March 14, 2013: Transmissible Spongiform Encephalopathies Advisory Committee Meeting Webcast
Webcast
Variant CJD and the TMER study - RG Will 34
00:31:50
vCJD and Transfusion of Blood Components: An Updated Risk Assessment for the UK - Peter Bennett 9
02:11:32
FDA vCJD RBC Risk Model: Model Assumptions and Changes since Previous Assessments - Luisa Gregori 13
03:12:29
Open Public Hearing 19
05:21:35
Volume 19, Number 7—July 2013
Dispatch
Asynchronous Onset of Clinical Disease in BSE-Infected Macaques
Judith Montag1, Walter Schulz-Schaeffer, Annette Schrod, Gerhard Hunsmann,
and Dirk Motzkus Author affiliations: German Primate Center, Göttingen, Germany
(J. Montag, A. Schrod, G. Hunsmann, D. Motzkus); University of Göttingen,
Göttingen (W. Schulz-Schaeffer)
Abstract
To estimate the effect of the variability of prion disease onset on primary
bovine spongiform encephalopathy transmission to humans, we studied 6 cynomolgus
macaques. The preclinical incubation period was significantly prolonged in 2
animals, implying that onset of variant Creutzfeldt-Jacob disease in humans
could be more diverse than previously expected.
Prion diseases, such as bovine spongiform encephalopathy (BSE) in cattle,
scrapie in sheep, and Creutzfeldt-Jakob disease (CJD) in humans, are fatal,
transmissible, neurodegenerative disorders associated with the aggregation of an
infectivity-associated isoform (PrPSc) of the cellular prion protein (PrP) (1).
Seventeen years ago, it became apparent that the BSE-infectious agent had
entered the food chain and was identified as the causative agent for a new
variant CJD (vCJD) (2). Since then, several risk assessment studies have
investigated the number of expected vCJD cases in human populations (reviewed in
[3]). Although thousands to millions of consumers of beef products were
estimated to be affected, thus far only a few more than 200 vCJD cases have been
observed worldwide.
This discrepancy was assumed to be attributable to the so-called species
barrier, defined as the hindrance of an infectious agent to change its natural
host. Upon crossing the species barrier, prion diseases often show a low attack
rate in conjunction with a high variability in the preclinical incubation time.
Thus, the consumption of BSE-contaminated products may have led either to a
restricted infection or to a prolonged asymptomatic phase in some exposed
persons. Therefore, concerns have been raised that asymptomatic carriers of vCJD
might exist, posing a risk for unintentional human-to-human transmission.
First indications that transmission of BSE to primates may lead to
variances in the preclinical incubation times were obtained by inoculating
cynomolgus macaques with cattle-derived BSE material (4–6), even though in those
studies not more than 3 animals were used. We have now used a group of 6
macaques that were infected with BSE at a comparable age and kept under
identical and controlled experimental conditions.
The Study Six captive-bred female cynomolgus macaques (Macaca fascicularis,
purchased from the Centre de Recherche en Primatologie, Mauritius) were
inoculated intracerebrally with 1 dose of 50 mg brain homogenate (10% wt/vol)
derived from 11 BSE-infected cattle. Animal experimentation was performed in
accordance with section 8 of the German Animal Protection Law in compliance with
Directive 86/609/EEC. Macaques were housed in a social group, and behavioral
changes were assessed on a daily basis by experienced animal care takers.
After inoculation, all 6 macaques remained healthy and asymptomatic for
>30 months (Table). At 931 days postinfection, 1 animal showed indications of
slight coordination disorders. Within a few days, afferent ataxia developed, and
when the animal was separated from the others animals, she apparently became
tame. After 2 weeks, the animal showed severe dysmetria of the extremities
without obvious myoclonia. Dementia was apparent but could not be diagnosed by
objective measures. For ethical reasons, the animal was euthanized 17 days after
disease onset. Within the next 14 weeks, 3 more animals became symptomatic.
After appearance of neurologic symptoms (ataxia, tremors), the affected animals
were occasionally separated from the group when symptoms became more severe or
attacks from asymptomatic animals occurred. The disease course in these animals
was comparable to that of the first animal, but the progression was slower
(91–103 days).
Figure 1
Figure 1. . Survival of intracerebrally BSE-infected cynomolgus macaques.
Six age- and sex-matched cynomolgus macaques were inoculated intracerebrally
with 50 mg brain homogenate (10% in sucrose) derived from 11 BSE-infected
cattle. Macaques were...
Two of the 6 animals remained asymptomatic for ≈1 additional year. Although
daily monitoring was facilitated by the fact that only 2 macaques remained and
that the caretakers were more experienced to recognize minor changes in
behavior, symptoms were first detected 1,340 and 1,398 days postinfection,
respectively. Clinical signs were similar to those observed in the previous 4
animals. The symptomatic periods before euthanasia for these macaques lasted 103
and 143 days, respectively (Table). Direct comparison revealed that the
difference between the short (931–1,025 days) and the long (1,340–1,398 days)
preclinical incubation time was statistically significant (Figure 1, log-rank
[Mantel-Cox] test, p<0 .05="" div="">
Test results of brain samples from all animals were positive for
macaque-adapted BSE by Western blot analysis. In brief, brain tissue from each
animal was homogenized and subjected to proteinase K (PK) treatment for 1 h at
37°C. Samples were separated on acrylamide gels and transferred to
nitrocellulose membranes. Macaque-adapted BSE (PrPSc) was detected by using the
monoclonal anti-PrP antibody 11C6. PK-resistant PrP was detected in all 6
macaques, confirming that BSE was transmitted to the animals.
Figure 2
Figure 2. . PrPSc profile of macaque-adapted BSE in comparison to human
CJD. Brain homogenates from human sCJD type 1, sCJD type 2, vCJD, and
BSE-infected macaques were subjected to PK treatment, separated...
