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

Saturday, January 20, 2007 Fourth case of transfusion-associated vCJD infection in the United Kingdom

Subject: Fourth case of transfusion-associated vCJD infection in the United Kingdom Date: January 18, 2007 at 8:32 am PST

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

Editorial team (eurosurveillance.weekly@hpa.org.uk), Eurosurveillance editorial office

A suspected case of variant Creutzfeldt-Jakob disease (vCJD) has recently been diagnosed in a patient in the United Kingdom (UK), who received a blood transfusion from a donor who later developed vCJD [1]. This is the fourth case of probable transfusion transmission of vCJD infection in the UK. Three of the four recipients developed symptoms of vCJD. The first symptomatic case of vCJD associated with blood transfusion was identified in December 2003. This individual developed vCJD six and a half years after transfusion of red cells donated by an individual who developed symptoms of vCJD three and a half years after donation.

A second case of vCJD 'infection' was identified a few months later in a person who had received red cells from a donor who developed symptoms of vCJD 18 months after donation. This patient (the second case) died from causes unrelated to vCJD five years after transfusion. Post-mortem investigations found abnormal prion protein in the spleen and a cervical lymph node., However, prion protein was not found in the brain, and no pathological features of vCJD were found.

A third case developed symptoms of vCJD six years after receiving a transfusion of red blood cells, and died two years and eight months later. The donor of the blood involved developed vCJD about 20 months after donating it.

These three cases have been published as case reports and in the findings of the ongoing collaborative study between the National Blood Services, the National CJD Surveillance Unit, and the Office for National Statistics. This study aims to collect evidence about transmission of CJD or vCJD via the blood supply [2,3,4,5].

The new, fourth case is in a patient who developed symptoms of vCJD eight and a half years after receiving a transfusion of red blood cells from a donor who developed vCJD about 17 months after this blood was donated [1]. The donor to this case also donated the vCJD-implicated blood transfused to the third case. As for all other reported clinical vCJD cases that have been tested for genotype, this patient is a methionine homozygote at codon 129 of the prion protein gene. The patient is currently alive.

All four cases had received transfusions of non-leucodepleted red blood cells between 1996 and 1999. Since October 1999, leucocytes have been removed from all blood used for transfusion in the UK. The effect of leucodepletion on the reduction of the risk of transmission of vCJD from an infective donation is uncertain.

This fourth case of vCJD infection associated with blood transfusion further increases the level of concern about the risk of vCJD transmission between humans by blood transfusion, although much remains unknown. This reinforces the importance of the existing precautions that have been introduced to reduce the risk of transmission of vCJD infection by blood and blood products [6]. No cases of vCJD have been associated with fractionated plasma products. The small group of living recipients of vCJD-implicated blood transfusion in the UK have been informed of their potential exposure to vCJD by blood transfusion, asked to take certain precautions to reduce the risk of onward person-to-person transmission of vCJD during health care, and offered specialist neurological evaluation and advice.

This article has been adapted from reference 1

References: Health Protection Agency. Fourth case of variant CJD associated with blood transfusion (press release). Press release, 18 January 2007. (http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070118_vCJD.htm ) Llewelyn CA, Hewitt PE, Knight RSG, Amar K, Cousens S, Mackenzie J, et al. Possible transmission of variant CJD disease by blood transfusion. Lancet 2004; 363:417-21. Peden AH, Head MW, Ritchie DL, Bell JE, Ironside JW. Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 2004 ; 364: 527-9. Wroe SJ, Pal S, Siddique D, Hyare H, Macfarlane R, et al Clinical presentation and pre-mortem diagnosis of blood transfusion-associated variant CJD. Lancet 2006;368:2061-67. Hewitt PE, Llewelyn CA, Mackenzie J, Will RG. Creutzfeldt-Jakob disease and blood transfusion: results of the UK Transfusion Medicine Epidemiology review study. Vox Sang. 2006;91(3):221-230. Department of Health [London]. Further precautions to protect blood supply. Press release 2004/0104, 16 March 2004. (http://www.dh.gov.uk/PublicationsAndStatistics/PressReleases/PressReleasesN otices/fs/en?CONTENT_ID=4076608&chk=MTwE%2Bl)

http://www.eurosurveillance.org/ew/2007/070118.asp#4


HPA Press Statement

18 January 2007

4th case of variant CJD infection associated with blood transfusion

A new case of variant-Creutzfeldt-Jakob disease (vCJD ) associated with a blood transfusion has recently been diagnosed.

This latest patient has been diagnosed with vCJD about nine years after receiving a blood transfusion from a donor who later went on to develop vCJD. A transfusion from the same blood donor was also associated with one of the previously identified cases. The patient is still alive and is under specialist care.

This fourth case of vCJD infection associated with blood transfusion increases the concern about the risk of vCJD transmission between humans via blood transfusion. All four cases relate to the transfusion of blood components: no cases have been reported relating to treatment with plasma products.

The patient is one of a small number (less than 30) of living individuals who are known to have received a blood transfusion in the UK from a donor who later developed vCJD. All these individuals have previously been informed of their potential exposure to vCJD and asked to take certain precautions to reduce the chance of passing on vCJD to other people via healthcare procedures, such as surgery.

The Health Protection Agency has been in contact with doctors caring for the other patients who have been exposed to blood transfusions from donors who later developed vCJD. This is to ensure that they are informed of this new development and provide access to the latest information and specialist advice about their risk due to blood transfusion.

Professor Peter Borriello, Director of the HPA's Centre for Infections said, "This new case of vCJD infection increases our concern about the risk to the small group of people who had blood transfusions from donors who unknowingly at the time of donation must have had vCJD infection. However, this new case does not change our understanding of the risk for other people in any specific way. It does however reinforce the importance of the precautions that have already been taken to reduce the risk of transmission of vCJD infection by blood."

