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Fourth case of transfusion-associated vCJD infection UK

flounder

Well-known member
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 ([email protected]), 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/PressReleasesNotices/fs/en?CONTENT_ID=4076608&chk=MTwE%2Bl)

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


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

###


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


----- Original Message -----
From: Terry S. Singeltary Sr.
To: [email protected]
Cc: [email protected] ; [email protected]
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

###


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

###

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

###

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: [email protected]
Cc: [email protected] ; [email protected]
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. [[email protected]] Monday, January 08,200l 3:03 PM freas ...


Freas, William

From: Terry S. Singeltary Sr. [[email protected]]

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

To: [email protected]

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
 

flounder

Well-known member
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 search 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


TSS
 

flounder

Well-known member
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


TSS
 

PORKER

Well-known member
CJD (new var.) update 2007 (02): South Korea, susp
15.jan.07
ProMED Mail Post
http://www.promedmail.org
Date: Mon 15 Jan 2007
Source: Korea Times - Seoul, South Korea [edited]
South Korea: suspected case of mad cow disease
The authorities are conducting an epidemic inspection on a suspected victim
of mad cow disease (BSE, bovine spongiform encephalopathy). A patient who
was hospitalized due to dementia symptoms at Soon Chun Hyang University
Hospital in Seoul on Fri [5 Jan 2006] showed symptoms consistent with those
of a variant of Creutzfeldt-Jakob disease [abbreviated as CJD (new var.) or
vCJD in ProMED-mail], according to the hospital, the Ministry of
Agriculture and Forestry, and the Ministry of Health and Welfare on Monday
[16 Jan 2007].
An official of the hospital said the patient, a man in his 70s whose
identity was not disclosed, was confirmed to have Creutzfeldt-Jakob disease
(CJD) symptoms and has been hospitalized. "But the final checkup result
about whether he was infected with vCJD has not yet come out," the official
said. The hospital reported the case to the authorities, and the
authorities dispatched related experts to inspect the patient, as the
hospital did not have people and equipment needed for close examination of
vCJD.
People infected with vCJD have similar symptoms to that of bovine
spongiform encephalopathy (BSE), so-called mad cow disease. With that
disease, brains develop holes like sponges. Those in their 20s or 30s
usually fall victim to the disease, and the patients have symptoms such as
madness, loss of eyesight and paralysis. They develop dementia and die
within one year. Currently, there is no cure.
People can get vCJD through eating beef infected with BSE. According to the
Korea Center for Disease Control and Prevention, there were 75 people in
Korea from 2001 through last September [2006] who were suspected of having
the disease. Korea has had cases of CJD, which occurs from gene mutation,
but not a case of vCJD yet.
[No cases of vCJD have been reported from South Korea previously, and the
risk of exposure to BSE in East Asia is negligible unless the patient had
spent some time in the UK or France. The age of the patient is not typical
of vCJD, and without laboratory examination, the patient's illness could be
confused with sporadic CJD, familial CJD, iatrogenic CJD, or
Gerstmann-Straussler-Scheinker (GSS) syndrome. Further information from
South Korea is awaited. - Mod.CP]
 
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