The individual glycopattern and band migration of macaque-adapted PrPSc was
compared with human sporadic CJD (sCJD) type 1, sCJD type 2, and vCJD.
PK-resistant PrP from BSE-infected macaques co-migrated with type 2 sCJD and was
clearly distinguishable from type 1 sCJD (Figure 2). The glycosylation pattern
of macaque-adapted BSE was comparable with vCJD (6,7), which is characterized by
an overrepresentation of diglycosylated PrPSc (8,9). Using 11C6 antibody (10),
we detected a slightly decreased signal of the diglycosylated PrPSc isoform for
sCJD, vCJD, and macaque-adapted BSE. We assume that this effect is related to a
reduced affinity of the diglycosylated isoform to 11C6 that otherwise shows high
sensitivity to macaque-adapted PrPSc. Nevertheless, direct comparison showed a
higher amount of the diglysosylated PrPSc isoform in vCJD and macaque-adapted
BSE than sCJD, which was also shown with a different monoclonal antibody, 3F4.
This finding confirms that BSE transmission to macaques is comparable with, and
can be used as a model for, human vCJD infection.
Conclusions
Several susceptibility studies using nonhuman primates as a model for human
prion diseases hint to heterogeneity of the preclinical incubation period upon
crossing the species barrier (5,11,12). However, because of the low number of no
more than 3 animals, this variability was not always evident (4). Therefore,
there was an urgent need to determine whether the transmission of BSE to humans
is likely to lead to a similar diversity.
Our study using 6 cynomolgus macaques shows that the transmission of BSE to
primates led to a significantly prolonged asymptomatic phase in 2 animals.
Disease onset is influenced by several factors (13). Our study design enabled us
to exclude that the route of transmission influenced the disease progression
because the infectious agent was injected into the same brain region of each
animal. Also, a limited infectious dose cannot be responsible, as shown by the
attack rate of 100%. In addition, endogenous factors, such as age, the MM
genotype at codon 129 (Table), and housing conditions, were comparable for all
macaques.
Thus, we conclude that the variable asymptomatic phase is most likely
influenced by the infectious agent (14) or the genomic diversity of the macaques
(13). The animals in our study were not inbred. Therefore, differences in the
genomic background may have influenced the time of disease onset. In contrast,
the PrPSc migration patterns of the animals give no indications for different
types or strains that evolved from the mixed BSE inoculum. However, further
studies will have to verify this.
Nevertheless, during the BSE epidemics, the human population with its
natural genomic diversity was also exposed to a nonhomogenous prion source.
Therefore, our study closely mimics the human situation. Our results imply that
a prolonged asymptomatic phase can be expected for vCJD. In light of the
transmissibility of vCJD through blood transfusions (15), our findings emphasize
the need for continued attention to the risks of secondary human-to-human
transmission.
Dr Montag is a microbiologist at the Department of Molecular and Cell
Physiology at the Hannover Medical School. Her primary research interests are
the molecular mechanisms of disease pathology, including prion disorders and
inherited cardiac diseases.
Acknowledgments We thank J.P. Deslys for providing vCJD material.
This study was supported by European Union grant QLK1-CT-2002-01096 and
BMH4-CT-98-6029.
References
snip...see full text ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
snip...
EFSA and the European Centre for Disease Prevention and Control (ECDC)
recently delivered a scientific opinion on any possible epidemiological or
molecular association between TSEs in animals and humans (EFSA Panel on
Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical
BSE prions as the only TSE agents demonstrated to be zoonotic so far but the
possibility that a small proportion of human cases so far classified as
"sporadic" CJD are of zoonotic origin could not be excluded. Moreover,
transmission experiments to non-human primates suggest that some TSE agents in
addition to Classical BSE prions in cattle (namely L-type Atypical BSE,
Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic
wasting disease (CWD) agents) might have zoonotic potential.
snip...
Thursday, August 12, 2010
Seven main threats for the future linked to prions
First threat
The TSE road map defining the evolution of European policy for protection
against prion diseases is based on a certain numbers of hypotheses some of which
may turn out to be erroneous. In particular, a form of BSE (called atypical
Bovine Spongiform Encephalopathy), recently identified by systematic testing in
aged cattle without clinical signs, may be the origin of classical BSE and thus
potentially constitute a reservoir, which may be impossible to eradicate if a
sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently
sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases
constitute an unforeseen first threat that could sharply modify the European
approach to prion diseases.
Second threat
snip...
Tuesday, March 05, 2013
A closer look at prion strains Characterization and important implications
Prion
7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
Friday, April 19, 2013
APHIS 2013 Stakeholder Meeting (March 2013) BSE TSE PRION
Monday, May 6, 2013
Warning of mad cow disease threat to blood transfusions
Sunday, May 19, 2013
CJD BLOOD SCREENING, DONORS, AND SILENT CARRIERS House of Commons Written
Answers 16 May 2013
Tuesday, May 21, 2013
CJD, TSE, PRION, BLOOD Abstracts of the 23rd Regional Congress of the
International Society of Blood Transfusion, Amsterdam, The Netherlands, June
2-5, 2013
Tuesday, March 5, 2013
Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening
of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)
FDA believes current regulation protects the public from BSE but reopens
comment period due to new studies
FC5.1.1
Transmission Results in Squirrel Monkeys Inoculated with Human sCJD, vCJD,
and GSS Blood Specimens: the Baxter Study
Brown, P1; Gibson, S2; Williams, L3; Ironside, J4; Will, R4; Kreil, T5;
Abee, C3 1Fondation Alliance BioSecure, France; 2University of South Alabama,
USA; 3University of Texas MD Anderson Cancer Center, USA; 4Western General
Hospital, UK; 5Baxter BioSience, Austria
Background: Rodent and sheep models of Transmissible Spongiform
Encephalopathy (TSE) have documented blood infectivity in both the pre-clinical
and clinical phases of disease. Results in a (presumably more appropriate)
non-human primate model have not been reported.
