Revised Preventive Measures to Reduce the Possible Risk of Transmission of
Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and
Blood Products Guidance for Industry
U.S. Department of Health and Human Services Food and Drug Administration
Center for Biologics Evaluation and Research May 2010 Updated January 2016
i
Table of Contents
I.
INTRODUCTION..............................................................................................................1
II.
BACKGROUND................................................................................................................3
A. CJD and
vCJD.......................................................................................................
3
B. Evolution of the Global BSE
epidemic................................................................ 6
C. TSE Agents and
Blood..........................................................................................
7
D. FDA Regulatory History
....................................................................................
10
E. Rationale for Geographic Donor Deferrals
...................................................... 15
III. EXPLANATION OF CURRENT VCJD
RECOMMENDATIONS...........................17
A. Exposure to British Beef in the
U.K.................................................................. 17
B. Exposure to British Beef Products Distributed Outside of the
U.K............... 17
C. Indigenous BSE Exposure Outside the U.K.
.................................................... 18
D. Potential Infection with vCJD Agent Acquired by Transfusion
.................... 21
E. Exposure to Bovine Insulin
................................................................................
21
F. Reports of Biological Product Deviations
......................................................... 21
G.
Definitions............................................................................................................
22
IV. RECOMMENDATIONS FOR DONOR DEFERRAL
................................................24
A. Donor Deferral Criteria
.....................................................................................
24
B. Questions to Identify Donors at an Increased Risk for CJD
.......................... 25
C. Donor Reentry after Donor Deferral for Risk of Familial
CJD..................... 26
D. Questions for Identifying Donors at Risk for Exposure to
BSE..................... 26
V. POST-DONATION INFORMATION: RECOMMENDATIONS FOR PRODUCT RETRIEVAL AND
QUARANTINE, CONSIGNEE NOTIFICATION, AND BIOLOGICAL PRODUCT DEVIATION
REPORTING...........................................29
A. Whole Blood and Blood Components Intended for Transfusion, Cellular
Blood Components Intended for Further Manufacture into Injectable Products, and
Source Plasma From Donors with CJD or CJD Risk Factors29
B. Whole Blood and Blood Components Intended for Transfusion, Source
Leukocytes and Other Cellular Blood Components Intended for Further Manufacture
into Injectable Products, from Donors with Geographic Risk Deferrals and/or
Exposure to Bovine Insulin Made in the U.K. since 1980.. 30
C. Source Plasma and Recovered Plasma from Donors with Geographic Risk
Deferrals and/or Exposure to Bovine Insulin Made in the U.K. Since 1980 .
31
D. Whole Blood and Blood Components Intended for Transfusion, Recovered
Plasma, Source Leukocytes, Other Cellular Blood Components Intended for
Manufacturing into Injectable Products, and Source Plasma from Donors with vCJD,
suspected vCJD, or CJD and Age Less Than 55 Years............... 31
E. Plasma
Derivatives..............................................................................................
32
F. Disposal of Retrieved and Quarantined Products
........................................... 33
VI. RECOMMENDATIONS FOR RECIPIENT TRACING AND NOTIFICATION...34
Contains Nonbinding Recommendations
ii VII. LABELING
RECOMMENDATIONS...........................................................................34
VIII. IMPLEMENTATION OF
RECOMMENDATIONS...................................................36
IX. THE IMPACT OF GEOGRAPHIC DONOR DEFERRALS THAT ARE MORE STRINGENT THAN
THOSE RECOMMENDED BY THIS GUIDANCE...............37
X. SOURCES OF ADDITIONAL INFORMATION
........................................................38
XI.
REFERENCES.................................................................................................................39
APPENDIX TABLE 1: DONOR DEFERRAL, PRODUCT DISPOSITION, RECIPIENT
NOTIFICATION FOR WHOLE BLOOD, BLOOD COMPONENTS INTENDED FOR TRANSFUSION, SOURCE
LEUKOCYTES, AND OTHER CELLULAR BLOOD COMPONENTS INTENDED FOR FURTHER
MANUFACTURE...........45
APPENDIX TABLE 2: DONOR DEFERRAL, PRODUCT DISPOSTION, AND RECIPIENT
NOTIFICATION FOR SOURCE PLASMA (SP), RECOVER PLASMA (RP) AND PLASMA DERIVATIVES
(PD) ................................................47
Contains Nonbinding Recommendations
1
Revised Preventive Measures to Reduce the Possible Risk of Transmission of
Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and
Blood Products
Guidance for Industry
This guidance represents the current thinking of the Food and Drug
Administration (FDA or Agency) on this topic. It does not establish any rights
for any person and is not binding on FDA or the public. You can use an
alternative approach if it satisfies the requirements of the applicable statutes
and regulations. To discuss an alternative approach, contact the FDA staff
responsible for this guidance as listed on the title page.
