sheep also contains infectivity. Rodent models of prion disease implicated both cellular and plasma fractions. However, direct detection of PrPsc from blood in the absence of in vitro amplification or bioassay has proved difficult. Methods for the direct detection of PrPsc in blood would be advantageous for the study of the pathogenesis of TSEs and as a basis for a blood test. Objectives: To develop a method for the direct detection of PrPsc in blood cells from scrapie and BSE infected sheep; to study the temporal distribution of PrPsc in blood and to determine the identity of the cells bearing prions in blood. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from sheep naturally infected with scrapie or experimentally infected with BSE at the clinical stage of disease and from scrapie infected sheep from 3 months of age through to clinical end-point. PBMCs were tested for PrPsc content by a direct immunoassay based on the IDEXX CWD HerdChek kit. Different subsets of PBMCs were isolated by subset specific cell surface markers and magnetic bead separation and analysed for PrPsc content. Results: PrPSc was detected in 54% of sheep with clinical scrapie and 71% of sheep with clinical BSE. A longitudinal study of the temporal distribution of blood PBMC associated PrPsc showed that the detection rate increases during the course of disease and is more likely to be observed during the second half of the incubation period. Additionally detection is more likely in scrapie infected sheep if they carry the PRNP genotype of VRQ/VRQ. Cell separation studies showed that the PrPsc is associated with a specific cell subset implicating a subset of B lymphocytes. Discussion. This is the first report of the direct detection of PrPsc in cells isolated from sheep blood in the absence of in vitro amplification or bioassay. Since PrPsc can be detected from as early as 3 months of age in sheep naturally infected with scrapie, correlating with initial replication in the gut-associated lymphoid tissue, the assay could be the basis of a preclinical test. The identification of the cell subset carrying PrPsc progresses our understanding of the pathogenesis of the disease. However, it remains unclear whether this cell subset is responsible for the dissemination of prions or in clearance of circulating PrPsc. Funded by defra, UK and IDEXX.



O.2.6



Human urine and PrP



Silvio Notari1*, Liuting Qing1*, Ayuna Dagdanova1*, Sergei Ilchenko1, Mark E. Obrenovich1, Wen-Quan Zou1, Maurizio Pocchiari2, Pierluigi Gambetti1, Qingzhong Kong1, Shu G. Chen1 1Case Western Reserve University, USA; 2Istituto Superiore di Sanità, Italy



Background: The presence and the characteristics of prion protein (PrP) in human urine under normal conditions are controversial. Similarly, there are no definite data on the presence of infectivity in urine in the course of naturally occurring human prion diseases. Objectives: 1) To definitely determine the presence and characteristics of PrPC in normal urine. 2) To evaluate the prion infectivity in human urine in sporadic Creutzfeldt-Jakob disease (sCJD), we have carried out a set of bioassays in humanized transgenic mouse with urine samples collected from sCJD subjects. Methods: 1) Advanced mass spectrometry and experimental treatments have been used to demonstrate the presence, primary structure and posttranslational modifications of purified urinary PrPC (uPrP). 2) Bioassays were performed by intracerebral inoculation of 100 times concentrated and dialyzed urine, collected from three sCJD-MM1 cases to humanized transgenic mice and from appropriate controls. Results: We found that human urine contains significant amount of PrP (approximately 10 ng/ml) that is truncated with the major N-terminus at residue 112 as the PrPC fragment identified as C1, and it carries an anchor, which is soluble because likely lacks the phosholipid component. None of the humanized transgenic mice inoculated with sCJD concentrated urine had evidence of prion disease during a period of over 700 days (their normal life expectancy) leading to the conclusion that prion infectivity in sCJD urine, if present, must be less than 6 infectious units/100ml. Discussion: The issues raised in the discussion will include: 1) The origin of the truncated uPrP; 2) How the present data compare with the experimental studies published to date that indicate presence of infectivity; 3) The practical implications of our findings. *



O.4.6



All separated components, prepared from BSE-infected sheep blood, are infectious upon transfusion



Sandra McCutcheon1, Anthony Richard Alejo Blanco1, Christopher de Wolf1, Boon Chin Tan1, Nora Hunter1, Valerie Hornsey2, Christopher Prowse2, Marc Turner2, Martin H Groschup3, Dietmar Becher4, Fiona Houston5, Jean C Manson1 1The Roslin Institute and R (D) SVS, University of Edinburgh, UK; 2Scottish National Blood Transfusion Service, UK; 3FLIFederal Research Institute for Animal Health, Germany; 4Micromun, Germany; 5University of Glasgow, UK



Background: The possibility that vCJD may be transmitted by blood transfusion is serious public health issue, of which 4 probable (3 clinical) cases have been attributed. Recently a case of asymptomatic vCJD infection was identified in a haemophiliac; following treatment with clotting factors from UK plasma pools. Sheep orally infected with BSE provide a suitable model, to assess vCJD infection in humans & risk reduction methods, as the distribution of PrPSc & infectivity in lymphoid tissues resembles that of vCJD patients.