Dr Angela Robinson, Medical Director of NHS Blood and Transplant said, "Blood transfusions are often given to save or prolong the life of patients who are very ill and the benefit of receiving a transfusion when needed must always be balanced against any possible risk. Nonetheless, our primary concern is the safety of our patients through maintaining the quality of blood used for medical treatment. Since 1997, the NBS has introduced a range of precautionary measures against the risk of vCJD."

vCJD is a rare disease, and less than 2% of the vCJD cases reported to date in the UK have been associated with blood transfusion.

Notes to Editors:

To date, there have been 66 people identified in the UK who have received vCJD implicated blood transfusions. The transfusions received by these 66 individuals were donated by eighteen different donors who were diagnosed with vCJD after their blood donation. Of these 66 people, 40 have died of illnesses other than vCJD, including one patient who was found to have evidence of vCJD in parts of their body after their death. Including the new (4th) case, 3 of these people who have received vCJD implicated blood transfusions have developed symptoms of vCJD. There are 23 people who have received vCJD implicated blood transfusions who are alive and have not been diagnosed with vCJD.

The identification of cases of variant-CJD associated with blood transfusion has depended on the Transfusion Medicine Epidemiology Review, a collaborative study between the National Blood Services, the National CJD Surveillance Unit and the Office of National Statistics. For further information about this study see Hewitt et al Creutzfeldt-Jakob disease and blood transfusion: results of the UK Transfusion Epidemiology Review study. Vox Sanguinis 2006 91:221-230.

'Blood Transfusion' means transfusion with labile blood components (e.g. red cells, platelets, fresh frozen plasma). This latest case (and the previous three referred to) relate to transfusion of blood components and not treatment with plasma products (i.e. products that are manufactured from plasma). To date, no case of vCJD has been associated with treatment with plasma-products (e.g. clotting factors used to treat individuals with bleeding disorders such as haemophilia).

This fourth case has been classified by the National CJD Surveillance Unit ( www.cjd.ed.ac.uk ) as a 'probable' case of vCJD. Of the 158 vCJD cases that have died (data to 5 Jan 2007), all 112 that have undergone post-mortem (46 have not) have been 'confirmed' by neuropathological examination (examination of brain tissue).

The first clinical case of vCJD associated with transfusion was identified in December 2003. A case of vCJD 'infection' associated with transfusion was identified a few months later. The patient had no symptoms but evidence of infection (abnormal prion proteins) was identified in a post mortem investigation. The individual died from causes unrelated to vCJD.

Following the first case of vCJD associated with a blood transfusion in 2003, the Department of Health asked all recipients of blood transfusions not to donate blood as a precautionary measure to protect the blood supply from vCJD.

Patients who are informed that they are considered to be 'at risk' of vCJD for public health purposes are asked to take the following precautions to reduce the chance of passing on vCJD to other people: Not to donate blood, tissues or organs and To inform their healthcare providers of their 'at-risk' status so that special procedures may be arranged for certain instruments used in their healthcare (NB. Their GPs are also asked to do this.)

A range of measures have been put in place by the Department of Health to minimise the possible risk of vCJD being passed through blood:

Since 1997 all cases of vCJD that are reported to the National CJD Surveillance Unit and diagnosed as having 'probable' vCJD, result in a searc h of the UK Blood Services blood donor records. If the patient has donated blood, any unused parts of that blood are immediately removed from stock. The fate of all used components of blood from the donor is traced, and surviving recipients informed of their risk. In July 1998, the Department of Health announced that plasma for the manufacture of blood products, such as clotting factors, would be obtained from non-UK sources. Since October 1999, white blood cells (which may carry the greatest risk of transmitting vCJD) have been removed from all blood used for transfusion. In August 2002 the Department of Health announced that fresh frozen plasma for treating babies and young children born after 1 January 1996 would be obtained from the USA, extended to all children under 16 years of age (Summer 2005). In December 2002, the Department of Health completed its purchase of the largest remaining independent US plasma collector, Life Resources Incorporated. This secures long-term supplies of non-UK blood plasma for the benefit of NHS patients. Since April 2004, blood donations have not been accepted from people who have themselves received a blood transfusion in the UK since 1980. This has been extended to include apheresis donors and donors who are unsure if they had previously had a blood transfusion (August 2004). Since late 2005, blood donations have not been accepted from donors whose blood was transfused to patients who later developed vCJD. The UK Blood Services continue to promote the appropriate use of blood and tissues and alternatives throughout the NHS.

The likelihood of a person who may be infected with vCJD going onto develop symptoms of the disease is uncertain, and may depend on individual susceptibility. It is possible that infected individuals may never develop symptoms.

For further information contact the HPA press office on 0208 327 7098/7097/6055

Specialist care for vCJD is available from The NHS National Prion Clinic, based at The Hospital for Neurology and Neurosurgery, Queen Square, London http://www.nationalprionclinic.org/

The National CJD Surveillance Unit is based at the Western General Hospital Edinburgh: www.cjd.ed.ac.uk

For further information about vCJD go to: http://www.hpa.org.uk/infections/topics_az/cjd/menu.htm http://www.dh.gov.uk/PolicyAndGuidan...pics/CJD/fs/en http://www.blood.co.uk/ http://www.cjd.ed.ac.uk http://www.nationalprionclinic.org/

http://www.hpa.org.uk/hpa/news/articles/press_releases/2007/070118_vCJD.htm


FDA NVCJD BLOOD LATEST RECALLS

PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0576-7; b) Red Blood Cells, Recall # B-0577-7; c) Fresh Frozen Plasma, Recall # B-0578-7; d) Recovered Plasma, Recall # B-0579-7 CODE a) Units: 4588939, 4685381,4800041, 4892978, 4882799, 4883439, 4956157; b) Unit: 4662465; c) Units: 4800041, 4883439; d) Units: 4588939, 4662465, 4685381, 4800041, 4892978, 4882799, 4956157 RECALLING FIRM/MANUFACTURER Recalling Firm: Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on March 11, 2005. 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 17 units DISTRIBUTION OK, MS, MI, CA, and Switzerland ______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0580-7; b) Recovered Plasma, Recall # B-0581-7 CODE a) and b) Unit: 5346932 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on October 27, 2005. 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 OK and Switzerland