I. INTRODUCTION
II. BACKGROUND
A. CJD and vCJD
CJD is a rare but invariably fatal degenerative disease of the central
nervous system, one of a group of transmissible diseases called transmissible
spongiform encephalopathies (TSEs) or prion diseases. TSEs are associated with a
poorly understood transmissible agent (Refs. 1-6), now designated TSE agents or
prions (Ref. 7). Cases of sporadic CJD—the most common human TSE—occur at low
frequency by an unknown mechanism. CJD may be acquired by an identified
exogenous (usually iatrogenic) exposure to infectious material; or it may be
familial, associated with one of a number of mutations in the
prion-protein-encoding (PRNP) gene. Clinical latency for iatrogenic CJD,
following point exposures to contaminated materials, has sometimes exceeded 30
years (Ref. 8); incubation periods of kuru—another human TSE—appear to have
sometimes exceeded 50 years (Ref. 9).
In 1996, a previously unrecognized variant of CJD, now designated vCJD, was
reported in the United Kingdom (U.K.) (Ref. 10). vCJD is distinguished from CJD
by differences in clinical presentation, cerebral imaging and neuropathologic
changes, summarized in Table 1 (Refs. 10-14).
snip...
B. Evolution of the Global BSE Epidemic
================================
LOL, I omitted this part, see real facts on BSE typical and atypical risk
factors and the infamous BSE MRR policy, the legal trading of TSE prion disease
in links below. ...tss
================================
D. FDA Regulatory History
================================
LOL, see links below as well for past regulatory history by the FDA.
...TSS
================================
2. Evidence that vCJD Has Been Transmitted by Blood Products
Soon after the first description in the U.K. of vCJD affecting 10 young
patients in 1996 (Ref. 10), vCJD was recognized to be an emerging infectious
disease with several unique clinical and pathological characteristics differing
from those of previously known forms of CJD. It was uncertain whether human
blood might transmit the vCJD agent. FDA therefore recommended in the 1999
guidance a donor deferral policy more stringent for donors at increased risk of
vCJD than for those at increased risk of the “classical” forms of the disease
(see Section IV below), including a recommendation to withdraw plasma
derivatives should a plasma donor later be diagnosed with vCJD (a situation
never recognized in the U.S. to date) and a case-by-case review when a plasma
donor is suspected of having vCJD (including all donors with onset of CJD before
the age of 55 years) instead of a more common form of CJD.
In December 2003, U.K. authorities reported a case of vCJD in a recipient
of non-leukoreduced red blood cell concentrate obtained from a clinically
healthy donor who later developed typical vCJD (Ref. 53). In July 2004, a second
recipient of non-leukoreduced red blood cell concentrate from another such donor
in the U.K. was reported to have died of other causes without clinical or
neuropathological evidence of vCJD, but at autopsy the recipient had abnormal
accumulations of prion protein in lymphoid tissues (Ref. 54). This finding is
typical of vCJD, although the recipient had a PRNP genotype (heterozygous for
the sequences encoding methionine and valine at PRNP codon 129 [129 MV]) not
previously found in cases of vCJD (all of which have been 129 MM homozygous).
Two additional recipients of non-leukoreduced red blood cell concentrates from a
donor incubating vCJD were subsequently reported by U.K. authorities in February
2006 (Refs. 55-56) and January 200726 to have died with confirmed vCJD. These
four cases provided convincing epidemiological evidence that vCJD infections
have been transmitted by non-leukoreduced red blood cell concentrates. Although
no other blood components have been associated with transfusion-transmitted
vCJD, experience is still too limited to allow a conclusion that other blood
components cannot transmit the infection.
24 U.K. Health Protection Agency (HPA), “vCJD abnormal prion protein found
in a patient with haemophilia at post mortem,” dated February 17, 2009, and
“Variant CJD and plasma products,” dated July 27, 2009 at http://www.hpa.org.uk.
25 Transfusion Medicine Epidemiology Review: http://www.cjd.ed.ac.uk/TMER/TMER.htm.
26 Transfusion Medicine Epidemiology Review: http://www.cjd.ed.ac.uk/TMER/TMER.htm.
Contains Nonbinding Recommendations
10
In February 2009, the United Kingdom Health Protection Agency announced
evidence of vCJD infection in a patient with type-A hemophilia at postmortem.27
The patient had been treated with human plasma-derived Factor VIII clotting
factor manufactured using plasma from U.K. donors, including one batch that was
manufactured using plasma from a donor who later developed typical vCJD. This is
the first report that vCJD abnormal protein has been found in a patient with
hemophilia or any patient treated with plasma products. The patient, who was
over 70 years old, died of other causes and may have been exposed to other risk
factors for vCJD. A risk assessment performed by U.K. health authorities
concluded that, assuming that the abnormal prion protein finding was a marker
for asymptomatic vCJD infection, the most likely source of such an infection was
plasma-derived Factor VIII, rather than dietary exposure, endoscopy procedures,
or red blood cell transfusions.