Objectives: To determine qualitative and quantitative data on the changes in infectivity in blood and its clinically relevant components with time, to assess the effect of leucodepletion of such products and the potential for secondary transmission by blood transfusion.



Methods: We orally infected sheep with bovine BSE brain homogenate and collected two full-sized donations of whole blood, before the onset of clinical signs. The following components were transfused into naive recipients: whole blood, buffy coat and leucoreduced and non leucoreduced plasma, platelets and red cells. A sub sample of all components was inoculated into TgShpXI mice for determination of infectivity titers. A unit of whole blood from selected primary recipients was transfused into secondary recipients. We are creating a blood archive throughout this study.



Results: 33% of the infected donors have been confirmed as having BSE. We have 4 transmissions of BSE-infectivity following the transfusion of whole blood, buffy coat and plasma. Short incubation times were recorded in these recipients (468, 513, 567 and 594 days) & were similar to those seen in their respective donors (534, 628, 614 and 614 days). The donor of buffy coat also donated both leucodepleted and non leucodepleted blood components to other recipients.



Discussion: Our study will provide invaluable data on the safety of blood products, in relation to TSE infection, used in human medicine (DoH 007/0162)



O.8.1



Variant CJD and plasma products



Robert G. Will National CJD Surveillance Unit, Edinburgh, UK



Evidence from the Transfusion Medicine Epidemiology Review (TMER) project indicates that variant CJD is transmissible through transfusion of labile blood components. The question as to whether plasma products sourced from vCJD contaminated plasma pools has been addressed by a number of risk assessments, with conflicting conclusions. Recently a case of possible vCJD infection in an individual with haemophilia has been described and analysis has suggested that infection may have been related to prior treatment with vCJD implicated Factor VIII. The details of this case will be described together with an analysis of plasma product exposures in UK clinical cases of vCJD.



O.8.2



Blood safety: from screening tests to prion removal



Marc Turner Scottish National Blood Transfusion Service and Department of Haematology, Royal Infirmary, Edinburgh, UK



Although the number of clinical cases of variant CJD continues to fall, concern remains within UK and Western European Blood Services in relation to the risk of transmission of variant CJD due to the estimated prevalence of sub-clinical infection in the general population and the clinical cases of transmission of variant CJD prions by blood components and plasma products. The UK Advisory Committee on the Safety of Blood, Tissues and Organs (SaBTO) has considered a number of further precautionary measures including reducing exposure to blood transfusion, importation of blood components, implementation of prion assays and prion reduction for red cell concentrates. The latter two technologies are currently under independent evaluation and it is expected that contingent on the outcome of these an initial decision on whether or not to recommend implementation of these technologies will be made by SaBTO in Autumn 2009.



O.9.3



Updated risk assessment of variant Creutzfeldt-Jakob disease (vCJD) risks for recipients of plasma-derived blood clotting products in the U.S.



Hong Yang, Richard Forshee, Mark Walderhaug, Steven Anderson US Food and Drug Administration, USA



Background: A recent announcement by UK health authorities of a case of vCJD infection in a >70 year old person with hemophilia has prompted the US Food & Drug Administration (FDA) to re-evaluate vCJD risks in the U.S. via plasma-derived Factor VIII (pdFVIII) and to update its 2006 risk assessment. As of May 2009, confirmed vCJD deaths have occurred in persons who are homozygous methionine (MM) at codon 129 of the PRP gene. Several reports in the last few years have indicated signs of vCJD infection in persons of methionine-valine (MV) and homozygous valine (VV) genotypes. FDA updated risk assessment by assuming all genotypes are susceptible to vCJD and modeling the incubation periods for all three genotypes.



Objectives: To evaluate the vCJD risk for pdFVIII recipients with severe hemophilia and vonWillebrand diseases.



Methods: The model assumed equal susceptibility of three genotypes, a median incubation period of 12 years for the MM and 32 years for MV and VV genotypes, and vCJD infectivity was present in the blood of infected donors during the last 50% to 90% of incubation period. Model used statistical distributions for inputs including susceptibility to the disease, donation rates, frequency and duration of travel to the UK, France and other countries in Europe since 1980, the effectiveness of donor deferral policies and infectivity clearance during manufacturing processes.