______________________________ PRODUCT a) Red Blood Cells Leukocytes, Recall # B-0582-7; b) Recovered Plasma, Recall # B-0583-7 CODE a) and b) Unit: 5208304 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on April 20, 2006. Firm initiated recall is complete. REASON Blood products, collected from a donor considered to be at increased riskfor variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION OK and Switzerland

______________________________ PRODUCT Source Plasma, Recall # B-0585-7 CODE Units: 02JWIB9722, 02JWIC0263, 02JWIC0607, 02JWIC4253, 02JWIC4904, 02JWIC5216, 02JWID2018, 02JWID2958, 02JWID3310, 02JWID8505, 02JWID8842, 02JWID9390, 02JWID9844, 02JWIE0468, 02JWIE0836, 02JWIE1435, 02JWIE1812, 02JWIE2609, 02JWIE3289, 02JWIE3887, 02JWIE4309, 02JWIE4818, 02JWIE5277, 02JWIE5825, 03JWIA0857, 03JWIA1249, 03JWIA1850, 03JWIA2192, 03JWIA2825, 03JWIA3180, 03JWIA3724, 03JWIA4092, 03JWIA4691, 03JWIA5042, 03JWIA5586, 02JWIC1157, 02JWIC1458, 02JWIC2095, 02JWIC2551, 02JWIC3031, 02JWIC3491, 02JWIC3975, 02JWIC6689, 02JWIC7051, 02JWIC7609, 02JWIC7898, 02JWIC8547, 02JWIC8906, 02JWIC9494, 02JWIC9793, 02JWID0630, 02JWID1144, 02JWID1592, 02JWID3884, 02JWID4247, 02JWID4827, 02JWID5189, 02JWID5713, 02JWID6578, 02JWID6926, 02JWID7624, 02JWID7970 RECALLING FIRM/MANUFACTURER BioLife Plasma Services L.P., Janesville, WI, by fax on April 7, 2003. 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 62 units DISTRIBUTION MI and Austria

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-0586-7; b) Recovered Plasma, Recall # B-0587-7 CODE a) and b) Unit: 4499508 RECALLING FIRM/MANUFACTURER Sylvan N. Goldman Center, Oklahoma Blood Institute, Oklahoma City, OK, by fax on February 27, 2006. 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 OK and Switzerland

______________________________

PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-0644-7; b) Recovered Plasma, Recall # B-0645-7 CODE a) and b) Units: 5219381, 4759725 RECALLING FIRM/MANUFACTURER Oklahoma Blood Institute, Sylvan N. Goldman Center, Oklahoma City, OK, by facsimile on December 3, 2005 or by electronic notification on December 4, 2005. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 4 units DISTRIBUTION OK, VA, and Switzerland

______________________________

END OF ENFORCEMENT REPORT FOR JANUARY 17, 2007

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http://www.fda.gov/bbs/topics/enforce/2007/ENF00987.html


----- Original Message ----- From: Terry S. Singeltary Sr. To: FREAS@CBER.FDA.GOV Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov Sent: Wednesday, November 29, 2006 1:24 PM Subject: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION]

November 29, 2006

Greetings FDA, DHH, Dr. Freas, and Dr. Harvey et al,

a kind and warm Holiday Greetings to you all.

i kindly wish to submit the following to the TSE advisory committee for the meeting December 15, 2006, about the assessment for potential exposure to vCJD in human plasma-derived antihemophilic factor (FVIII) products manufactured from U.S. plasma donors and related communication material ;

http://a257.g.akamaitech.net/7/257/2422/01jan20061800/edocket.access.gpo.gov/2006/E6-20251.htm


i see the media picked up on this as a 'low risk', from what the gov. agency perceived to be to them;

http://www.newsday.com/news/health/ats-ap_health14nov27,0,7955259.story?coll=ny-leadhealthnews-headlines


however, i seem to disagree. from my primitive ciphering, i see it another way. this is a huge catastrophic risk. 3 in 160 is 1.9%. so call that 2% which is 1 in 50 or twenty per thousand or 20,000 per million. also, what about the mixed genotypes/mixed susceptibility? what about the silent carriers that donated tainted blood? what about the sporadic CJDs of UNKNOWN strain or phenotype? this risk assessment is just more BSe to me. just another in a long line of industry fed crap. i pray that my assessment is the one that is wrong. but it is THEY who roll the dice with your life. it is THEY who refuse to regulate an industry that has run amok. just from a recall aspect of potentially tainted blood, and these are just recent recalls ;