At this time, plasma derivatives have not been implicated in vCJD
transmission in any country other than the U.K. To date, no U.S.-licensed
plasma-derived products have been manufactured from a donor known to have
developed vCJD and no cases of vCJD have been reported from use of a
U.S.-licensed plasma derivative. In addition, published studies and information
submitted to FDA show that certain plasma derivative manufacturing steps can
remove TSE infectivity, although such experiments have inherent limitations
(Refs. 51, 57). Based on animal studies as well as on FDA risk assessments, the
possibility of vCJD transmission by a U.S.-licensed plasma derivative is
extremely small.
snip...
Criteria A.
Donor deferral criteria 1-7 apply to all donors. Donor deferral criterion 8
(residence in Europe for 5 years or more between 1980 and the present) applies
to all donors with the exception of donors of Source Plasma.
1. You should permanently defer donors who have been diagnosed with vCJD or
any other form of CJD.66
2. You should permanently defer donors at increased risk for CJD (as
identified by questions 2 and 3 in Section IV.B. Donors are considered to have
an increased risk for CJD if they have received a dura mater transplant or an
injection of human cadaveric pituitary-derived growth hormone. Donors with one
or more blood relatives diagnosed with CJD (as identified in Section IV.B.,
Question 1 below) are also considered to be at increased risk of CJD, and should
be indefinitely deferred (see Section IV.C. for donor reentry
recommendations).
3. You should indefinitely defer donors who have spent three months or more
cumulatively in the U.K. from the beginning of 1980 through the end of
1996.
4. You should indefinitely defer donors who have spent five years or more
cumulatively in France from the beginning of 1980 to the present.
5. You should indefinitely defer former or current U.S. military personnel,
civilian military personnel, and their dependents as follows:
a. Individuals who resided at U.S. military bases in Northern Europe
(Germany, United Kingdom, Belgium, and the Netherlands) for six months or more
from 1980 through 1990, or
b. Individuals who resided at U.S. military bases elsewhere in Europe
(Greece, Turkey, Spain, Portugal, and Italy) for six months or more from 1980
through 1996.
6. You should indefinitely defer donors who have received a transfusion of
blood or blood components in the U.K. or in France between the beginning of 1980
and the present.
66 For the purposes of this document, FDA considers the less common TSEs,
Gerstmann-Sträussler-Scheinker syndrome and fatal insomnia syndromes, to be
equivalent in risk to familial and sporadic CJD. The blood establishment need
not name these rare syndromes in the questionnaire but might consider them as
equivalent in risk to CJD if, in response to a question about CJD, the donor
offers information that a family member has been diagnosed with one of
them.
Contains Nonbinding Recommendations 25
7. You should indefinitely defer donors who have injected bovine insulin
since 1980, unless you can confirm that the product was not manufactured after
1980 from U.K. cattle.
8. You should indefinitely defer donors of Whole Blood, blood components
for transfusion, and Source Leukocytes, who have lived cumulatively for five
years or more in Europe from the beginning of 1980 until the present. (Note this
criterion includes time spent in the U.K. from 1980 through 1996 and time spent
in France from 1980 to the present.) Unless otherwise unsuitable (for example,
because they lived in the U.K. or France or on U.S. military bases for the
periods of time noted previously), these donors remain eligible for Source
Plasma donation.
NOTE: Donors who are otherwise deferred based upon the above criteria 2-8
may continue to donate if they are participating in a CBER-approved program that
allows collection of Source Plasma solely for use in manufacturing of
non-injectable products. We recommend special labeling for products obtained
from such donors (see Section VII.A).
Questions to Identify Donors at an Increased Risk for CJD B.
You should question frequent Source Plasma donors at the first donation
following implementation of the recommendations in this guidance, and annually
thereafter. You should question donors of Whole Blood and blood components,
infrequent Source Plasma donors and Source Leukocyte donors at each donation. If
the donor is not familiar with the term “Creutzfeldt-Jakob Disease,” you may
take that as a negative response. These questions are similar to those in the
1999 and 2002 guidances. We consider donors who answer “Yes” to any of the
questions below to have an increased risk for developing CJD.
Question 1: Have any of your blood relatives ever had Creutzfeldt-Jakob
Disease?67
Question 2: Have you ever received growth hormone made from human pituitary
glands?
NOTE: If the donor is uncertain about his or her treatment, the following
question describing human pituitary-derived growth hormone injections may be
asked: “Was the hormone treatment given repeatedly by injection?” This question
needs to be asked only once, since human cadaveric pituitary growth hormone is
no longer available.
67 See footnote 66.
Contains Nonbinding Recommendations
26
Question 3: Have you ever received a dura mater (brain covering)
graft?
NOTE: This question may be preceded by the more general question “Have you
ever had brain surgery?” Ask the specific question only if the donor responds
“yes” to the general question.
Donor Reentry after Donor Deferral for Risk of Familial CJD C.