Results: For severe hemophilia patients at the highest risk (prophylaxis, with inhibitor, with immune tolerance) the model estimated annual mean exposure to be ~7 x 10-8 iv ID50 or ~1 in 270,000 with the lower prevalence (4 per million) assumption, and ~1 x 10-4 iv ID50 or ~1 in 12,000 with the higher prevalence (1 per 4,225) assumption. Donor deferral policies reduce the risk by >92%.



Discussion: Due to limited data and knowledge of vCJD, the model estimates are uncertain. However, it suggests the risk is small, and donor deferral and manufacturing processes greatly reduce the risk.



P.10.7



Serial passage of sCJD in humanised transgenic mice indicates two major transmission strains associated with PrPSc of either type 1 or 2



Matthew Bishop, Robert Will, Enrico Cancellotti, Jean Manson University of Edinburgh, UK



Background: Questions remain about the aetiology of sporadic CJD and whether phenotypic variation is solely controlled by factors such as codon 129 genotype and biochemistry of PrPC. Variation in infective strain has not been clearly demonstrated in sCJD.



Objectives: By serial passage of sCJD in transgenic mice expressing human prion protein with MM, MV, and VV codon 129 genotypes we aimed to understand strain transmission characteristics for the three most commonly observed phenotypes of sCJD.



Methods: We performed intracerebral inoculation of humanised transgenic mice with brain homogenates derived from similar mice previously inoculated with frontal cortex from sCJD patients of subgroups MM1, MV2, and VV2. These mice were assessed for clinical TSE signs, for TSE vacuolation, and deposition of PrPSc.



Results: sCJD(MM1) passage via all mice showed transmission profiles similar to primary inoculation. sCJD(MV2) passage via HuMM and HuVV mice showed a transmission profile similar to primary inoculation. Passage via a HuMV mouse showed transmission properties similar to not only the primary inoculum but also sCJD(MM1). sCJD(VV2) passage via HuMV and HuVV mice showed transmission profiles similar to the primary inoculation. Passage via a HuMM mouse showed transmission properties similar to not only the sCJD(VV2) primary inoculum but also sCJD(MM1). Cluster analysis of the lesion profile data showed that three clusters seen after primary inoculation were reduced to two following second passage, identified by the biochemical type of PrPSc (1 or 2) found in the host mice.



Discussion: Serial passage of sCJD subgroups MM1, MV2, and VV2 shows that PrPSc type and mouse codon 129 genotype determine the secondary transmission profile, independently of the originating inoculum strain. There are associations between type 1 PrPSc and C129-Met, and type 2 PrPSc and C129-Val. This should allow us to investigate further the relationship between PrPSc, genotype, infection, and pathology.



P.5.1



Detection of cellular prion protein (PrPc) in plasma from healthy cynomolgus monkeys (Macaca fascicularis) and changes observed after BSE infection



Barbara Yutzy, Edgar Holznagel, Johannes Löwer Paul-Ehrlich-Institut, Germany



Background: Orally BSE-dosed cynomolgus monkeys represent a valuable model to examine the kinetic of blood infectivity and to assess the risk of blood-borne transmission of variant Creutzfeldt-Jacob disease (vCJD).



Methods: Blood samples were collected monthly from BSE-infected (n = 18) and non-infected female cynomolgus monkeys (n = 8) over a period of up to 9 years. PrPc concentrations were retrospectively analyzed in plasma samples by a dot blot assay and by a sandwich ELISA using a highly sensitive dissociation- enhanced lanthanide fluoro-immunoassay (DELFIA) for detection. Different blood preparation protocols were evaluated to obtain plasma.



Objective: To detect changes in the levels of soluble plasmaderived PrPc. Results: Different blood preparation protocols had a significant effect on the measured plasma PrPc concentrations. In non-infected macaques, concentrations of soluble, plasmaderived PrPc were at least 10-fold lower compared to plasma concentrations in healthy humans. Levels of plasma PrPc increased 6 - 12 months after experimental BSE infection, remained high during the asymptomatic phase, and dropped towards the clinical phase. Soluble, plasma-derived PrPc molecules were PK-sensitive in BSE-infected macaques.



Discussion: There is a species-specific difference in the PrPc concentrations between human and macaque. At least a part of the plasma-derived PrPc fraction originates from blood cells. Andfinally, BSE infection caused an increase in plasma PrPc levels during the asymptomatic phase of infection. Blood transfusion studies have been initiated to examine whether these PK-sensitive PrP molecules carry infectivity.