Objective: To determine if blood components (red cells, white cells,
platelets, and plasma) from various forms of human TSE are infectious.
Methods: Blood components were inoculated intra-cerebrally (0.1 ml) and
intravenously (0.5 ml) into squirrel monkeys from 2 patients with sporadic
Creutzfeldt- Jakob disease (sCJD) and 3 patients with variant Creutzfeldt-Jakob
disease (vCJD). Additional monkeys were inoculated with buffy coat or plasma
samples from chimpanzees infected with either sCJD or
Gerstmann-Sträussler-Scheinker disease (GSS). Animals were monitored for a
period of 5 years, and all dying or sacrificed animals had post-mortem
neuropathological examinations and Western blots to determine the presence or
absence of the misfolded prion protein (PrPTSE).
Results: No transmissions occurred in any of the animals inoculated with
blood components from patients with sporadic or variant CJD. All donor
chimpanzees (sCJD and GSS) became symptomatic within 6 weeks of their
pre-clinical phase plasmapheresis, several months earlier than the expected
onset of illness. One monkey inoculated with purified leukocytes from a
pre-clinical GSS chimpanzee developed disease after 36 months.
Conclusion: No infectivity was found in small volumes of blood components
from 4 patients with sporadic CJD and 3 patients with variant CJD. ***However, a
single transmission from a chimpanzee-passaged strain of GSS shows that
infectivity may be present in leukocytes, and the shock of general anaesthesia
and plasmspheresis appears to have triggered the onset of illness in
pre-clinical donor chimpanzees.
Saturday, September 5, 2009
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
snip...
Saturday, September 5, 2009
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
snip...see full text ;
Monday, May 6, 2013
Warning of mad cow disease threat to blood transfusions
Tuesday, April 30, 2013
Mad cow infected blood 'to kill 1,000’
Sunday, February 10, 2013
Creutzfeldt-Jakob disease (CJD) biannual update (February 2013) Infection
report/CJD
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a
methodological outline for evidence-based guidance
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Sunday, June 2, 2013
Characterisation of an Unusual TSE in a Goat by Transmission in Knock-in
Transgenic Mice
Monday, June 3, 2013
Unsuccessful oral transmission of scrapie from British sheep to
cattle
snip...
I have often pondered if the whole damn mad cow follies started over here
in the USA, and somehow, the USA shipped it over to the UK ?
snip...
but I still am not so sure that the mad cow follies did not start long ago
right here in the USA i.e. Richard Marsh and deadstock downer cattle to those
mink, and then the USA shipped it to hell and back. just pondering out loud
here. ...tss
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
_____________________________________________________________________
snip...
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1
Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and
Jean-Philippe Deslys1
1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State
University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain;
5Health Canada; Ottawa, ON Canada†Presenting author; Email:
emmanuel.comoy@cea.fr
The epidemiology of Transmissible mink encephalopathy (TME) indicates an
alimentary origin. Several inter-species transmission experiments have not
succeeded in establishing with certainty any natural reservoir of this prion
strain, although both ovine and bovine sources have been suspected. Cattle
exposed to TME develop a spongiform encephalopathy that is distinct from
classical Bovine Spongiform Encephalopathy (c-BSE).
Inoculation of c-BSE to cynomolgus macaque provided early evidence of a
possible risk to humans, and remains an important model to define the risk of
both primary (oral transmission from cattle to primate) and secondary
(intravenous intra-species transmission) exposures. We have also evaluated the
transmissibility of other cattle prion strains to macaques, including L- and H-
atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.
BSE-L induced a neurological disease distinct from c-BSE. Peripheral
exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and
intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted
TME also induced a rapid disease in cynomolgus macaque. The clinical features,
lesion profile, and biochemical signature of the induced disease was similar to
the features observed in animals exposed to BSE-L, suggesting a link between the
two prion strains. Secondary transmissions to a common host (transgenic mouse
overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in
primates induced diseases with similar incubation periods: like the c-BSE
strain, these cattle strains maintained their distinctive features regardless of
the donor species and passages.
If the link between TME and BSE-L is confirmed, our results would suggest
that BSE-L in North America may have existed for decades, and highlight a
possible preferential transmission of animal prion strains to primates after
passage in cattle.
=====================end...tss====================
link url not available, please see PRION 2011 ;
ALSO, SEE Scrapie Mission, Texas, did not produce _typical_ BSE...
see page 17 here ;
snip...see full text ;
Monday, June 3, 2013
Unsuccessful oral transmission of scrapie from British sheep to
cattle
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Volume 33, Issue 3, Article first published online: 20 JAN 2013
Special Lecture
Human prion diseases: Molecular, cellular and population biology
Mark W. Head
National CJD Research & Surveillance Unit, Centre for Clinical Brain
Sciences, School of Clinical Sciences,
The University of Edinburgh, Edinburgh, UK
snip...
Potential future zoonoses
Scrapie is endemic in many countries around the world, yet there is no
evidence to suggest that it is pathogenic for humans. The intense investigations
of ruminant TSEs that followed the BSE epidemic have resulted in the
identification of several distinct animal prion diseases, atypical or Nor98
scrapie in sheep and H-type and L-type BSE in cattle.32 Moreover, BSE is
experimentally transmissible to sheep and there are concerns that if BSE were to
have infected the national flock in the UK its presence might be masked by
endemic scrapie, but it might retain its pathogenicity for humans.33,34 Another
concern, particularly for the North American countries, is the spread of chronic
wasting disease in farmed and free-ranging deer and elk.35 There is no known
epidemiological link between any of these animal prion diseases and human
disease, but there are active efforts to try to quantify strain-related species
barriers between the diseases known to be a risk (BSE/ vCJD), those thought not
to represent a risk (scrapie) and those for which data is lacking (atypical
scrapie, H- and L-type BSE and BSE in sheep).36 In assessing whether or not
human prion diseases might have an animal origin, it is important to have a
proper understanding of the clinicopathological heterogeneity of the sporadic
human prion diseases, because it is against this backdrop that any new acquired
forms of the disease will be seen and from which it will need to be
distinguished.