If you defer a donor because of family history of CJD, you may reenter that
donor if:
1) The diagnosis of CJD in the family member(s) is confidently excluded, or
CJD in the family member(s) is iatrogenic, or the family member(s) is (are) not
a blood relative(s); or
2) Laboratory testing (gene sequencing) shows that the donor does not have
a mutation associated with familial CJD. Note that gene sequencing of the donor
is not necessary to demonstrate that the donor is not at risk for familial CJD.
Sequencing of the family member with CJD or the appropriate parent of the donor,
if the CJD-affected family member was a second-degree relative, may be
sufficient to demonstrate that the donor does not have a mutation associated
with familial CJD.
Questions for Identifying Donors at Risk for Exposure to BSE D.
1. Method of Donor Questioning
Due to the added complexity of screening donors for cumulative periods of
potential exposure to BSE, a trained staff member should administer the revised
geographic donor deferral criteria by face-to-face interview to each new donor
(as defined in your blood establishment’s standard operating procedures (SOP)).
Instead of face-to-face interviews, you may use a computerized interactive donor
interview program that includes an audio component (audio-CASI) as described in
the FDA guidance entitled “Guidance for Industry: Streamlining the Donor
Interview Process: Recommendations for Self-Administered Questionnaires,” dated
July 2003.68 You should submit changes to your donor interview procedure
according to 21 CFR 601.12. For repeat donors, you may use alternative methods
for introducing and emphasizing the new questions. Your alternative method
should provide the repeat donor with a detailed description of the changes to
the donor questionnaire, to highlight any new questions and modifications.
68 Available at http://www.fda.gov/BiologicsBloodVaccines/GuidanceComplianceRegulatoryInformation/Guidances/Blood/ucm075086.htm.
Contains Nonbinding Recommendations 27
2. Donor Questions
You should indefinitely defer donors who answer “Yes” to the following
questions:
To identify donors with geographic risk of BSE exposure.
SNIP...
LOL...
NO NEED TO GO ANY FURTHER, BECAUSE THE GEOGRAPHICAL RISK ASSESSMENT ON BSE
EXPOSURE IS BASED ON FALSE INFORMATION AND LIES, thanks to the USDA, FDA, and
OIE, in my opinion, see information and links below. ...tss
see full text ;
P197
Misfolded prion protein (PrPTSE) can be detected in the blood of squirrel
monkeys infected with variant Creutzfeldt-Jakob disease (vCJD)
Larisa Cervenakova1, Oksana Yakovleva1, Paula Saá1, David M. Asher2, Thomas
R. Kreil3, Susan Gibson4, Christian Abee5, James W. Ironside6, Paul W. Brown7
1Scientific Affairs, American Red Cross, Rockville, MD, USA, 2Office of Blood
Research and Review, Center for Biologics Evaluation and Research, FDA, Silver
Prion2015 Program Guide
36
Prion 2015 Fort Collins Spring, MD, USA, 3Global Pathogen Safety, Baxter
BioScience, Vienna, Austria, 4University of South Alabama, Mobile, AL
(deceased), USA, 5University of Texas, Anderson Cancer Center, Bastrop, TX, USA,
6National CJD Surveillance Unit, Edinburgh, UK, 7NINDS, National Institutes of
Health, Bethesda, MD (retired), USA
Variant CJD infections have been recognized in 4 recipients of
non-leukocyte-depleted red blood cell (RBC) transfusions (and in a hemophilia
patient treated with a plasmaderived coagulation factor). In the UK, PrPTSE has
been detected in blood of 70% of vCJD patients and in appendices of as many as 1
in 2000 asymptomatic individuals. Reliable tests are needed to detect blood
donors infected with vCJD before the appearance of overt illness to protect
transfusion recipients. We previously reported the co-localization of PrPTSE
with extracellular vesicles (EVs) in plasma of vCJD-infected mice. Here we
report detecting PrPTSE in EVs from archived plasma samples of vCJD-infected
squirrel monkeys. Blood was collected from infected and uninfected monkeys into
anticoagulant every 3 months and separated into RBCs, buffy coat and plasma. EVs
were extracted from plasma using ExoQuickTM. PMCA was performed using uninfected
TgHu mouse brain homogenate as PrPC substrate. We tested samples of blood from 2
groups of monkeys inoculated intracerebrally with vCJD brain diluted 10-1 (4
monkeys) or 10-3 (3 monkeys) and from 4 control monkeys inoculated with 10-1
normal human brain. PrPTSE was detected in plasma EV of 5 of 7 vCJD-inoculated
monkeys (3/4 10-1 and 2/3 10-3). Multiple tests of control plasma EV samples
from the 4 control monkeys were all negative. Whole blood collected from 4
monkeys during incubation and clinical stages of vCJD was transfused into
individual recipient monkeys. We continue to test archived plasma samples from
donor and transfusion-recipient monkeys. Baxter and FABS funded the study.
prion2013
ORIGINAL RESEARCH
Blood transmission studies of prion infectivity in the squirrel monkey
(Saimiri sciureus): the Baxter study
Diane L. Ritchie1,*, Susan V. Gibson2,†, Christian R. Abee3, Thomas R.