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




http://vcjdtransfusion.blogspot.com/2007_01_01_archive.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.



Second threat



In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.



Third threat



The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.



Fourth threat



Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,



whereas other countries, including the US,



Brazil, and Argentine do not have these constraints.



However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.



Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.



Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.



Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.



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




Wednesday, March 31, 2010



Atypical BSE in Cattle



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



This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.



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




TSS

Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA


Greetings,

WITH more and more atypical Transmissible Spongiform Encephalopathy cases showing up in more and more species here in North America, and the enormous monumental amount of banned mad cow protein in commerce since the infamous partial and voluntary mad cow feed ban inked on paper, with tons and tons crossing back and forth between the USA, Canada, and Mexico, it just does not surprise me of all these "PENDING CLASSIFICATIONS" of human TSE in Canada, and the USA. UK c-BSE transmitted to humans became nvCJD. WE now have atypical strains of BSE in cattle. Mission Texas experiments long ago showed that transmitted USA sheep scrapie to USA bovine, produced a TSE much different than the UK typical c-BSE. SO why would human TSE in the USA look like UK human TSE ? The corruption is mind boggling. The UK saw a suspicious TSE in humans, and science linked it to cattle. North America is awash with human and animal TSE, CJD is rising in young and old, with the same pathology and same symptoms, and none of it is related to the other. isn't that nice. who, what, bestowed such miracles upon North America $

Archive Number 20100405.1091 Published Date 05-APR-2010

Subject PRO/AH/EDR> Prion disease update 1010 (04)

snip...

[Terry S. Singeltary Sr. has added the following comment:

"According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed.


http://whqlibdoc.who.int/publications/2003/9241545887.pdf.


The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?"



http://www.promedmail.org/pls/apex/f?p=2400:1001:568933508083034::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1000,82101



CANADA CJD UPDATE 2011

CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011

3. Final classification of 49 cases from 2009, 2010, 2011 is pending.

snip...

http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf


USA 2011

USA

National Prion Disease Pathology Surveillance Center

Cases Examined1

(November 1, 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 87 51 43 7 1 0

1999 121 73 65 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 13

2005 344 194 157 36 1 0

2006 383 197 166 29 0 24

2007 377 214 187 27 0 0

2008 394 231 205 25 0 0

2009 425 258 215 43 0 0

2010 333 213 158 33 0 0

TOTAL 38315 22656 1907 328 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 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

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



Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.

I also urge you to again notice these disturbing factors in lines 5 and 6 ;

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

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.


========end=====tss=====2011


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



THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$

The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

http://www.oie.int/boutique/extrait/06heim937950.pdf



Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html


Saturday, March 05, 2011

MAD COW DISEASE BSE PRION MEXICO ???

http://bse-atypical.blogspot.com/2011/03/mad-cow-disease-bse-prion-mexico.html



Wednesday, March 31, 2010

Atypical BSE in Cattle

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

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

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



snip...

please see all seven threats listed in the USA, and more...FULL TEXT ;



Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

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

Second threat

snip...

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



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


http://prionpathy.blogspot.com/



Thursday, August 12, 2010




Seven main threats for the future linked to prions



First threat



The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.



***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.



Second threat



snip...



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



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




http://prionpathy.blogspot.com/




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



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


P26 TRANSMISSION OF ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN HUMANIZED MOUSE MODELS

Liuting Qing1, Fusong Chen1, Michael Payne1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5*, and Qingzhong Kong1 1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; 2CEA, Istituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University, Diagnostic Medicine/Pathobiology Department, Manhattan, KS 66506, USA. *Previous address: USDA National Animal Disease Center, Ames, IA 50010, USA

Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Two atypical BSE strains, BSE-L (also named BASE) and BSE-H, have been discovered in three continents since 2004. The first case of naturally occurring BSE with mutated bovine PrP gene (termed BSE-M) was also found in 2006 in the USA. The transmissibility and phenotypes of these atypical BSE strains/isolates in humans were unknown. We have inoculated humanized transgenic mice with classical and atypical BSE strains (BSE-C, BSE-L, BSE-H) and the BSE-M isolate. We have found that the atypical BSE-L strain is much more virulent than the classical BSE-C. The atypical BSE-H strain is also transmissible in the humanized transgenic mice with distinct phenotype, but no transmission has been observed for the BSE-M isolate so far.