Sporadic CJD and variably protease-sensitive prionopathy
Sporadic CJD is the most commonly occurring human prion disease; it occurs
world-wide and it has long been known to be clinically and pathologically
heterogeneous. The molecular basis for this heterogeneity is currently thought
to reside in a combination of the PRNP codon 129 polymorphic status of the
patient (MM, MV, or VV) and the type (type 1 or type 2) of the
protease-resistant component of PrPSc determined by protease K digestion and
Western blotting (termed PrPres).37,38 The original sCJD sub-classification
system of Parchi et al. that recognized six sCJD subtypes (MM1/MV1, MM2c, MM2t,
MV2,VV2 and VV1) has had to be modified to accommodate the growing number of
cases recognized to contain both type 1 and type 2 PrPres in different or
sometimes the same regions of the brain.39,40 Moreover, intensive surveillance
and investigation of forms of human prion disease that lack PRNP mutation and
known risk factors has identified another sporadic human prion disease, termed
protease-sensitive prionopathy (VPSPr).41While intensively investigated, the
etiology and diversity of the sporadic human prion diseases remain poorly
understood.
snip...
There is also a potentially important practical corollary to the idea of
prion-like spread, which may affect future stem cell therapies for
neurodegenerative diseases. Presumably therapeutic stem cell-derived neurons
would be equally susceptible to “infection” (with misfolded protein aggregates)
as the patient’s own cells, unless steps were taken to prevent this,55 the most
obvious of which would be to prevent expression of the gene product that can be
converted to a pathological prion-like isoform.The suggestion that a prion-like
mechanism of spread of molecular pathology underlies diseases as diverse as
Alzheimer’s disease and Parkinson’s disease has led some researchers to explore
whether the molecular pathology of these diseases is transmissible in an
experimental setting56–58 and to suggest that perhaps some cases of these more
common neurodegenerative illnesses might, like CJD, be acquired.58,59
snip...
MOLECULAR BASIS OF HUMAN PRION DISEASES Molecular strain typing Molecular
strain typing in the form of classifying the mobility and glycoform ratio of
protease-resistant prion protein byWestern blotting is a remarkably useful
adjunct to neuropathological assessment during the post-mortem diagnosis of
human prion diseases (Fig. 1). The glycoform ratio difference between vCJD and
all forms of sCJD is a remarkably robust phenomenon, although the mechanism
underlying it remains obscure. All cases of vCJD examined show type 2B PrPres,
irrespective of brain region assayed and the PrPres type is also found in
lymphoreticular tissues, albeit with presumably tissue-specific minor
modification of mobility and an accentuation of the glycoform ratio. Similarly
sCJD cases are characterized by a narrow range of glycoform ratios, distinct
from vCJD, and the presence of either type 1 or type 2 PrPres (type 1A and type
2A).The PrPres types found in the brain in iCJD and kuru resemble those found in
sCJD (type 1A and type 2A), from which they were presumably derived. Individual
cases of gCJD, GSS and FFI usually have type 1 or type 2 PrPres, but with a
glycoform ratio in which the non-glycosylated component is under-represented
(which we have termed A/B). However, this is not always true and a broad
spectrum of glycoform ratios can be found in genetic prion diseases. Moreover,
some cases of GSS are characterized by an approximately 8 kDa (N- and
C-terminally truncated) PrPres fragment, and some cases of FFI have little
detectable PrPres at all. Despite the diagnostic utility, a simple one-to-one
correspondence between PrPres type and disease phenotype (and by implication to
agent strain) seems unlikely in principle and is complicated by the facts.
First, the choice of analyzing only that fraction of PrPSc which survives a
particular concentration of protease may seem arbitrary. Second, the
interpretation of a molecular population variable, such as glycosylation site
occupancy, as conforming to two or three discrete types, could be seen as
simplistic. Lastly, protease digestion may be considered to be a somewhat blunt
instrument to distinguish secondary and higherorder conformational differences
in PrPSc. Even when genotype (mutations and polymorphisms) is taken into
account, three major types (1, 2, 8 kDa) and three wild-type genotypes (MM,MV
and VV) provide insufficient molecular variation to account for all the
phenotypic variations observed. For example, two forms of sCJD share methione
homozygosity and type 2A PrPres but one form closely resembles FFI (without the
causative mutation) and the other is CJD-like.8 Two more substantial problems,
which may point toward a more subtle and perhaps informative approach to PrPSc
analysis, are discussed below. The co-occurrence of PrPres types 1 and 2 Once
controversial, the idea that PrPSc in individual cases might be composed of
mixtures (or different types co-occurring) is now well recognized and
accepted.40,70 There are probably two phenomena at play here. One is the finding
of different predominant types in individual samples from different parts of the
brain or more rarely approximately equal amounts of type 1A and type 2A in the
same sCJD brain samples.The other is the observation made using antibodies that
specifically recognize type 1 or type 2 PrPres, that a minority type always
accompanies a majority type in sCJD and vCJD, albeit at sub-detectable levels
when conventional antibodies are used.71–75 The former issue is more tractable
and a consensus is beginning to emerge that when multiple brain sampling and
sensitive co-detection is performed on cohorts of sCJD cases, a plateau is
reached at between 30–40% of cases showing co-occurrence. Our own data examining
four regions (temporal cortex, parietal cortex, occipital cortex and thalamus)
instead of frontal cortex only, shows a rise in detected co-occurrence from 3%
to 24% of cases.76 Interestingly, only very rarely did this re-analysis involve
a change in the predominant type found in the brain overall. Parchi et al. have
offered a revised version of their 1999 sporadic CJD classification system that
adds mixed type to the original “pure” types and have shown that the most common
of these 12 sCJD subtypes can be recognized on histological grounds, without
reference to biochemical analysis.39,40,77 It will be interesting to see in the
fullness of time whether this additional complexity reflects a more refined
series of discrete clinicopathological phenotypes or whether it is indicative of
a spectrum of phenotypes depending on the spacio-temporal accumulation of PrPSc