Kreil4, James W. Ironside1 and Paul Brown5
Article first published online: 23 NOV 2015
DOI: 10.1111/trf.13422
© 2015 AABB
Issue
Cover image for Vol. 55 Issue 11
Transfusion
Early View (Online Version of Record published before inclusion in an
issue)
Abstract
BACKGROUND
Four secondary transmissions of variant Creutzfeldt-Jakob disease (vCJD)
infectivity have been associated with the transfusion of nonleukoreduced red
blood cells collected from vCJD patients during the asymptomatic phase of the
disease. Establishing efficient experimental models for assessing the risk of
future transmissions of vCJD infectivity via blood transfusion is of paramount
importance in view of a study of archived appendix samples in which the
prevalence of asymptomatic vCJD infection in the United Kingdom was estimated at
approximately 1 in 2000 of the population. In this study, we investigated
transmission of vCJD and sporadic CJD (sCJD) infectivity from blood using the
squirrel monkey, which is highly susceptible to experimental challenge with
human prion disease.
STUDY DESIGN AND METHODS
Whole blood collected from vCJD- and sCJD-infected squirrel monkeys was
transfused at multiple time points into recipient squirrel monkeys. Blood
recipients were euthanized approximately 7 years after their first blood
transfusion.
RESULTS
No clinical or pathologic signs of a prion disease were observed in either
the sCJD- or the vCJD-transfused monkeys, and immunohistochemistry and
biochemical investigations showed no PrPTSE in central nervous system or
lymphoreticular tissues. Similarly, monkeys inoculated intracerebrally (IC) and
intravenously (IV) with either buffy coat or plasma from vCJD and sCJD patients
failed to develop disease. However, white blood cells from a chimpanzee-passaged
strain of human Gerstmann-Sträussler-Scheinker (GSS) disease transmitted
autopsy-proven disease to two IC-inoculated monkeys after incubation periods of
34 and 39 months.
CONCLUSION
Blood transmits GSS but not sCJD or vCJD infectivity to IC- or
IV-inoculated squirrel monkeys within a 7-year observation period.
2015 PRION CONFERENCE
*** RE-P.164: Blood transmission of prion infectivity in the squirrel
monkey: The Baxter study
***suggest that blood donations from cases of GSS (and perhaps other
familial forms of TSE) carry more risk than from vCJD cases, and that little or
no risk is associated with sCJD. ***
P.164: Blood transmission of prion infectivity in the squirrel monkey: The
Baxter study
Paul Brown1, Diane Ritchie2, James Ironside2, Christian Abee3, Thomas
Kreil4, and Susan Gibson5 1NIH (retired); Bethesda, MD USA; 2University of
Edinburgh; Edinburgh, UK; 3University of Texas; Bastrop, TX USA; 4Baxter
Bioscience; Vienna, Austria; 5University of South Alabama; Mobile, AL USA
Five vCJD disease transmissions and an estimated 1 in 2000 ‘silent’
infections in UK residents emphasize the continued need for information about
disease risk in humans. A large study of blood component infectivity in a
non-human primate model has now been completed and analyzed. Among 1 GSS, 4
sCJD, and 3 vCJD cases, only GSS leukocytes transmitted disease within a 5–6
year surveillance period. A transmission study in recipients of multiple whole
blood transfusions during the incubation and clinical stages of sCJD and vCJD in
ic-infected donor animals was uniformly negative. These results, together with
other laboratory studies in rodents and nonhuman primates and epidemiological
observations in humans, suggest that blood donations from cases of GSS (and
perhaps other familial forms of TSE) carry more risk than from vCJD cases, and
that little or no risk is associated with sCJD. The issue of decades-long
incubation periods in ‘silent’ vCJD carriers remains open.
ran across an old paper from 1984 ;
***The occurrence of contact cases raises the possibility that transmission
in families may be effected by an unusually virulent strain of the agent.
***
Monday, November 23, 2015
*** Blood transmission studies of prion infectivity in the squirrel monkey
(Saimiri sciureus): the Baxter study
Article | Open
Preclinical detection of infectivity and disease-specific PrP in blood throughout the incubation period of prion disease
Elizabeth B. Sawyer , Julie Ann Edgeworth , Claire Thomas , John Collinge
& Graham S. Jackson
Scientific Reports 5, Article number: 17742 (2015) doi:10.1038/srep17742 Download Citation Diagnostic markers | Experimental models of disease | Prion diseases
Received:18 June 2015Accepted:06 November 2015Published online:03 December 2015
Abstract
Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disorder characterised by accumulation of pathological isoforms of the prion protein, PrP. Although cases of clinical vCJD are rare, there is evidence there may be tens of thousands of infectious carriers in the United Kingdom alone. This raises concern about the potential for perpetuation of infection via medical procedures, in particular transfusion of contaminated blood products. Accurate biochemical detection of prion infection is crucial to mitigate risk and we have previously reported a blood assay for vCJD. This assay is sensitive for abnormal PrP conformers at the earliest stages of preclinical prion disease in mice and precedes the maximum infectious titre in blood. Not only does this support the possibility of screening asymptomatic individuals, it will also facilitate the elucidation of the complex relationship that exists between the ensemble of abnormal PrP conformers present in blood and the relationship to infectivity.