III International Symposium on THE NEW PRION BIOLOGY: BASIC SCIENCE, DIAGNOSIS AND THERAPY 2 - 4 APRIL 2009, VENEZIA (ITALY)

http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf


Saturday, March 05, 2011

MAD COW DISEASE BSE PRION MEXICO ???

http://bse-atypical.blogspot.com/2011/03/mad-cow-disease-bse-prion-mexico.html


Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.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



Friday, February 18, 2011

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

http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html


Wednesday, February 9, 2011

[Docket No. FSIS-2010-0041] Non-Ambulatory Disabled Veal Calves and Other Non-Ambulatory Disabled Livestock at Slaughter; Petitions for Rulemaking

http://downercattle.blogspot.com/2011/02/docket-no-fsis-2010-0041-non-ambulatory.html



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



BANNED MAD COW FEED IN COMMERCE IN ALABAMA (where h-g-BSEalabama mad cow was documented)

Date: September 6, 2006 at 7:58 am PST PRODUCT

a) EVSRC Custom dairy feed, Recall # V-130-6;

b) Performance Chick Starter, Recall # V-131-6;

c) Performance Quail Grower, Recall # V-132-6;

d) Performance Pheasant Finisher, Recall # V-133-6.

CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.

REASON

Dairy and poultry feeds were possibly contaminated with ruminant based protein.

VOLUME OF PRODUCT IN COMMERCE 477.72 tons

DISTRIBUTION AL

______________________________

http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html


PRODUCT Bulk custom dairy pre-mixes,

Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 350 tons

DISTRIBUTION AL and MS

______________________________

PRODUCT

a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;

b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;

c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;

d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;

e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;

f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;

g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6

CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.

REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags

DISTRIBUTION AL, GA, MS, and TN

END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006

###

http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006

Date: August 6, 2006 at 6:16 pm PST PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE

Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.

REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE 125 tons

DISTRIBUTION AL and FL

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html


MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;

b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;

c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;

d) Feather Meal, Recall # V-082-6 CODE

a) Bulk

b) None

c) Bulk

d) Bulk

RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.

REASON

Possible contamination of animal feeds with ruminent derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons

DISTRIBUTION Nationwide

END OF ENFORCEMENT REPORT FOR July 12, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html


let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.

This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$

ALABAMA MAD COW g-h-BSEalabama

In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.

http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156


http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF


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


Saturday, June 12, 2010

PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse

http://bse-atypical.blogspot.com/2010/06/publication-request-and-foia-request.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


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


Monday, January 17, 2011

MAD COW Update on Feed Enforcement Activities to Limit the Spread of BSE January 13, 2011

January 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/mad-cow-update-on-feed-enforcement.html


Wednesday, March 2, 2011

Transmissible Spongiform Encephalopathies Advisory Committee Meeting Transcript Posted: 3/2/2011 Posted: 3/2/2011

October 28, 2010

http://tseac.blogspot.com/2011/03/transmissible-spongiform.html


http://www.inspection.gc.ca/english/anima/disemala/bseesb/comenqe.shtml


http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml


http://www.fda.gov/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/BovineSpongiformEncephalopathy/default.htm


http://www.fsis.usda.gov/Fact_Sheets/Bovine_Spongiform_Encephalopathy_BSE/



layperson


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

Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

Alberta dairy cow found with mad cow disease

Fri Mar 4, 2011 10:05am EST


WINNIPEG, Manitoba (Reuters) - Canadian government officials have found a dairy cow in Alberta with mad cow disease, but the finding is not surprising and shouldn't affect beef exports, a spokesman for the Canadian Food Inspection Agency said on Friday. The agency confirmed the case of bovine spongiform encephalopathy, or BSE as the disease is also known, on February 18 in a 77-month-old dairy cow, spokesman Guy Gravelle said.

In 2003, the first discovery of a cow in Canada with the disease led to closures of numerous export markets to Canadian beef. Most have reopened, other than South Korea and China, and importers are no longer as sensitive to new cases as countries such as Canada now have monitoring systems in place.

Canada continues to be rated a "controlled risk" for the disease by the World Organization for Animal Health, Gravelle said. The newest case may delay any upgrade to Canada's international risk status as a country cannot apply for negligible status sooner than 11 years after the latest-born case.

The cow has been destroyed and no part of its carcass entered the human food or animal feed systems, Gravelle said.

The case, which is believed to be Canada's 18th, should not affect exports of Canadian cattle or beef, he said, as a small number of BSE cases are expected as Canada monitors for the disease.