PRODUCT Source Plasma, Recall # B-0054-7 CODE Units: 03MMNC5465, 03MMNC6361, 03MMNC6801, 03MMNC7510, 03MMNC7891, 03MMNC8252, 03MMNC8801, 03MMNC9144, 03MMND1122, 03MMND1478, 03MMND1969, 03MMND2350, 03MMND2825, 03MMND3211, 03MMND3708, 03MMND4072, 03MMND4588, 03MMND4831, 03MMND5320, 03MMND5719, 03MMND6268, 03MMND6683, 03MMND7228, 03MMND7656, 03MMND8211, 03MMND8652, 03MMND9195, 03MMND9618, 03MMNE0628, 03MMNE0884, 03MMNE1597, 03MMNE1979, 03MMNE2644, 03MMNE3064, 03MMNE3707, 03MMNE4122, 03MMNE4750, 03MMNE5080, 03MMNE5876, 03MMNE6218, 03MMNE7189, 03MMNE7587, 03MMNE8027, 03MMNE8645, 03MMNE9029, 03MMNE9641, 03MMNE9979, 03MMNF0491, 03MMNF0685, 03MMNF0937, 03MMNF1260, 04MMNA0351, 04MMNA0707, 04MMNA1241, 04MMNA1650, 04MMNA2291, 04MMNA2646, 04MMNA3340, 04MMNA3719, 04MMNA4312, 04MMNA4683, 04MMNA5298, 04MMNA5750, 04MMNA6407, 04MMNA6816, 04MMNA7482, 04MMNA7915, 04MMNA8632, 04MMNA9076, 04MMNA9723, 04MMNB0063, 04MMNB0696, 04MMNB1100, 04MMNB1845, 04MMNB2285, 04MMNB3035, 04MMNB3485, 04MMNB4213, 04MMNB4672, 04MMNB5841, 04MMNB6652, 04MMNB7162, 04MMNB7930, 04MMNB8453, 04MMNB9239, 04MMNB9747, 04MMNC0456, 04MMNC0931, 04MMNC1578 RECALLING FIRM/MANUFACTURER BioLife Plasma Services, L.P., Mankato, MN, by facsimile on June 4, 2004. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 89 units DISTRIBUTION CA and Austria

END OF ENFORCEMENT REPORT FOR October 25, 2006

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http://www.fda.gov/bbs/topics/enforce/2006/ENF00975.html


USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)

RECALLS AND FIELD CORRECTIONS: BIOLOGICS -- CLASS II ______________________________ PRODUCT Source Plasma, Recall # B-1708-6 CODE Units: MI180733, MI180927, MI181625, MI181780, MI182337, MI182519, MI183140, MI183311, MI183955, MI185006, MI185278, MI185822, MI186081, MI186855, MI187183, MI187903, MI188273, MI188695, MI189257, MI189553, MI190136, MI190473, MI191073, MI191395, MI191972, MI192303, MI193473, MI194343, 04MINA0377, 04MINA0801, 05MINA7147, 05MINA7451, 05MINA8094, 05MINA8504, 05MINA9548, 05MINA9883, 05MINB0489, 05MINB0875, 05MINB1469, 05MINB1874, 05MINB3116, 05MINB7192, 05MINB7529, 05MINB8246, 05MINB8612, 05MINB9236, 05MINB9366, 05MINB9475, 05MINB9641, 05MINC0031, 05MINC0237, 05MINC0336, 05MINC0894, 05MINC0964, 05MINC1138, 05MINC1619, 05MINC1750, 05MINC1907, 05MINC1977, 05MINC2375, 05MINC2774, 05MINC3113, 05MINC3484, 05MINC4277, 05MINC4623, 05MINC5623, 05MINC5914, 05MINC7545, 05MINC7870, 05MINC8355, 05MINC8689, 05MINC9437, 05MINC9775, 05MIND0067, 05MIND0393, 05MIND0892, 05MIND0951, 05MIND1836, 05MIND2183 and 05MIND2962 RECALLING FIRM/MANUFACTURER BioLife Plasma Services L.P., Muncie, IN, by facsimile on November 22, 2005. Firm initiated recall is complete. REASON Blood products, collected from unsuitable donors based on risk factors for Creutzfeldt-Jakob Disease (CJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 80 units DISTRIBUTION CA, NC, and MD

______________________________

PRODUCT a) Red Blood Cells, Leukocytes Reduced, Recall # B-1714-6; b) Fresh Frozen Plasma, Recall # B-1715-6; c) Platelets, Recall # B-1716-6 CODE a), b), and c) Unit: 2443732 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by letters dated November 11, 2003 and December 18, 2003. Firm initiated recall is complete. REASON Blood products, collected from a donor who was at increased risk for new variant Creutzfeldt-Jakob Disease (nvCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION TX and WI

END OF ENFORCEMENT REPORT FOR SEPTEMBER 13, 2006

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http://www.fda.gov/bbs/topics/enforce/2006/ENF00969.html


PRODUCT Fresh Frozen Plasma, Recall # B-1751-6 CODE Unit: 4936623 RECALLING FIRM/MANUFACTURER Gulf Coast Regional Blood Center, Houston, TX, by facsimile dated September 16, 2005. Firm initiated recall is complete. REASON Blood product, which was collected from an unsuitable donor based on risk factors for variant Creutzfeldt-Jakob Disease (vCJD), was distributed. VOLUME OF PRODUCT IN COMMERCE 1 unit DISTRIBUTION TX

END OF ENFORCEMENT REPORT FOR SEPTEMBER 6, 2006

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


Mon Aug 7, 2006 10:24 71.248.132.189

PRODUCT a) Red Blood Cells, Recall # B-1587-6; b) Cryoprecipitated AHF, Recall # B-1588-6; c) Recovered Plasma, Recal # B-1589-6 CODE a), b) and c) Unit: 2016719 RECALLING FIRM/MANUFACTURER Walter Shepeard Community Blood Center, Inc., Augusta, GA, by facsimile on March 13, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION GA and Germany

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1590-6; b) Fresh Frozen Plasma, Recall # B-1591-6 CODE a) and b) Unit: 2443595 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on June 30, 2004. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1592-6; b) Fresh Frozen Plasma, Recall # B-1593-6 CODE a) and b) Unit: 2545596 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on December 14, 2004 and January 3, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________