Discussion
The ability to accurately diagnose prion infection using biochemical methods is crucial to protect public health from iatrogenic transmissions, particularly arising from the transfusion of contaminated blood and blood products10,11,12,33. In the United Kingdom (UK) measures taken to prevent secondary infections of vCJD have included leucodepletion of donor blood, sourcing of plasma from non-UK sources, exclusion of transfusion recipients from donation, use of recombinant clotting factors for patients with bleeding disorders and ceasing the use of UK plasma for fractionation and export34. We have previously reported the development19 and validation20,35 of a blood test for vCJD based upon the detection of abnormal disease-specific isoforms of PrP, which is now in clinical use for the diagnosis of prion disease. The wider application of this test, or indeed other emerging assays36,37, for screening asymptomatic individuals for potential infection is confounded by an inability to confirm that an assay detection limit is sufficient for the detection of preclinical infections. This problem arises as there are currently no samples available from individuals confirmed as sub-clinical carriers of vCJD with which to assess either the prevalence of prionaemia in BSE prion-exposed populations or the sensitivity of any potential blood tests. A definitive answer will require prolonged longitudinal study of individuals testing positive to determine what proportion of patients with vCJD prionaemia go on to develop clinical vCJD and how many are chronic carriers38.
It has been suggested that carriers would have lower concentrations of abnormal PrP compared to individuals with clinical CJD13, and this seems likely. Despite potentially lower levels, animal models indicate clear preclinical blood involvement23,24,39,40 and very efficient transmission of prion infection has been demonstrated from blood taken from sheep in early preclinical stages of scrapie9. The use of the RML-prion strain allows rapid and precise estimates of low prion titre using cell-based assays41,42. Previous attempts to detect infectivity in low titre sources have required either the use of large numbers of recipient animals or the transfusion or large volumes of infected analyte in large animals. By using the SSBA18 we have not only verified but accurately quantified the presence of infectivity in blood even at the earliest stages of preclinical prion disease. A comparison of RML-infected brain diluted into either FVB/N-Prnp0/0 brain homogenate or blood showed that although the presence of whole blood impacted on the overall detection limit of the assay, it remained capable of detecting RML prions at concentrations of less than 1 LD50 units/ml. Infectivity was found to rise by approximately 10–20-fold throughout the incubation period (Fig. 4) as might be anticipated from historical estimates derived from conventional large scale rodent bioassays26, albeit with significant fluctuations approaching the clinical end-point of disease. The significant increase in infectious titre in the last few days of the incubation period are unexpected with the change in titre identifiable only as a result of the high precision of SSBA and related cell-culture assays which are providing unique insights into the replication of prion isoforms during pathogenesis43,44. Levels of MMP-9 in serum provide an indication of BBB integrity and although complicated by age-related decline45, sudden elevation towards the clinical end point for prion disease (Fig. 5) may indicate a sudden perturbation leading to exchange of prion material between the CNS and circulating blood and fluctuations in the concentration of prion disease-related PrP isoforms in blood.
Surprisingly, analysis of the same samples using our DDA assay revealed relatively consistent positive signals throughout the RML incubation period (Fig. 3). Positive detection was achieved from the earliest time point sampled and could not be ascribed to the detection of residual inoculum as similar signals were not observed in the blood of FVB/N-Prnp0/0 mice unable to replicate prions (data not shown), and the half-life of prion-infected inocula has previously been shown to be short: 36 hours in rodent brain tissue46 and less in cell-culture47. The lack of correlation between DDA reactivity and infectivity seen by SSBA indicates DDA is capable of detecting a wider ensemble of abnormal PrP conformers associated with prion infection44,48 of which infectivity may only constitute a minority component. Such observations are not without precedent and there is increasing evidence to suggest that abnormal PrP conformers may be as much as 106-fold more abundant than assayable infectivity49. The ability to detect the plethora of abnormal PrP increases the analytical sensitivity of assays and in the case of DDA an analytical sensitivity equivalent to a 109-fold dilution of prion-infected brain is sufficient for clinical sensitivity at the earliest stages of preclinical prion disease.
http://www.nature.com/articles/srep17742
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Transmission of scrapie prions to primate after an extended silent
incubation period
Authors
item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire,
Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item
Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item
Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron,
Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item
Deslys, Jean-Philippe -
Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal
Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015
Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E.,
Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C.,
Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J.