types set against the patient genotype.78
Variably protease-sensitive prionopathy The phenotypic complexity of the
sporadic forms of human prion disease has increased with the report of a new
sporadic human prion disease, termed variably proteasesensitive prionopathy
(VPSPr) that is distinct from previously recognized sub-types of sCJD.41,79
There are no mutations in the open reading frame of PRNP. The patients have no
known risk factors for the disease, but the disease is most common in theVV
genotype, as opposed to sCJD, which is most common in the MM genotype. The
neuropathology involves medium-sized vacuolation and characteristic
microplaques. Durations of illness can be very long and this coupled with
symptoms that do not conform well to CJD have prompted speculation that the
condition may be under-ascertained. The most interesting aspect of the disease
from a biochemical perspective is that although PrPSc is abundantly present in
the brain, PrPres is difficult to detect because of its sensitivity to
proteolysis and because what remains after proteinase K (PK) digestion is both
C- and N-terminally cleaved by PK digestion and seen as a faint 8 kDa band on
Western blots (Fig. 2). The degree of protease resistance is reported to reflect
the codon 129 genotype, withVV being least resistant andMM being most resistant,
despite having the same 8 kDa PrPres fragment predominating.79We have identified
two cases of VPSPr prospectively in the UK80,81 and recently completed a
retrospective review for such cases confirming many of the original observations
by Gambetti and colleagues.41,79 Our work has shown that some areas of the VPSPr
brain contain PrPres similar in appearance to that found in sCJD and conversely
that some cases of sCJD have a very minor PrPres band similar to the 8 kDa
PrPres band that typifies VPSPr.82
snip...
The biochemical basis of the strain phenomenon The results of transmission
of individual samples from single examples of the six different Parchi et al.39
sCJD subtypes (MM1/MV1, VV1, MM2c, MV2, VV2) into humanized transgenic mice
suggest the existence of four distinct sCJD agents, termed M1, M2, V1 and V2,
and a fifth strain corresponding to MM2t or sporadic fatal insomnia.99,100
Interestingly, when we performed formally analogous experiments in the cell-free
PMCA reaction, similar results were obtained: The PrPres type of the seed was
conserved in the PMCA product and the efficiency of conversion appeared to be
determined by compatibility at codon 129 of PRNP.101 The behavior of the seeds
from heterozygous patients were particularly interesting, in that MV1 sCJD seeds
selectively amplified in MM substrate producing type 1 PrPres and MV2 sCJD seeds
selectively amplified in VV substrate producing type 2 PrPres (Fig. 6). These
results reinforce the association between methionine at codon 129 and the
production of type 1 PrPres and valine at codon 129 and the production of type 2
PrPres.
EMERGING RISKS Zoonotic disease BSE is the only animal prion strain with
demonstrated pathogenicity for humans.While it is tempting to suggest that
scrapie might represent the animal reservoir that results in some cases of sCJD,
there is no epidemiological evidence to support this hypothesis. The
pathogenicity of new or newly described animal prion diseases for humans is
unclear and this is particularly true for H- and L-type BSE, atypical scrapie
and for chronic wasting disease (CWD), all of which are probably consumed. Human
susceptibility has been modeled by attempted transmission to (humanized)
transgenic mice with sometimes conflicting results, depending on the transgenic
model used and depending upon whether central or peripheral tissues are
examined.102–106 We have attempted to establish whether PMCA can model the
molecular component of these hypothetical cross-species transmission events.107
The existing data correspond well with the established facts. First, PrPSc in
vCJD brain samples amplifies most efficiently in humanized mouse MM substrate,
less efficiently in MV substrate and not at all in VV. Cattle BSE PrPres is less
efficient than vCJD, but shows the same substrate genotypic preference. Sheep
scrapie fails to amplify detectably in any of the three substrates; however,
sheep BSE PrPres does amplify, again with a codon 129 preference for methionine
(Fig. 7). We are currently extending this approach to encompass atypical
scrapie, H- and L-type BSE and CWD using human rather than humanized PMCA
substrates.
Secondary infection
In the same way that animal reservoirs cannot be completely excluded as
causes of individual sCJD cases, neither can other environmental sources, such
as medical procedures. The known routes of iatrogenic CJD acquisition are
historically growth hormone therapy, dura mater grafting, corneal grafting and
certain highly specialized neurosurgical procedures. The secondary transmission
of vCJD by blood transfusion and experimental evidence showing the efficiency of
the transfusion of viable blood cells between scrapie and BSE-infected and naive
sheep have prompted a reappraisal of transfusion-transmitted CJD, including
consideration being given to the possibility of prion blood testing or
filtration.25,26,108,109
Blood transfusion is the original and most extensively used cellular
therapy, but we may be on the threshold of a new era of cellular therapies based
on embryonic stem cell and induced pluripotent stem cell technologies. Although
the potential for stem cell therapy-mediated prion transmission might be judged
remote, this was also considered to be the case for transfusion transmission of
CJD before 2004.
snip...
SUMMARY AND PERSPECTIVE
While the prospect of a major epidemic of vCJD in the UK and elsewhere
seems to be receding, there remain a series of uncertainties surrounding the
eventual numbers of individuals that will suffer from this devastating
condition.The issues include the effects of genotype on susceptibility and the
possible existence of substantial numbers of asymptomatic infected individuals
that may pose risks of onward transmission. sCJD remains the most frequently
occurring human prion disease and arguably the least well understood. Other
idiopathic forms of human prion disease (such as VPSPr), characterized by
protease-sensitive forms of the prion protein, also exist and their true
prevalence may be hard to ascertain. The possible risks from newly described
animal prion diseases and from emerging cellular therapies are currently poorly
quantified. On a more theoretic level the prion hypothesis has provided a
unifying conceptual framework for TSE research and provided a paradigm to
interrogate the similarities and differences between the diverse
neurodegenerative conditions involving prion-like mechanisms of molecular
pathology.
