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From: TSS ()
Subject: nvCJD MAD COW blood products recall update USA MAY 2006
Date: May 24, 2006 at 8:26 am PST

nvCJD MAD COW blood products recall update USA

PRODUCT
Recovered Plasma, Recall # B-1032-6
CODE
Units: 12K76696, 12X00935
RECALLING FIRM/MANUFACTURER
The American National Red Cross, Carolinas Region, Charlotte, NC, by fax on January 24, 2004, 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
CA

______________________________


PRODUCT
Source Plasma, Recall # B-1033-6
CODE
Unit: 02lWID2565
RECALLING FIRM/MANUFACTURER
BioLife Plasma Services L.P., Onalaska, WI, by fax on August 6, 2002, firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
MN

______________________________

PRODUCT
Source Plasma, Recall # B-1101-6
CODE
Units 05MINA8244, 05MINA8587, 05MINA9587
RECALLING FIRM/MANUFACTURER
BioLife Plasma Services, L.P., Muncie, IN, by fax on January 18, 2006, 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
CA

______________________________

END OF ENFORCEMENT REPORT FOR MAY 24, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00953.html

PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1072-6
b) Platelets, Recall # B-1073-6
c) Recovered Plasma, Recall # B-1074-6
CODE
a), b) and c) Unit: 3770030
RECALLING FIRM/MANUFACTURER
LifeShare Blood Centers, Shreveport, LA, by e-mail on December 15, 2004, firm initiated recall is complete.
REASON
Blood products, collected from a donor considered to be at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
3 units.
DISTRIBUTION
LA, MI and Switzerland

______________________________

END OF ENFORCEMENT REPORT FOR MAY 17, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00952.html

______________________________
PRODUCT
Irradiated Cancellous Bone & Marrow, 0.25, 0.5, 1.0 and 2.0 gram vials, Recall # B-0809-6
CODE
Lot # 03049, 1.0 gram, Vial numbers: 1 thru 51
Lot # 03051, 0.25 gram, Vial numbers 1 thru 205
Lot # 04091, 0.25 gram, Vial numbers 1 thru 393
Lot # 04102, 0.5 gram, Vial numbers 1 thru 44
Lot # 04103, 1.0 gram, Vial numbers 1 thru 47
Lot # 04104, 1.0 gram, Vial numbers 1 thru 44
Lot # 04109, 1.0 gram, Vial numbers 1 thru 60
Lot # 04113, 2.0 gram, Vial numbers 1 thru 23
Lot # 04120, 1.0 gram, Vial numbers 1 thru 31
Lot # 04123, 2.0 gram, Vial numbers 1 thru 23
Lot # 04124, 0.5 gram, Vial numbers 1 thru 70
RECALLING FIRM/MANUFACTURER
Recalling Firm: Rocky Mountain Tissue Bank, Aurora, CO, by telephone on October 5, 2005, and by letter dated November 1, 2005.
Manufacturer: BioMedical Tissue Services, Ltd., Fort Lee, NJ, firm initiated recall is complete.
REASON
Human tissues, procured from donors without adequate donor eligibility determinations, were distributed.
VOLUME OF PRODUCT IN COMMERCE
991 vials
DISTRIBUTION
Nationwide

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced Irradiated, Recall # B-0987-6;
b) Plasma Frozen, Recall # B-0988-6
CODE
a) and b) Unit number: 16GR21277
RECALLING FIRM/MANUFACTURER
American Red Cross Blood Services, Columbus, OH, by telephone on September 8, 2005 and by letter dated September 9, 2005. Firm initiated recall is complete.
REASON
Blood products, which were collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
OH

______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-0989-6;
b) Fresh Frozen Plasma, Recall # B-0990-6
CODE
a) and b) Unit number: 1173839
RECALLING FIRM/MANUFACTURER
Hoxworth Blood Center, Cincinnati, OH, by telephone on June 23, 2005. Firm initiated recall is complete.
REASON
Blood products which were collected from a donor who was at increased risk for variant Creutzfeldt-Jakob Disease (vCJD), were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
OH
_____________________________

ENFORCEMENT REPORT FOR MAY 10, 2006

###

http://www.fda.gov/bbs/topics/enforce/2006/ENF00951.html


A new human genotype prone to variant Creutzfeldt-Jakob disease
New evidence may rekindle fears of a larger epidemic and greater risk of iatrogenic spread

The first 150 words of the full text of this article appear below.