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


PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6; b) Fresh Frozen Plasma, Recall # B-1551-6 CODE a) and b) Unit 2395371 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on August 20, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX ______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1552-6; b) Platelets, Recall # B-1553-6; c) Fresh Frozen Plasma, Recall # B-1554-6 CODE a), b) and c) Unit 2438702 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on May 29, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 3 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells Leukocytes Reduced, Recall # B-1555-6; b) Fresh Frozen Plasma, Recall # B-1556-6 CODE a) and b) Unit 2454970 RECALLING FIRM/MANUFACTURER South Texas Blood and Tissue Center, San Antonio, TX, by fax on July 23 and December 11. 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION TX

______________________________ PRODUCT a) Red Blood Cells, Recall # B-1494-6 b) Cryoprecipitated AHF, Recall # B-1495-6 CODE a) and b) Unit 5013100 RECALLING FIRM/MANUFACTURER Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on May 17, 2005. Firm initiated recall is complete. REASON Blood products, which were collected from a donor who may be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION GA

______________________________ PRODUCT Source Plasma, Recall # B-1450-6 CODE Unit numbers ST0824313 and ST0824764 RECALLING FIRM/MANUFACTURER Stillwater Plasma Center LLC, Stillwater, OK, by fax on November 21, 2003. Firm initiated recall is complete. REASON Blood products, which were collected from a donor whose suitability pertaining to risk factors for Creutzfeldt-Jakob Disease (vCJD) was not adequately determined, were distributed. VOLUME OF PRODUCT IN COMMERCE 2 units DISTRIBUTION UK

______________________________ PRODUCT Plasma Frozen, Recall # B-1422-6;

SNIP...END

----- Original Message ----- 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 PART III]

Lancet Neurology DOI:10.1016/S1474-4422(06)70413-6

Predicting susceptibility and incubation time of human-to-human transmission of vCJD

MT Bishop a, P Hart b, L Aitchison b, HN Baybutt b, C Plinston b, V Thomson b, NL Tuzi b, MW Head a, JW Ironside a, RG Will a and JC Manson b

Summary Background Identification of possible transmission of variant Creutzfeldt-Jakob disease (vCJD) via blood transfusion has caused concern over spread of the disease within the human population. We aimed to model iatrogenic spread to enable a comparison of transmission efficiencies of vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the effect of the codon-129 polymorphism on human susceptibility.

Methods Mice were produced to express human or bovine prion protein (PrP) by direct replacement of the mouse PrP gene. Since the human PrP gene has variation at codon 129, with MM, VV, and MV genotypes, three inbred lines with an identical genetic background were produced to express human PrP with the codon-129 MM, MV, and VV genotypes. Mice were inoculated with BSE or vCJD and assessed for clinical and pathological signs of disease.

Findings BSE was transmitted to the bovine line but did not transmit to the human lines. By contrast, vCJD was transmitted to all three human lines with different pathological characteristics for each genotype and a gradation of transmission efficiency from MM to MV to VV.

Interpretation Transmission of BSE to human beings is probably restricted by the presence of a significant species barrier. However, there seems to be a substantially reduced barrier for human-to-human transmission of vCJD. Moreover, all individuals, irrespective of codon-129 genotype, could be susceptible to secondary transmission of vCJD through routes such as blood transfusion. A lengthy preclinical disease is predicted by these models, which may represent a risk for further disease transmission and thus a significant public-health issue.

Affiliations

a. National CJD Surveillance Unit, Bryan Matthews Building, Western General Hospital, Edinburgh, UK b. Institute for Animal Health, Neuropathogenesis Unit, King's Buildings, Edinburgh, UK

Correspondence to: Prof J C Manson, Institute for Animal Health, Neuropathogenesis Unit, Ogston Building, King's Buildings, West Mains Road, Edinburgh EH9 3JF, UK

snip...

Discussion

Although the cattle BSE epidemic in the UK has amounted to more than 180 000 cases since the 1980s, the extent of the human vCJD epidemic has so far remained limited with the total number of cases worldwide currently at 190. One explanation for this apparent discrepancy is that there exists a significant species barrier between cattle and human beings, which limits the susceptibility of the human population to BSE. The data shown here suggest that this could indeed be the case since BSE was readily transmissible to the bovine transgenic mice but not to the human transgenic mice. However, once BSE has passed through human beings in the form of vCJD, the transmissibility of this TSE strain is altered for the human population.

All the human transgenic lines inoculated with BSE were negative for TSE transmission, which suggests that either the human transgenic lines are relatively resistant to transmission of BSE or the incubation time is longer than the length of the experiment (approximately 700 days). BSE transmission previously observed by others, in human transgenic lines overexpressing the human prion protein, could be due to overexpression of the PrP gene and may not therefore give a true reflection of the species barrier between BSE and human beings.15,25,26 This apparent resistance of human transgenic mice to BSE could be explained by a large species barrier and this in turn could explain the low number of vCJD cases in the human population.

vCJD was transmitted to all three human lines with different pathological characteristics for each genotype, and a gradation of transmission efficiency from MM to MV to VV. The greater transmission efficiency in HuMM mice suggests that homozygosity for methionine at codon 129 leads to earlier onset of TSE-related pathological features and clinical disease than for the other two genotypes. The differences in PrPSc deposition in the HuMM and HuMV lines suggest that the codon- 129 polymorphism in human beings is likely to affect the distribution of PrPSc deposition in the brain. Moreover, the similar numbers that scored positive for PrP deposition in each of the MM and MV groups (11/15 and 11/13 respectively) suggest that the two genotypes might be equally susceptible to vCJD, but with different incubation periods. Titration experiments are needed to fully compare the susceptibility of each line. The single HuVV mouse positive for PrPSc shows that VV individuals may be susceptible to vCJD with very long incubation times, including a lengthy subclinical phase. Transmission studies from all three genotype mice are now underway to examine the infectious nature of the disease and determine any alterations in the strain characteristics on passage through human transgenic mice. By contrast with published data suggesting that VV individuals cannot propagate the vCJD biochemical phenotype,15 the data presented here suggest that the