(Reporting by Rod Nickel; Editing by Walter Bagley)


http://ca.reuters.com/article/domesticNews/idCATRE7233JT20110304



http://www.inspection.gc.ca/english/anima/disemala/bseesb/comenqe.shtml


http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml




Bovine spongiform encephalopathy (BSE) cases confirmed in Canada in 2011

BSE is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

The following table lists individual animals confirmed to be infected with BSE in Canada in 2011.

Current as of: 2011-02-28

Date confirmed Location Animal type infected Age of animal February 18 Alberta Dairy cow 77 months



http://inspection.gc.ca/english/anima/disemala/rep/2011bseesbe.shtml




Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA


http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html



Saturday, March 12, 2011

Variant Creutzfeldt-Jakob Disease in a Canadian resident Infectious Diseases News Brief - March 11, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/variant-creutzfeldt-jakob-disease-in.html





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, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 and how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html



Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html






TSS

Wednesday, February 2, 2011

Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay

Detection of prion infection in variant Creutzfeldt-Jakob disease: a blood-based assay

Julie Ann Edgeworth, Michael Farmer, Anita Sicilia, Paul Tavares, Jonathan Beck, Tracy Campbell, Jessica Lowe, Simon Mead, Peter Rudge, John Collinge, Graham S Jackson

Summary

Background

Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder originating from exposure to bovine-spongiform-encephalopathy-like prions. Prion infections are associated with long and clinically silent incubations. The number of asymptomatic individuals with vCJD prion infection is unknown, posing risk to others via blood transfusion, blood products, organ or tissue grafts, and contaminated medical instruments. We aimed to establish the sensitivity and specifi city of a blood-based assay for detection of vCJD prion infection.

Methods

We developed a solid-state binding matrix to capture and concentrate disease-associated prion proteins and coupled this method to direct immunodetection of surface-bound material. Quantitative assay sensitivity was assessed with a serial dilution series of 10.. to 10.1. of vCJD prion-infected brain homogenate into whole human blood, with a baseline control of normal human brain homogenate in whole blood (10..). To establish the sensitivity and specifi city of the assay for detection of endogenous vCJD, we analysed a masked panel of 190 whole blood samples from 21 patients with vCJD, 27 with sporadic CJD, 42 with other neurological diseases, and 100 normal controls. Samples were masked and numbered by individuals independent of the assay and analysis. Each sample was tested twice in independent assay runs; only samples that were reactive in both runs were scored as positive overall.



Findings

We were able to distinguish a 10.1. dilution of exogenous vCJD prion-infected brain from a 10.. dilution of normal brain (mean chemiluminescent signal, 1E3~10. [SD 1E1~10.] for vCJD vs 9E9~10. [4E5~103] for normal brain; p<0E0001).an assay sensitivity that was orders of magnitude higher than any previously reported. 15 samples in the masked panel were scored as positive. All 15 samples were from patients with vCJD, showing an assay sensitivity for vCJD of 71E4% (95% CI 47E8.88E7) and a specifi city of 100% (95% CIs between 97E8% and 100%). Interpretation These initial studies provide a prototype blood test for diagnosis of vCJD in symptomatic individuals, which could allow development of large-scale screening tests for asymptomatic vCJD prion infection. Funding UK Medical Research Council.


http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(10)62308-2/abstract



see full text ;



http://download.thelancet.com/pdfs/journals/lancet/PIIS0140673610623082.pdf?id=3d35b1b5aa0ec416:-4a4ca7b:12de9223051:-1b401296700700892




World’s first blood test for vCJD developed in MRC lab


Thursday 3 February 2011

The world’s first accurate blood test for variant Creutzfeldt-Jakob disease (vCJD) has been developed by Medical Research Council (MRC) scientists. The prototype, which is 100,000 times more sensitive than any previous attempt, could transform the diagnosis and screening of the brain disease.

Variant CJD, the human form of BSE (or mad cow disease) first emerged in 1995. The disease, which affects the brain, is believed to have passed from cattle to humans through infected food. It causes personality change, loss of body function, and eventually death.

The research team from the MRC Prion Unit, based at University College London, working with the National Prion Clinic at the National Hospital for Neurology and Neurosurgery (NHNN) tested 190 blood samples, including 21 from individuals known to have vCJD. The blood test was able to detect blood spiked with a dilution of vCJD to within one part per ten billion - 100,000 times more sensitive than any other method developed so far.

Prions, the infectious proteins which cause vCJD and other fatal prion diseases, can inhabit a person’s body for up to 50 years before presenting symptoms. During this time there is a chance a carrier of vCJD infection could pass on the infection to others, for example through blood transfusion or even through surgical and medical instruments as prions can easily attach onto metal surfaces.