From the initial discovery of variant Creutzfeldt-Jacob disease (vCJD) in the United Kingdom a decade ago, there has been concern about the ultimate extent and magnitude of the epidemic.1 Early estimates varied widely, with one model predicting up to 136 000 cases.2 Fortunately, the magnitude of the epidemic at present seems to match the lower limit of the early estimates, with 161 definite or probable cases in the United Kingdom. However, the article by Ironside and colleagues on p 1186 may rekindle fears that a larger epidemic is an ongoing threat.3

The study reports a genotype analysis that identified the presence of the homozygous valine (VV) genotype in two samples of appendix tissue that harboured prion proteins. The implication of this finding of most concern is that it raises the possibility that ongoing iatrogenic transmission of vCJD may sustain the epidemic.

Why are the findings from . . . [Full text of this article]


Policy implications

Related Articles


Variant Creutzfeldt-Jakob disease: prion protein genotype analysis of positive appendix tissue samples from a retrospective prevalence study James W Ironside, Matthew T Bishop, Kelly Connolly, Doha Hegazy, Suzanne Lowrie, Margaret Le Grice, Diane L Ritchie, Linda M McCardle, and David A Hilton
BMJ 2006 332: 1186-1188. [Abstract] [Full Text]

http://bmj.bmjjournals.com/cgi/content/full/332/7551/1186


Risk of acquiring Creutzfeldt-Jakob disease from blood transfusions: systematic review of case-control studies Kumanan Wilson, Catherine Code, and Maura N Ricketts
BMJ 2000 321: 17-19. [Abstract] [Full Text]

http://bmj.bmjjournals.com/cgi/content/full/321/7252/17

http://bmj.bmjjournals.com/cgi/content/extract/332/7551/1164

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.

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...

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

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


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


http://disc.server.com/discussion.cgi?id=167318;article=2847


4. The committee will hold a reserved business session in the

afternoon to allow discussion of unpublished scientific data relating

to TSE infectivity in blood. This is in accordance with the SEAC

Code of Practice. Short summaries of the open and reserved

business discussions will be posted on the SEAC website next

week. A list of website addresses of recently published reports

relevant to TSEs has been tabled. ...


http://www.seac.gov.uk/papers/draft92.pdf


see increase of sporadic CJD over the years ;


http://www.eurocjd.ed.ac.uk/sporadic.htm


USA


notice steady increase, but also notice in 2005, # 7 the 38 pendings cases through Oct. and #8 includes 53 type pending, 1 type unknown.

if you look at 2003 there were 3 type unknown.

wonder if they were the same or different than the unknown in 2005?

considering the soup that has been brewing over here in the USA for years via the rendering of BSE and atypical TSE in cattle, CWD, Scrapie, a few TME cases (not too much due to scent gland, but there were a few rendered, but all this, and you have one hell of a recipe for a new strains of TSE in humans. then who knows what 'friendly fire' cases would look like from this soup via secondary transmission via medical/surgical/dental arena. ...TSS


National Prion Disease Pathology Surveillance Center case exams...


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


Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al.
JAMA.2001; 285: 733-734


http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 26 March 2003


Terry S. Singeltary,
retired (medically)
CJD WATCH

Send Correspondence to journal:
Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


Email Terry S. Singeltary

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

''Answering critics like Terry Singeltary, who feels that the US
undercounts CJD, Schonberger _conceded_ that the current
surveillance system has errors but stated that most of the errors
will be confined to the older population''....

Philip Yam
The Pathological Protein

Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
2003. Hardcover, 285 pp.
Euro 29.95 (net price); £21.00; $27.50; sFr 51.50
ISBN 0-387-95508-9

Contact and review copies:

Joan Robinson
Springer-Verlag Press and Public Relations
Tel.: +49- (0) 6221-487-8130,
Fax: +49- (0) 6221-487-8141,
E-mail: robinson@springer.de


http://www.springer.de/press/newbooks/protein.html

The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly
Prion Diseases
Philip Yam

List Price: $27.50
Our Price: $19.25
You Save: $8.25 (30%)
Availability: Usually ships within 24 hours.


http://www.target.com/gp/detail.html/sr=1-1/qid=1054420048/ref=sr_1_1/602-9780634-9614260?asin=0387955089

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... 2 January 2000
Terry S Singeltary
retired

Send response to journal:
Re: U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...


In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.

The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;

"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."

Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.

Something else I find odd, page 16;

"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."

A few more factors to consider, page 15;

"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."

"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."

"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."

Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.

To be continued...

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

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

TSS




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