Sunday, March 31, 2013
Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years
old, shall we pray
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Monday, July 23, 2012
The National Prion Disease Pathology Surveillance Center July 2012
2011 Monday, September 26, 2011
L-BSE BASE prion and atypical sporadic CJD
Wednesday, June 29, 2011
TSEAC Meeting August 1, 2011 donor deferral Saudi Arabia vCJD risk blood
and blood products
Wednesday, June 29, 2011 TSEAC JUNE 2, 1999 Welcome to the FDA traveling
road show From: TSS
Subject: TSEAC JUNE 2, 1999 Welcome to the FDA traveling road show
Date: October 15, 2007 at 3:18 pm PST
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE MEETING
Thursday, June 2, 1999
Wednesday, March 2, 2011
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011 Posted: 3/2/2011
October 28, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of
Transmission of CJD and vCJD by Blood and Blood Products 2011 ???
October 29, 2010
Transmissible Spongiform Encephalopathies Advisory Committee Meeting
Transcript Posted: 3/2/2011
Monday, October 18, 2010
TSEAC Transmissible Spongiform Encephalopathies Advisory Committee Draft
Agenda and Meeting Materials,
Posted: 10/18/2010
Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee
Center Date Time Location
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Saturday, September 5, 2009
TSEAC MEETING FEBRUARY 12, 2004 THE BAXTER STUDY GSS
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
May 8, 2009
Greetings again Dr. Freas, TSEAC et al,
I would kindly, once again, wish to comment at this meeting about the
urgent actions that need to be taken asap, to the Meeting of the Transmissible
Spongiform Encephalopathies Committee On June 12, 2009. Due to my disability
from my neck injury, I will not be attending this meeting either, however I hope
for my submission to be read and submitted. ...
IN reply to ;
snip...see full text ;
Sunday, May 10, 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June
12, 2009 (Singeltary submission)
TO : william.freas@fda.hhs.gov
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October
31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety
and Inspection Service (FSIS) held a public meeting on July 25, 2006 in
Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine
Spongiform Encephalopathy Update, October 31, 2005 (report and model located on
the FSIS website:
Comments on technical aspects of the risk assessment were then submitted to
FSIS. Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary. This document provides itemized replies to the public comments
received on the 2005 updated Harvard BSE risk assessment. Please bear the
following points in mind:
From: Terry S. Singeltary Sr.
To: FREAS@CBER.FDA.GOV
Cc: william.freas@fda.hhs.gov ; rosanna.harvey@fda.hhs.gov
Sent: Friday, December 01, 2006 2:59 PM
Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS
SUBMISSION
snip...
ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear
with me)
THE USA is in a most unique situation, one of unknown circumstances with
human and animal TSE. THE USA has the most documented TSE in different species
to date, with substrains growing in those species (BSE/BASE in cattle and CWD in
deer and elk, there is evidence here with different strains), and we know that
sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie
documented and also BSE is very likely to have passed to sheep. all of which
have been rendered and fed back to animals for human and animal consumption, a
frightening scenario. WE do not know the outcome, and to play with human life
around the globe with the very likely TSE tainted blood from the USA, in my
opinion is like playing Russian roulette, of long duration, with potential long
and enduring consequences, of which once done, cannot be undone.
These are the facts as i have come to know through daily and extensive
research of TSE over 9 years, since 12/14/97. I do not pretend to have all the
answers, but i do know to continue to believe in the ukbsenvcjd only theory of
transmission to humans of only this one strain from only this one TSE from only
this one part of the globe, will only lead to further failures, and needless
exposure to humans from all strains of TSE, and possibly many more needless
deaths from TSE via a multitude of proven routes and sources via many studies
with primates and rodents and other species. ...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
snip... 48 pages...
Wednesday, October 17, 2007 TSEAC MEETINGS ----- 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
[TSSSUBMISSION]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-derivedantihemophilic factor (FVIII) productsmanufactured from U.S.
plasma donors and related communication material ;
i see the media picked up on this as a 'low risk', from what the gov.
agency perceived to be to them;
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, wha tabout 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 are call aspect of potentially tainted
blood, and these are just recent recalls ;
PRODUCT
Source Plasma, Recall # B-0054-7CODEUnits: 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
###
USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)RECALLS AND
FIELD CORRECTIONS: BIOLOGICS -- CLASS II
______________________________
PRODUCTSource Plasma, Recall # B-1708-6CODEUnits: 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-1716-6CODEa),
b), and c) Unit: 2443732RECALLING 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
###
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
###
Mon Aug 7, 2006 10:2471.248.132.189
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
June30, 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
CODEa) 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
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6;b) Fresh Frozen
Plasma, Recall # B-1551-6
CODEa) 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
increasedrisk 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
CODEa) 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-1494-6b) Cryoprecipitated AHF, Recall #
B-1495-6
CODEa) and b)
Unit 5013100
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on
May17, 2005. Firm initiated recall is complete.REASONBlood 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;Recovered Plasma, Recall # B-1423-6
CODE
a) Unit 03E42218;
b) Unit 03E38153
RECALLING FIRM/MANUFACTURER
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail
orletter on February 20 or 21, 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
GA and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6;
b) Recovered Plasma, Recall # B-1375-6CODEa) and b) unit 2453906
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31
and November 5, 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 and Austria
______________________________
PRODUCT
Source Plasma.
Recall # B-1295-6
CODE
Units: NG0046551, NG0045950
RECALLING FIRM/MANUFACTURERD
CI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
onDecember 20, 2002, Firm initiated recall is complete.