A widely available, accurate blood test would enable people to be diagnosed earlier and could also help identify carriers of the disease. This would help measure how widespread the prion infection is in the general population and identify those who are at risk of passing on the infection to others.

Lead author Dr Graham Jackson, Programme Leader at the MRC Prion Unit, said:

“This test comes at the end of many years of meticulous, painstaking research in our Unit and the NHS National Prion Clinic. Although further larger studies are needed to confirm its effectiveness, it’s the best hope yet of a successful early diagnostic test for the disease. This test could potentially go on to allow blood services to screen the population for vCJD infection, assess how many people in the UK are silent carriers and prevent onward transmission of the disease.”

Professor John Collinge, Director of the MRC Prion Unit, said:

“One of the reasons that vCJD is such a dreaded disease and has caused such disruption and expense to health services is the lack of knowledge of who is and who is not a carrier of this infection. The next step will be to test anonymously several thousand blood donors from a country unaffected by BSE in order to gain a better idea of how the test fares in practice. Longer term studies will also be needed to assess what proportion of individuals who test positive for prion infection will then go on to develop the disease later in life.

“The MRC Prion Unit’s research with the NHS National Prion Clinic to improve early diagnosis is an essential part of the wider MRC strategy to develop better treatments for patients. For this to develop, it will be crucial for clinicians to be able to offer treatment before extensive irreversible damage to the brain has occurred. At the moment, a firm diagnosis of vCJD can usually be made only once serious symptoms of the disease have developed which indicate extensive damage to the brain.”

The study ’A blood-based assay for the detection of vCJD prion infection’ is published today in the journal The Lancet.

Ends

Notes to editors:

To arrange an interview with the researchers of this paper, please call the MRC Press Office on 0207 395 2345.

For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including one of the first antibiotics penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk

While the number of vCJD samples available for analysis was inherently small, and to date only a small number of healthy donors has been studied, analysis of this blinded panel indicated an assay sensitivity for vCJD of over 71% (15/21, CI 48-89%) and a specificity of 100% (0/169, CI 98-100%).

The NHNN forms part of University College London Hospitals NHS Foundation Trust, one of the largest NHS trusts in the United Kingdom providing first-class acute and specialist services. The Trust is committed to research and development and forms part of UCL Partners which in March 2009 was officially designated as one of the UK's first academic health science centres by the Department of Health. UCLH works closely with UCL, translating research into treatments for patients. www.uclh.nhs.uk



http://www.mrc.ac.uk/Newspublications/News/MRC007683




Annals of Neurology Volume 67, Issue 6, pages 761–770, June 2010


Validation of diagnostic criteria for variant Creutzfeldt–Jakob disease†


Craig A. Heath MD1,*, Sarah A. Cooper MD2, Katy Murray MD1, Andrea Lowman MB ChB (Hons), MRCP3, Colm Henry MB MRCPI MRCGP4, Margaret A. MacLeod MD, MRCP5, Gillian E. Stewart MB ChB1, Martin Zeidler FRCP6, Jan M. MacKenzie7, James W. Ironside FRCPath7, David M. Summers MD1, Richard S. G. Knight FRCP7, Robert G. Will FRCP7Article first published online: 27 JAN 2010

DOI: 10.1002/ana.21987



http://onlinelibrary.wiley.com/doi/10.1002/ana.21987/abstract



Annals of Neurology Volume 69, Issue 1, page 212, January 2011

Letter to the Editor Comment on validation of diagnostic criteria for variant Creutzfeldt-Jakob disease

Ana Lukic MRCP1,2, Simon Mead MRCP, PhD1,2,3, Peter Rudge FRCP1,2, John Collinge FRCP, PhD, FRS1,2,3

Article first published online: 28 JAN 2011

DOI: 10.1002/ana.22273

Copyright © 2010 American Neurological Association

There is no doubt that the development of diagnostic criteria has contributed greatly to epidemiological research in prion diseases, and Heath and colleagues1 emphasize this in surveillance studies of variant Creutzfeldt-Jakob disease (vCJD). We caution, however, against a more broad application in clinical practice, particularly in governing decisions about clinical diagnosis, communication with patients/caregivers, and access to experimental therapies. The physician looking after a young patient with an unexplained rapidly progressive neuropsychiatric syndrome, dementia, or ataxia needs to make prompt clinical decisions. There are treatable alternative diagnoses, and an early firm diagnosis is essential. The pulvinar sign on magnetic resonance imaging is often not identified when patients are first imaged, and a requirement for a clinical duration of 6 months or greater makes a probable diagnosis impossible in the early stages of disease. Physicians who have cared for families affected by vCJD are aware of the complicated psychological issues generated by the perceived mismanagement of the bovine spongiform encephalopathy epidemic, which are often exacerbated by a delay or equivocation about diagnosis. Several families also choose experimental intracerebroventricular pentosan polysulfate therapy, which requires neurosurgery.