2015. Transmission of scrapie prions to primate after an extended silent
incubation period. Scientific Reports. 5:11573.
Interpretive Summary:
The transmissible spongiform encephalopathies (also called prion diseases)
are fatal neurodegenerative diseases that affect animals and humans. The agent
of prion diseases is a misfolded form of the prion protein that is resistant to
breakdown by the host cells. Since all mammals express prion protein on the
surface of various cells such as neurons, all mammals are, in theory, capable of
replicating prion diseases. One example of a prion disease, bovine spongiform
encephalopathy (BSE; also called mad cow disease), has been shown to infect
cattle, sheep, exotic undulates, cats, non-human primates, and humans when the
new host is exposed to feeds or foods contaminated with the disease agent. The
purpose of this study was to test whether non-human primates (cynomologous
macaque) are susceptible to the agent of sheep scrapie. After an incubation
period of approximately 10 years a macaque developed progressive clinical signs
suggestive of neurologic disease. Upon postmortem examination and microscopic
examination of tissues, there was a widespread distribution of lesions
consistent with a transmissible spongiform encephalopathy. This information will
have a scientific impact since it is the first study that demonstrates the
transmission of scrapie to a non-human primate with a close genetic relationship
to humans. This information is especially useful to regulatory officials and
those involved with risk assessment of the potential transmission of animal
prion diseases to humans.
Technical Abstract:
Classical bovine spongiform encephalopathy (c-BSE) is an animal prion
disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the
past decades, c-BSE's zoonotic potential has been the driving force in
establishing extensive protective measures for animal and human health. In
complement to the recent demonstration that humanized mice are susceptible to
scrapie, we report here the first observation of direct transmission of a
natural classical scrapie isolate to a macaque after a 10-year incubation
period. Neuropathologic examination revealed all of the features of a prion
disease: spongiform change, neuronal loss, and accumulation of PrPres throughout
the CNS.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
SUMMARY: We are reopening the comment period for our proposed rule that
would revise completely the scrapie regulations, which concern the risk groups
and categories established for individual animals and for flocks, the use of
genetic testing as a means of assigning risk levels to animals, movement
restrictions for animals found to be genetically less susceptible or resistant
to scrapie, and recordkeeping requirements. This action will allow interested
persons additional time to prepare and submit comments.
DATES: The comment period for the proposed rule published on September 10,
2015 (80 FR 54660-54692) is reopened. We will consider all comments that we
receive on or before December 9, 2015. ...
COMMENT SUBMISSION TERRY S. SINGELTARY SR.
WITH regards to Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats, I
kindly submit the following ;
>>>The last major revision of the scrapie regulations occurred on
August 21, 2001, when we published in theFederal Register(66 FR 43964, Docket
No. 97-093-5) a final rule amending part 79 by imposing additional restrictions
on the interstate movement of sheep and goats.<<<
Indeed, much science has changed about the Scrapie TSE prion, including
more science linking Scrapie to humans. sadly, politics, industry, and trade,
have not changed, and those usually trump sound science, as is the case with all
Transmissible Spongiform Encephalopathy TSE Prion disease in livestock producing
animals and the OIE. we can look no further at the legal trading of the Scrapie
TSE prion both typical and atypical of all strains, and CWD all stains. With as
much science of old, and now more new science to back this up, Scrapie of all
types i.e. atypical and typical, BSE all strains, and CWD all strains, should be
regulated in trade as BSE TSE PRION. In fact, I urge APHIS et al and the OIE,
and all trading partners to take heed to the latest science on the TSE prion
disease, all of them, and seriously reconsider the blatant disregards for human
and animal health, all in the name of trade, with the continued relaxing of TSE
Prion trade regulations through the ‘NEGLIGIBLE BSE RISK’ PROGRAM, which was set
up to fail in the first place. If the world does not go back to the ‘BSE RISK
ASSESSMENTS’, enhance, and or change that assessment process to include all TSE
prion disease, i.e. ‘TSE RISK ASSESSMENT’, if we do not do this and if we
continue this farce with OIE and the USDA et al, and the ‘NEGLIGIBLE BSE RISK’
PROGRAM, we will never eradicate the TSE prion aka mad cow type disease, they
will continue to mutate and spread among species of human and animal origin, and
they will continue to kill. ...
please see ;
O.05: Transmission of prions to primates after extended silent incubation
periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni,
Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys
Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies
reputed to be transmissible under field conditions since decades. The
transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that
an animal PD might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, PD, like the other proteinopathies, are
reputed to occur spontaneously (atpical animal prion strains, sporadic CJD
summing 80% of human prion cases). Non-human primate models provided the first
evidences supporting the transmissibiity of human prion strains and the zoonotic
potential of BSE. Among them, cynomolgus macaques brought major information for
BSE risk assessment for human health (Chen, 2014), according to their
phylogenetic proximity to humans and extended lifetime. We used this model to
assess the zoonotic potential of other animal PD from bovine, ovine and cervid
origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical
scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD,
albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked
in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases. We will present an
updated panorama of our different transmission studies and discuss the
implications of such extended incubation periods on risk assessment of animal PD
for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
snip...see ;
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
==========================================
***our findings suggest that possible transmission risk of H-type BSE to
sheep and human. Bioassay will be required to determine whether the PMCA
products are infectious to these animals.