REASON
Blood products, collected from a donor who did not answer the questions on
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately,
were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma. Recall # B-1296-6
CODE
Unit: NG 0044520RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches
LLC, Nacogdoches, TX, by telephone and fax onDecember 12, 2002. Firm initiated
recall is complete.
REASON
Blood product, collected from a donor who did not answer the questions on
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was
distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma. Recall # B-1297-6
CODE
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797,
NG0044020,NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412,
NG0045555RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC,
Nacogdoches, TX, by telephone and fax onDecember 20, 2002. 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
13 units
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma, Recall # B-1298-6
CODE
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095,
NG0042525, NG 0042341RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC,
Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall
is complete.
REASON
Blood products, collected from a donor who answered questions on the
variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were
distributed.
VOLUME OF PRODUCT IN COMMERCE
7 units
DISTRIBUTION
KY
______________________________
PRODUCT
Recovered Plasma, Recall # B-1299-6CODEUnit: 4357117
RECALLING FIRM/MANUFACTURER
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and
letter on September 25, 2003. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at risk of exposure
to Creutzfeldt-Jacob Disease (CJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Germany
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
CJD WATCH MESSAGE BOARD
TSS
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY Fri Jul 7, 2006
09:3770.110.83.160
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6;
b) Platelets, Recall # B-1380-6;
c) Fresh Frozen Plasma, Recall # 1381-6;
d) Recovered Plasma, Recall # B-1382-6
CODE
a) Unit numbers: 2343106, 2377779, and 2403533;
b) and c) Unit numbers: 2377779;
d) Unit numbers: 2343106 and 2403533
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
June12, 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
7 units
DISTRIBUTIONTX and Austria
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6;
b) Recovered Plasma, Recall # B-1468-6
CODE
a) and b)
Unit numbers: 2329380
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May
8,2003. 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
DISTRIBUTIONTX and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6;
b) Cryoprecipitated AHF, Recall # B-1480-6;
c) Recovered Plasma, Recall # B-1481-6
CODE
a), b), and c)
Unit numbers: 2383280
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
July23 and 29, 2004. Firm initiated recall is complete.
REASONBlood 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 and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6;
b) Fresh Frozen Plasma, Recall # B-1483-6
CODE
a) and b)
Unit number: 2501452
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile
onOctober 5, 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 and NY
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6;
b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6;
c) Recovered Plasma, Recall # B-1486-6
CODE
a) and c)
Unit number: 2554077;
b) Unit number: 2415708
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
August13, 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
3 units
DISTRIBUTION
TX and Austria
_____________________________________
END OF ENFORCEMENT REPORT FOR July 5, 2006
###
Greetings again Dr. Freas et al at FDA,
WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and
the fact that the new BASE TSE in cattle being very very similar to sporadic
CJD, rather than the nvCJD, the fact that now science showing the TSE agent of
the atypical cattle in Japan showing infectivity other than CNS tissue, the fact
that the latest Texas mad cow and the recent Alabama mad cow both being of the
atypical strain, it would seem prudent to include all human TSE in the blood
ban, in my opinion. with sporadic CJD, you have many strains and or phenotypes,
some of which are 'UNKNOWN', so we do not know how this will transmit, what
tissues are infectious and or if blood transmits. that's the bottomline, however
it has been reported that the BASE is more virulent to humans.With this, and the
fact that sporadic CJD has tripled in the past few years or so, i see itas being
prudent to take serious and immediate action ;
snip...see full text ;
Wednesday, October 17, 2007 TSEAC MEETINGS ----- 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
[TSSSUBMISSION]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-derivedantihemophilic factor (FVIII) productsmanufactured from U.S.
plasma donors and related communication material ;
i see the media picked up on this as a 'low risk', from what the gov.
agency perceived to be to them;
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, wha tabout 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 are call aspect of potentially tainted
blood, and these are just recent recalls ;
PRODUCT
Source Plasma, Recall # B-0054-7CODEUnits: 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
###
USA FDA MAD COW BLOOD HUMANS RECALL (these are dime a dozen)RECALLS AND
FIELD CORRECTIONS: BIOLOGICS -- CLASS II
______________________________
PRODUCTSource Plasma, Recall # B-1708-6CODEUnits: 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-1716-6CODEa),
b), and c) Unit: 2443732RECALLING 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
###
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
###
Mon Aug 7, 2006 10:2471.248.132.189
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
June30, 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
CODEa) 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
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1550-6;b) Fresh Frozen
Plasma, Recall # B-1551-6
CODEa) 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
increasedrisk 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
CODEa) 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-1494-6b) Cryoprecipitated AHF, Recall #
B-1495-6
CODEa) and b)
Unit 5013100
RECALLING FIRM/MANUFACTURER
Walter L. Shepeard Community Blood Center, Inc., Augusta, GA, by fax on
May17, 2005. Firm initiated recall is complete.REASONBlood 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;Recovered Plasma, Recall # B-1423-6
CODE
a) Unit 03E42218;
b) Unit 03E38153
RECALLING FIRM/MANUFACTURER
American Red Cross Blood Services, Atlanta, GA, by telephone, e-mail
orletter on February 20 or 21, 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
GA and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1374-6;
b) Recovered Plasma, Recall # B-1375-6CODEa) and b) unit 2453906
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by fax on October 31
and November 5, 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 and Austria
______________________________
PRODUCT
Source Plasma.
Recall # B-1295-6
CODE
Units: NG0046551, NG0045950
RECALLING FIRM/MANUFACTURERD
CI Biologicals Nacogdoches LLC, Nacogdoches, TX, by telephone and fax
onDecember 20, 2002, Firm initiated recall is complete.
REASON
Blood products, collected from a donor who did not answer the questions on
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire appropriately,
were distributed.