PrPSc type will remain a useful diagnostic feature of secondary vCJD infection irrespective of codon-129 genotype, as has been observed for the two extant cases of transfusion-associated vCJD infection. 5,27

Transmission of vCJD to the three lines of human transgenic mice indicates that the human population could be at significantly heightened risk of developing disease after iatrogenic exposure to vCJD. Secondary transmission of vCJD has partly removed the cattle-to- human species barrier and has resulted in an agent that can be transmitted from human to human with relative efficiency. Transmission studies in cynomolgus macaques provide further evidence for this agent adaptation as they show reduction in incubation times after serial passage of BSE.28 Our BSE inoculation at 10-1 dilution was compared with vCJD inoculation at 10-2 because the latter inoculum was found to be toxic to the mice at 10-1. Use of a higher dose ofvCJD inoculum would have maintained or increased the transmission efficiency of vCJD and enhanced the current findings.

Our findings raise concerns relevant to the possibility of secondary transmission of vCJD through blood transfusion, fractionated blood products, or contaminated surgical instruments. For this study mice were injected intracerebrally, whereas the probable human exposure to these agents is by peripheral routes (eg, oral or intravenous), and thus human-to-human exposures might be significantly less efficient. However, it is difficult to know for sure what the practical implications might be in human beings. Peripheral route challenge is in progress; however, BSE transmission studies in primates have shown the intravenous route to be as efficient as the intracerebral route, with an extension of the incubation time.28

Although all cases of vC]D up to now have been observed in the MM genotype, this model of human-to- human vCJD transmission suggests that other genotypes are also susceptible. In our experimental setting, all PRNP codon-129 genotypes are susceptible to vCJD infection; however, progressive development of pathological TSE features (vacuolation and PrP deposition) is more rapid in the MM-genotype mice. An explanation for this finding might be provided by in-vitro conversion of recombinant human PrP by BSE and vCJD agents, which has shown that PrP with methionine at position 129 is more efficiently converted than PrP with valine, and that conversion by vCJD is significantly more efficient than by BSE.29 Long incubation periods during which PrPSc is deposited predicts that, in human beings, infection could be present in all genotypes for a significant period before clinical onset. Incubation periods of more than 30 years have been reported in the human TSE disease kuru.30

The possibility that an MV or VV genotype could result in a phenotype distinct from that recognised in vCJD draws attention to the importance of systematic assessment of the clinical, genetic, pathological, and

biochemical features of all human prion diseases. Our findings indicate that for human-to-human vCJD infection

it should be assumed that all codon-129 genotype individuals (not just MM) can be infected, that long incubation times can occur, and that a significant level of subclinical disease might be present in the population.

Contributors

MTB, PH, and CP did immunocytochemical and western blot analysis;

JCM, NT, HNB, and LA produced the transgenic mouse lines; JWI supplied vCJD case material and reviewed the neuropathology; VT did the mouse inoculations; and MTB, PH, MWH, RGW, JWI, and JCM prepared the manuscript.

Conflicts of interest

We have no conflicts of interest.

Acknowledgments

snip... end

http://www.thelancet.com/journals/laneur/article/PIIS1474442206704136/abstract?isEOP=true


SNIP...

Greetings again Dr. Freas et al at FDA,

THIS was like closing the barn door after the mad cows got loose. not only the red cross, but the FDA has failed the public in protecting them from the TSE aka mad cow agent. TSE agent i.e. bse, base, cwd, scrapie, tme, and any sub strains thereof. we do not know if these strains will or have transmitted to humans as subclinical TSE or clinical disease, and we do not know if they have or will transmit second, third, forth passage via friendly fire i.e. multiple potential routes via medical, surgical, pharmaceutical etc.

IF you remember correctly Dr. Freas et al, i called this long ago, almost 6 years ago ;

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 ...

Freas, William

From: Terry S. Singeltary Sr. [flounder@wt.net]

Sent: Monday, January 08,200l 3:03 PM

To: freas@CBS5055530.CBER.FDA.GOV

Subject: CJDIBSE (aka madcow) Human/Animal TSE's--U.S.--Submission To Scientific Advisors and

Consultants Staff January 2001 Meeting (short version)

Greetings again Dr. Freas and Committee Members,

I wish to submit the following information to the

Scientific Advisors and Consultants Staff

2001 Advisory Committee (short version).

I understand the reason of having to shorten my submission,

but only hope that you add it to a copy of the long version,

for members to take and read at their pleasure,

(if cost is problem, bill me, address below).

So when they realize some time in the near future

of the 'real' risks i speak of from human/animal TSEs and

blood/surgical products. I cannot explain the 'real' risk

of this in 5 or 10 minutes at some meeting,

but will attempt here:

remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?

no need to go into that, you know of this blunder:

DO NOT make these same stupid mistakes again with

human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD,

and my neighbor lost his Mother to sCJD as well (both cases

confirmed). I have seen many deaths, from many diseases.

I have never seen anything as CJD, I still see my Mom laying helpless,

jerking tremendously, and screaming "God, what's wrong

with me, why can't I stop this". I still see this, and will

never forget. Approximately 10 weeks from 1st of symptoms to death.

This is what drives me. I have learned more in 3 years about not only

human/animal TSE's but the cattle/rendering/feeding industry/government

than i ever wished to.

I think you are all aware of CJD vs vCJD, but i don't think

you all know the facts of human/animal TSE's as a whole,

they are all very very similar, and are all tied to the

same thing, GREED and MAN.

I am beginning to think that the endless attempt to track

down and ban, potential victims from known BSE Countries

from giving blood will be futile. You would have to ban

everyone on the Globe eventually? AS well, I think we

MUST ACT SWIFTLY to find blood test for TSE's,

whether it be blood test, urine test, eyelid test,

anything at whatever cost, we need a test FAST.

