Recalls raise questions on safety practices for donated blood CJD TSE PRION
Recalls raise questions on safety practices for donated blood
September 29, 2013
In March 2012, someone at increased risk for the human form of mad cow
disease walked into a Red Cross blood center in Michigan to donate for the fifth
time in recent years.
The donor — unidentified in public records — filled out the questionnaire
used to determine whether someone’s blood can safely flow into the Red Cross’
national network, which generated $2.2 billion in sales last year, and be
transfused into human patients.
The donor provided the usual information. This time, however, the
Lansing-based Great Lakes Region Blood Services employee reviewing the
questionnaire realized the person’s blood should not be collected that day and
shouldn’t have been drawn the four previous times. Under federal guidelines,
disqualification was automatic.
The U.S. Food and Drug Administration was notified. Screening procedures
were reviewed. The donor was permanently barred. And, belatedly, a recall was
issued for one unit of the donor’s blood that had been collected a year earlier
and sent from Lansing to California.
Interviews with Red Cross officials and a review of 10 pages of FDA records
associated with the recall don’t reveal whether the potentially dangerous blood
product was transfused or whether a transfused patient was ever notified —
leading to questions about accountability in the U.S. blood trade.
“That data is not specifically tracked and compiled by the FDA,” said
Morgan Liscinsky, spokeswoman for the agency.
The FDA requires blood banks to track products recalled for HIV and
hepatitis C and to notify transfused patients. For other infectious diseases,
such as the human form of mad cow disease, “look-back procedures” are encouraged
but not required, Liscinsky said.
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Oral.05: Contaminated blood products induce a highly atypical prion disease
devoid of PrPres in primates
Emmanuel Corney,1 Nina Jaffre,1 Jacqueline Mikol,1 Valerie Durand,1
Christelle Jas-Duval,1,2 Sophie Luccantoni-Freire,1 Evelyne Correia,1 Nathalie
Lescoutra-Etcheqaray,3 Nathalie Streichenberqer,4 Stephane Haik,5 Chryslain
Sumian,3 Paul Brown1 and Jean-Philippe Deslys1
1Commissariat a l'Energie Atomique; Institute of Emerging Diseases and
Innovative Therapies (iMETI); Division of Prions and Related Diseases (SEPIA);
Fontenay-aux- Roses, France; 2EFS·Nord de France; Lille, France; 3MacoPharm;
Tourcoing, France; 4Hospices Civils de Lyon; Prion Unit; Neurobiology
Department; Bron, France; 5Inserm; U 975·CNRS; UMR 7225 - Universite Pierre et
Marie Curie; Paris, France
Background, Concerns about the blood-borne risk of prion infection have
been confirmed by the occurrence in the UK of four transfusion-related
infections of vCJD and an apparently silent infection in an hemophiliac patient.
Asymptomatic incubation periods in prion diseases can extend over decades in
humans. We present here unexpected results of experiments evaluating blood
transmission risk in a non-human primate model.
Material and Methods, Cynomolgus macaques were inoculated with brain or
blood specimens from vCJD infected humans or monkeys. Neuropathological and
biochemical findings were obtained using current methods used for human
patients.
Results, Thirteen out of 23 primates exposed to various human or macaque
blood products exhibited a previously undescribed myelopathic syndrome, devoid
of the classical features of prion disease, notably abnormal prion protein
(PrPres) deposition, whereas the 14 corresponding brain-inoculated donor animals
and 1 transfused animal exhibited the classical vCJD pattern. In passage
experiments, plasma transfusion induced the same atypical phenotype after two
years (again, with no detectable PrPres), whereas the intracerebral inoculation
of spinal cord led to a typical prion disease with cerebral spongiosis and
PrPres accumulation in the brain of the primate recipient. Interestingly,
passage experiments in transgenic mice were largely unsuccessful.
In another experiment designed to test the efficacy of antiprion filters,
three recipients of filtered red blood cells suspended in plasma are still
healthy 4.5 y after transfusion whereas the recipients of unfiltered inocula
died after 2.5 y with the atypical neurological profile.
Conclusion. We describe a new fatal neurological myelopathic syndrome in
monkeys exposed to various vCJD/BSE-infected blood components.
Secondary transmission in primates confirms
(I) the transmissibility of this myelopathy, and
(2) its prion origin which could not be diagnosed as such in the first
recipients.