VOLUME OF PRODUCT IN COMMERCE
2 units
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma. Recall # B-1296-6
CODE
Unit: NG 0044520RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches
LLC, Nacogdoches, TX, by telephone and fax onDecember 12, 2002. Firm initiated
recall is complete.
REASON
Blood product, collected from a donor who did not answer the questions on
the new variant Creutzfeldt-Jacob disease (nvCJD) questionnaire, was
distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma. Recall # B-1297-6
CODE
Units: NG0042874, NG0043139, NG0043312, NG0043618, NG0043797,
NG0044020,NG0044209, NG0044507, NG0044718, NG0044977, NG0045161, NG0045412,
NG0045555RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC,
Nacogdoches, TX, by telephone and fax onDecember 20, 2002. 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
13 units
DISTRIBUTION
KY
______________________________
PRODUCT
Source Plasma, Recall # B-1298-6
CODE
Units: NG 0046823, NG 0046671, NG 0045205, NG 0044635, NG 0043095,
NG0042525, NG 0042341RECALLING FIRM/MANUFACTURERDCI Biologicals Nacogdoches LLC,
Nacogdoches, TX, by telephone and fax onDecember 20, 2002. Firm initiated recall
is complete.
REASON
Blood products, collected from a donor who answered questions on the
variant Creutzfeldt-Jacob disease (vCJD) questionnaire inappropriately, were
distributed.
VOLUME OF PRODUCT IN COMMERCE
7 units
DISTRIBUTION
KY
______________________________
PRODUCT
Recovered Plasma, Recall # B-1299-6CODEUnit: 4357117
RECALLING FIRM/MANUFACTURER
Department of the Navy, Naval Medical Center, San Diego, CA, by fax and
letter on September 25, 2003. Firm initiated recall is complete.
REASON
Blood product, collected from a donor considered to be at risk of exposure
to Creutzfeldt-Jacob Disease (CJD), was distributed.
VOLUME OF PRODUCT IN COMMERCE
1 unit
DISTRIBUTION
Germany
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
CJD WATCH MESSAGE BOARD
TSS
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY Fri Jul 7, 2006
09:3770.110.83.160
FDA mad cow nvCJD 'only' blood recalls 1ST WEEK JULY
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1379-6;
b) Platelets, Recall # B-1380-6;
c) Fresh Frozen Plasma, Recall # 1381-6;
d) Recovered Plasma, Recall # B-1382-6
CODE
a) Unit numbers: 2343106, 2377779, and 2403533;
b) and c) Unit numbers: 2377779;
d) Unit numbers: 2343106 and 2403533
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
June12, 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
7 units
DISTRIBUTIONTX and Austria
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1467-6;
b) Recovered Plasma, Recall # B-1468-6
CODE
a) and b)
Unit numbers: 2329380
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on May
8,2003. 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
DISTRIBUTIONTX and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1479-6;
b) Cryoprecipitated AHF, Recall # B-1480-6;
c) Recovered Plasma, Recall # B-1481-6
CODE
a), b), and c)
Unit numbers: 2383280
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
July23 and 29, 2004. Firm initiated recall is complete.
REASONBlood 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 and Switzerland
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1482-6;
b) Fresh Frozen Plasma, Recall # B-1483-6
CODE
a) and b)
Unit number: 2501452
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile
onOctober 5, 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 and NY
______________________________
PRODUCT
a) Red Blood Cells Leukocytes Reduced, Recall # B-1484-6;
b) Plasma Cryoprecipitated Reduced, Recall # B-1485-6;
c) Recovered Plasma, Recall # B-1486-6
CODE
a) and c)
Unit number: 2554077;
b) Unit number: 2415708
RECALLING FIRM/MANUFACTURER
South Texas Blood and Tissue Center, San Antonio, TX, by facsimile on
August13, 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
3 units
DISTRIBUTION
TX and Austria
_____________________________________
END OF ENFORCEMENT REPORT FOR July 5, 2006
###
Greetings again Dr. Freas et al at FDA,
WITH new atypical TSE in the bovine, in the sheep, goat, and humans, and
the fact that the new BASE TSE in cattle being very very similar to sporadic
CJD, rather than the nvCJD, the fact that now science showing the TSE agent of
the atypical cattle in Japan showing infectivity other than CNS tissue, the fact
that the latest Texas mad cow and the recent Alabama mad cow both being of the
atypical strain, it would seem prudent to include all human TSE in the blood
ban, in my opinion. with sporadic CJD, you have many strains and or phenotypes,
some of which are 'UNKNOWN', so we do not know how this will transmit, what
tissues are infectious and or if blood transmits. that's the bottomline, however
it has been reported that the BASE is more virulent to humans.With this, and the
fact that sporadic CJD has tripled in the past few years or so, i see itas being
prudent to take serious and immediate action ;
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 ...
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Thursday, February 24, 2011
The risk of variant Creutzfeldt-Jakob disease among UK patients with
bleeding disorders, known to have received potentially contaminated plasma
products
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
Saturday, May 25, 2013
Brain homogenates from human tauopathies induce tau inclusions in mouse
brain
Tuesday, May 21, 2013
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by blood transfusion are posed
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Proteinopathies, a core concept for understanding and ultimately treating
degenerative disorders?
Monday, September 26, 2011
Variably Protease-Sensitive Prionopathy, Prionpathy, Prionopathy, FFI, GSS,
gCJD, hvCJD, sCJD, TSE, PRION, update 2011
Friday, September 3, 2010
Alzheimer's, Autism, Amyotrophic Lateral Sclerosis, Parkinson's, Prionoids,
Prionpathy, Prionopathy, TSE
Tuesday, June 4, 2013
INTERPRETING RESULTS OF FSIS VERIFICATION SAMPLING OF DOMESTIC BEEF PRODUCT
DERIVED FROM ADVANCED MEAT RECOVERY SYSTEMS (AMR01/FAMR01) FSIS Notice
38-12
TSS