DO NOT let the incubation time period of these TSEs fool you.

To think of Scrapie as the prime agent to compare CJD,

but yet overlook the Louping-ill vaccine event in 1930's

of which 1000's of sheep where infected by scrapie

from a vaccine made of scrapie infected sheep brains,

would be foolish. I acquired this full text version of the

event which was recorded in the Annual Congress of 1946

National Vet. Med. Ass. of Great Britain and Ireland.

From the BVA and the URL is posted in my (long version).

U.S.A. should make all human/animal TSE's notifiable at all ages,

with requirements for a thorough surveillance and post-mortem

examinations free of charge, if you are serious about eradicating

this horrible disease in man and animal.

There is histopathology reports describing "florid plaques"

in CJD victims in the USA and some of these victims are getting

younger. I have copies of such autopsies, there has to

be more. PLUS, sub-clinical human TSE's will most definitely

be a problem.

THEN think of vaccineCJD in children and the bovine tissues

used in the manufacturing process, think of the FACT that

this agent surviving 6OO*C.

PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C

Then think of the CONFIDENTIAL documents of what was known of

human/animal TSE and vaccines in the mid to late 8Os, it was all about

depletion of stock, to hell with the kids, BUT yet they knew.

To think of the recall and worry of TSE's from the polio vaccine,

(one taken orally i think?), but yet neglect to act on the

other potential TSE vaccines (inoculations, the most effective mode to

transmit TSEs) of which thousands of doses were kept and used,

to deplete stockpile, again would be foolish.

--Oral polio; up to 1988, foetal calf serum was used from UK and

New Zealand (pooled); since 1988 foetal calf serum only from New

Zealand. Large stocks are held.

--Rubella; bulk was made before 1979 from foetal calf serum from UK

and New Zealand. None has been made as there are some 15 years stock.

--Diphtheria; UK bovine beef muscle and ox heart is used but since the

end of 1988 this has been sourced from Eire. There are 1,250 litres of

stock.

. .

--Tetanus; this involves bovine material from the UK mainly Scottish.

There are 21,000 litres of stock.

--Pertussis; uses bovine material from the UK. There are 63,000 litres

of stock.

--They consider that to switch to a non-UK source will take a minimum of

6-18 months and to switch to a non-bovine source will take a minimum of

five years.

3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These

are sourced from the USA and the company believes that US material only

is used.

89/2.14/2.1

============

BSE3/1 0251

4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK.

there are 440,000 units of stock. They have also got MMR using bovine

serum from the UK.

5. XXXXXXXXXXX have influenza, rubella, measles,' MMR vaccines

likely to be used in children. Of those they think that only MMR

contains bovine material which is probably a French origin.

6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial.

hese use veal material, some of which has come from the UK and has been

ade by XXXXXXXXXXX (see above).

I have documents of imports from known BSE Countries,

of ferments, whole blood, antiallergenic preparations,

2

human blood plasma, normal human blood sera, human immune

blood sera, fetal bovine serum, and other blood fractions

not elsewhere specified or included, imported glands,

catgut, vaccines for both human/animal, as late as 1998.

Let us not forget about PITUITARY EXTRACT. This was used to help COWS

super ovulate. This tissue was considered to be of greatest risk of

containing BSE and consequently transmitting the disease.

ANNEX 6

MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO

BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL

How much of this was used in the U.S.?

Please do not keep making the same mistakes.

'Absence of evidence is not evidence of absence'.

What are the U.S. rules for importing and manufacturing vaccines,

medicines and medical devices?

Does the U.S.A. allow sourcing of raw material of ruminants from

the U.S.A.?

U.S. cattle, what kind of guarantee can you give for serum or

tissue donor herds.?

The U.S. rendering system would easily amplify T.S.E.'s:

Have we increased the stability of the system (improved heat treatments)

since the EU SSC report on the U.S.A. was published

in july 2000?

What is done to avoid cross-contaminations in the U.S.A.?

How can the U.S. control absence of cross-contaminations of animal

TSE's when pig and horse MBM and even deer and elk are allowed in

ruminant feed, as well as bovine blood? I sadly think of the rendering

and feeding policy before the Aug. 4, 1997 'partial'

feed ban, where anything went, from the city police horse, to the circus

elephant, i will not mention all the scrapie infected sheep.

I am surprised that we have not included man 'aka soyent green'.

It is a disgusting industry and nothing more than greed fuels it.

When will the U.S.. start real surveillance of the U.S. bovine

population (not passive, this will not work)?

When will U.S. start removing SRMs?

Have they stopped the use of pneumatic stunners in the U.S.?

If so, will we stop it in all U.S. abattoirs or only in those

abattoirs exporting to Europe?

If not, WHY NOT?

same questions for removal of SRM in the U.S.A.,

or just for export?

If not, WHY NOT?

How do we now sterilize surgical/dental instruments in the U.S.A.?

Where have we been sourcing surgical catgut?

(i have copies of imports to U.S., and it would floor you)

When will re-usable surgical instruments be banned?

'Unregulated "foods" such as 'nutritional supplements' containing various

extracts from ruminants, whether imported or derived from

US cattle/sheep/cervids ("antler velvet" extracts!) should be

forbidden or at least very seriously regulated.

(neighbors Mom, whom also died from CJD, had been taking

bovine based supplement, which contained brain, eye, and many

other bovine/ovine tissues for years, 'IPLEX').

What is the use of banning blood or tissue donors from Germany, France,

etc... when the U.S.A. continues exposing cattle, sheep and people to

SRM, refuses to have a serious feed ban, refuses

to do systematic BSE-surveillance?