This myelopathy might be compared in some respects to certain forms of
human lower motor neuron disease, including neuromyelitis optica, the flail arm
syndrome of amyotrophic lateral sclerosis (ALS), and the recently described
FOSMN (facial onset sensory and motor neuronopathy) syndrome.
Friday, August 16, 2013
Creutzfeldt-Jakob disease (CJD) biannual update August 2013 U.K. and
Contaminated blood products induce a highly atypical prion disease devoid of
PrPres in primates
Sunday, August 11, 2013
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing
an extreme increase of 48% between 2008 and 2010
Thursday, September 26, 2013
Minimise transmission risk of CJD and vCJD in healthcare settings Guidance
Wednesday, September 25, 2013
Cleaning, disinfection and sterilization of surface prion contamination
Sunday, September 08, 2013
Iatrogenic Creutzfeldt-Jakob disease via surgical instruments and
decontamination possibilities for the TSE prion
Tuesday, May 28, 2013
Late-in-life surgery associated with Creutzfeldt-Jakob disease: a
methodological outline for evidence-based guidance
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
Tuesday, September 24, 2013
NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow
TSE prion Contamination Suit Cethrin(R)
Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1
of 15
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE
in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki
Okada, Shirou Mohri and Takashi Yokoyama
National Institute of Animal Health; Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE,
and has been detected in several European countries, and North America.
Transmission studies of H-type BSE led to the emergence of the classical BSE
(C-BSE) phenotypes during passages in inbred wild type and bovinized
PrP-overexpressing transgenic mice. In this study, we conducted serial passages
of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice
(TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods
of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage
were constant (~= 220 d), no clear differences were observed in their biological
and biochemical properties. However, at the forth passage, 2 different BSE
phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the
other is longer survival times. TgBoPrP mice with longer incubation period
showed the H-type phenotype of PrPsc profile and pathology. However, those of
shorter incubation period were different phenotypes from previously existed BSE
prions (C-BSE, L-type BSE, and H-type BSE).
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
see also ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
Monday, September 02, 2013
Atypical BSE: role of the E211K prion polymorphism
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research Unit
Sunday, September 1, 2013
Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy
We previously described the biochemical similarities between PrPres derived
from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations
suggest a link between these two uncommon prion phenotypes in a primate model
(it is to note that such a link has not been observed in other models less
relevant from the human situation as hamsters or transgenic mice overexpressing
ovine PrP [28]). We speculate that a group of related animal prion strains
(L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion
diseases in humans with a type 2 PrPres molecular signature (and more
specifically type 2B for vCJD)
snip...
Together with previous experiments performed in ovinized and bovinized
transgenic mice and hamsters [8,9] indicating similarities between TME and
L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME
outbreaks in North America and Europe during the mid-1900s.
To date the OIE/WAHO assumes that the human and animal health standards set
out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE
which include the H-type and L-type atypical forms. This assumption is
scientifically not completely justified and accumulating evidence suggests that
this may in fact not be the case. Molecular characterization and the spatial
distribution pattern of histopathologic lesions and immunohistochemistry (IHC)
signals are used to identify and characterize atypical BSE. Both the L-type and
H-type atypical cases display significant differences in the conformation and
spatial accumulation of the disease associated prion protein (PrPSc) in brains
of afflicted cattle. Transmission studies in bovine transgenic and wild type
mouse models support that the atypical BSE types might be unique strains because
they have different incubation times and lesion profiles when compared to C-type
BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian
hamster the resulting molecular fingerprint had changed, either in the first or
a subsequent passage, from L-type into C-type BSE. In addition, non-human
primates are specifically susceptible for atypical BSE as demonstrated by an
approximately 50% shortened incubation time for L-type BSE as compared to
C-type. Considering the current scientific information available, it cannot be
assumed that these different BSE types pose the same human health risks as
C-type BSE or that these risks are mitigated by the same protective
measures.
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
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SEE MORE CJD TSE PRION BLOOD PRODUCTS RECALLS HERE;
Sunday, June 9, 2013
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory
Committee Meeting Webcast
http://creativegumbo.net/cjdvoice/
tss
posted by Terry S. Singeltary Sr. at
11:42 AM
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