In the context of these issues, the role of tonsillar biopsy is underemphasized by Heath et al and the criteria. In our experience of 60 biopsies, by far the largest series worldwide, tonsillar biopsy has 100% sensitivity and specificity, at any stage of the disease. Prion protein deposition in the tonsil can be patchy, and at least 20 germinal centers need to be examined.2The number examined in 1 French case3 reported by Heath et al may not have been adequate to avoid a false-negative result. It is notable that of the 6 most recent patients suspected clinically of having vCJD in the United Kingdom, 3 did not meet epidemiological criteria for probable vCJD while alive. Two of these patients would have been misdiagnosed as sporadic CJD according to the updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob Disease4 criteria; typical vCJD was diagnosed at autopsy in both. In a third patient, with a heterozygous codon 129 genotype reported by Kaski et al,5 the pulvinar sign was not thought to be present by all neuroradiologists, and no tissue was examined. It is reasonable to expect that tonsillar biopsy may have made the correct diagnosis in each of these cases.

Given experience with transfusion-associated secondary vCJD, vCJD prions are likely to be present in significant titer in human blood, a diagnostic blood test based on detection of the infectious agent is clearly possible in principle, and if technologically achieved, will necessitate a complete revision of how we approach diagnosis in this disease.

Potential Conflicts of Interest Nothing to report.

References 1 Heath CA, Cooper SA, Murray K, etal. Validation of diagnostic criteria for variant Creutzfeldt-Jakob disease. Ann Neurol 2010; 67: 761–770. PubMed,Web of Science® Times Cited: 3 2 Ironside JW, Hilton DA, Ghani A, etal. Retrospective study of prion-protein accumulation in tonsil and appendix tissues. Lancet 2000; 355: 1693–1694. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 65 3 Brandel JP, Heath CA, Head MW, etal. Variant CJD in France and the United Kingdom: evidence for the same agent strain. Ann Neurol 2009; 65: 249–256. Direct Link: AbstractFull Article (HTML)PDF(255K)References 4 Zerr I, Kallenberg K, Summers DM, et al. Updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob disease. Brain 2009; 132: 2659–2668. CrossRef,PubMed,ChemPort,Web of Science® Times Cited: 15 5 Kaski D, Mead S, Hyare H, etal. Variant CJD in a PRNP codon 129 heterozygous individual. Lancet 2009; 374: 2128. CrossRef,PubMed,Web of Science® Times Cited: 10


http://onlinelibrary.wiley.com/doi/10.1002/ana.22273/abstract




Tuesday, January 25, 2011

Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions

http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html



Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html



Thursday, October 07, 2010

Experimental Transmission of H-type Bovine Spongiform Encephalopathy to Bovinized Transgenic Mice

http://bse-atypical.blogspot.com/2010/10/experimental-transmission-of-h-type.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



Wednesday, January 19, 2011

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html



Tuesday, January 18, 2011

Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html



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



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, September 24, 2010

USA Blood products, collected from a donor who was at risk for vCJD, were distributed SEPTEMBER 2010

http://vcjdtransfusion.blogspot.com/2010/09/usa-blood-products-collected-from-donor.html



Wednesday, September 08, 2010

Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010

http://vcjdtransfusion.blogspot.com/2010/09/emerging-infectious-diseases-cjd-bse.html



Saturday, July 17, 2010

Variant Creutzfeldt-Jakob disease Ironside JW., Haemophilia.

2010 Jul;16 Suppl 5:175-80 REVIEW ARTICLE

http://vcjdtransfusion.blogspot.com/2010/07/variant-creutzfeldtjakob-disease.html



Tuesday, September 14, 2010

Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)

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

From: Terry S. Singeltary Sr.

To: william.freas@fda.hhs.gov

Cc: rosanna.harvey@fda.hhs.gov ; Emery, Bryan (CBER)


SEE FULL TEXT ;

http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.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




USA

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.

2010

PLEASE NOTE REFERENCE LINES 5. AND 6.

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


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


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


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


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


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


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