The FDA should feel responsible for the safety of what people eat.

prohibit the most dangerous foods, not only prohibit a few more donors,

the FDA should be responsible for the safe sourcing of medical devices,

not only rely on banning donors "from Europe",

The 'real' risks are here in the U.S. as well, and have been for some

time.

We must not forget the studies that have proven

infectivity in blood from TSE's.

The Lancet, November 9, 1985

" Sir, --Professor Manuelidis and his colleagues (Ott 19, p896) report

transmission to animals of Creutzfeldt-Jakob disease (CJD) from the

buffy coat from two patients. We also transmitted the disease from ,

whole blood samples of a patient (and of mice) infected with CJD.l

Brain, Cornea, and urine from this patient were also infectious,

and the clinicopathological findings2 are summarised as follows.

snip...

full text ;

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


Greetings again Dr. Freas et al at FDA,

NOW, here we are in 2006, worried and still fumbling around with what should have been done long, long ago ;

Subject: 91ST MEETING OF THE SEAC MEETING LONDON 24TH FEB 2006 Date: March 10, 2006 at 7:36 am PST 1

© SEAC 2006

NINETY FIRST MEETING OF THE SPONGIFORM

ENCEPHALOPATHY ADVISORY COMMITTEE

The Spongiform Encephalopathy Advisory Committee held its 91st

meeting in London on 24th February 2006.

snip...

MEDICAL IMPLANTS CONTAINING BOVINE MATERIAL

SEAC considered the risk to human health from medical implants

that include bovine material sourced from the USA. This material

was used for a wide range of medical devices, some of which are

life saving and for which there are no alternative products.

SEAC considered that the source of the animal was crucial to

manage the risk. The committee suggested that other

precautionary steps be taken where practicable, such as using

material from young animals, sourcing material from countries with

good surveillance procedures and a low prevalence of disease. ......

snip...

http://www.seac.gov.uk/minutes/final90.pdf


A BIT OF HISTORY ON THIS TOPIC

TWA LITTLE minute

http://www.bseinquiry.gov.uk/files/yb/1988/06/10001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/13010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/14006001.pdf


COMMERCIAL IN CONFIDENCE

http://www.bseinquiry.gov.uk/files/yb/1988/09/06005001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/10/06005001.pdf


NOT FOR PUBLICATION

http://www.bseinquiry.gov.uk/files/yb/1988/11/01012001.pdf


http://www.bseinquiry.gov.uk/yb/1988/11/04003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/04/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/07/00007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/09/00004001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/10/00003001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/04001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/26007001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/01/30001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf


NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE

snip...

I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.

snip...

The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...

http://www.bseinquiry.gov.uk/files/ws/s467bx.pdf


more on the 1968 medicine act, they forgot to follow

http://www.bseinquiry.gov.uk/files/yb/1989/01/30008001.pdf


8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).

http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf


although 176 products do _not_ conform to the CSM/VPC guidelines.

http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf


Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

http://www.bseinquiry.gov.uk/files/yb/1989/02/22008001.pdf


http://www.bseinquiry.gov.uk/files/yb/1989/02/22011001.pdf


(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)

http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/08011001.pdf


http://www.bseinquiry.gov.uk/files/yb/1988/06/07010001.pdf


TWA LITTLE STATEMENT 331

http://www.bseinquiry.gov.uk/files/ws/s331.pdf


SNIP...

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bare 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

JOURNAL OF NEUROLOGY

MARCH 26, 2003

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

disease in the United States

Email Terry S. Singeltary:

flounder@wt.net

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?

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


Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/


BRITISH MEDICAL JOURNAL

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2


BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1


[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf


THE SEVEN SCIENTIST REPORT ***

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf


PAUL BROWN M.D.

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf


9 December 2005 Division of Dockets Management (RFA-305)

SEROLOGICALS CORPORATION James J. Kramer, Ph.D. Vice President, Corporate Operations

http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf


Embassy of Japan http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm


Dockets Entered on December 22, 2005 2005D-0330, Guidance for Industry and FDA Review Staff on Collection of Platelets by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ... http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm


03-025IF 03-025IF-631 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12. http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf


03-025IF 03-025IF-634 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf


Page 1 of 17 9/13/2005 [PDF] ... 2005 6:17 PM To: fsis.regulationscomments@fsis.usda.gov Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food ... http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf


03-025IFA 03-025IFA-6 Jason Frost [PDF] ... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al [Docket No. 03- 025IF] Prohibition of the Use of Specified Risk Materials for Human Food and ... http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf


In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF] Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone: 732-741-2290 Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...

http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf


PLEASE READ FULL TEXT ;

http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e


3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit Hall

3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.

6:30 Close of Day One

http://www.healthtech.com/2007/tse/day1.asp


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...

http://www.cjdsurveillance.com/resources-casereport.html


There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf


***UPDATE ATYPICAL BSE USA I.E. BASE AND SPORADIC CJD

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

snip...

4. Members had received information about the notification by the Health Protection Agency (HPA) of recipients of four batches of plasma products that had been produced from blood donated by individuals that had later developed variant Creutzfeldt Jakob Disease (vCJD). THESE batches HAD NOT been included in a similar notification exercise in 2004, as the fate of these products COULD NOT BE TRACED at that time. The fourteenth annual report of the National CJD Surveillance Unit had been published. The European Food Safety Authority (EFSA) had issued a consultation on a revised methodology for geographical bovine spongiform encephalopathy (BSE) risk assessment. Members could submit individual responses. Submission of a SEAC response was under consideration.

snip...

ITEM 9 - ANY OTHER BUSINESS

snip...

***$$$***

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE. Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD. A study also demonstrated that in a mouse model it was possible to alleviate the pathological changes of prion disease by suppressing expression of the prion protein gene after infection.

http://www.seac.gov.uk/minutes/95.pdf


Terry S. Singeltary Sr. Bacliff, Texas USA 77518