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

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