==========================================
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
O18
Zoonotic Potential of CWD Prions
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1,
Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve
University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy,
3Encore Health Resources, Houston, Texas, USA
*** These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.
==================
***These results indicate that the CWD prion has the potential to infect
human CNS and peripheral lymphoid tissues and that there might be asymptomatic
human carriers of CWD infection.***
==================
P.105: RT-QuIC models trans-species prion transmission
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover
Prion Research Center; Colorado State University; Fort Collins, CO USA
Conversely, FSE maintained sufficient BSE characteristics to more
efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was
competent for conversion by CWD and fCWD.
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.
================
***This insinuates that, at the level of protein:protein interactions, the
barrier preventing transmission of CWD to humans is less robust than previously
estimated.***
================
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
*** 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.
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ???? “Our conclusion stating that we found no
strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD. That
assumption would be wrong. I encourage you to read the whole article and call me
if you have questions or need more clarification (phone: 404-639-3091). Also, we
do not claim that "no-one has ever been infected with prion disease from eating
venison." Our conclusion stating that we found no strong evidence of CWD
transmission to humans in the article you quoted or in any other forum is
limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008
Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip... full text ;
CJD is so rare in people under age 30, one case in a billion (leaving out
medical mishaps), that four cases under 30 is "very high," says Colorado
neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in
the newspaper], six cases of CJD in people associated with venison is very, very
high." Only now, with Mary Riley, there are at least seven, and possibly eight,
with Steve, her dining companion. "It's not critical mass that matters,"
however, Belay says. "One case would do it for me." The chance that two people
who know each other would both contact CJD, like the two Wisconsin sportsmen, is
so unlikely, experts say, it would happen only once in 140 years.
Given the incubation period for TSEs in humans, it may require another
generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting
disease pass into humans? We'll be able to answer that in 2022," says Race.
Meanwhile, the state has become part of an immense experiment.
I urge everyone to watch this video closely...terry
*** you can see video here and interview with Jeff's Mom, and scientist
telling you to test everything and potential risk factors for humans ***
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).***
Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel
PrPSc Type in a Young British Woman
Simon Mead, PhD, MRCP; Susan Joiner, MSc; Melanie Desbruslais, BSc; et al
Arch Neurol. 2007;64(12):1780 doi:10.1001/archneur.64.12.1780
Observation | December 2007 Creutzfeldt-Jakob Disease, Prion Protein Gene
Codon 129VV, and a Novel PrPSc Type in a Young British Woman Simon Mead, PhD,
MRCP; Susan Joiner, MSc; Melanie Desbruslais, BSc; Jonathan A. Beck, BSc;
Michael O’Donoghue, PhD; Peter Lantos, FRCP; Jonathan D. F. Wadsworth, PhD; John
Collinge, FRS [+-] Author Affiliations Author Affiliations: MRC [Medical
Research Council] Prion Unit and Department of Neurodegenerative Disease,
Institute of Neurology, University College London, National Hospital for
Neurology and Neurosurgery, London, England (Drs Mead, Wadsworth, and Collinge;
Mss Joiner and Desbruslais; and Mr Beck); and Institute of Psychiatry, King's
College London (Dr Lantos). Dr O’Donoghue is now with the Department of Clinical
Neurology, Nottingham University Hospitals NHS [National Health Service] Trust,
Nottingham, England.
Arch Neurol. 2007;64(12):1780-1784. doi:10.1001/archneur.64.12.1780.
ABSTRACT Background Variant Creutzfeldt-Jakob disease (vCJD) is an acquired
prion disease causally related to bovine spongiform encephalopathy that has
occurred predominantly in young adults. All clinical cases studied have been
methionine homozygotes at codon 129 of the prion protein gene (PRNP) with
distinctive neuropathological findings and molecular strain type (PrPSc type 4).
Modeling studies in transgenic mice suggest that other PRNP genotypes will also
be susceptible to infection with bovine spongiform encephalopathy prions but may
develop distinctive phenotypes.
Objective To describe the histopathologic and molecular investigation in a
young British woman with atypical sporadic CJD and valine homozygosity at PRNP
codon 129.
Design Case report, autopsy, and molecular analysis.
Setting Specialist neurology referral center, together with the laboratory
services of the MRC [Medical Research Council] Prion Unit.
Subject Single hospitalized patient.
Main Outcome Measures Autopsy findings and molecular investigation
results.
Results Autopsy findings were atypical of sporadic CJD, with marked gray
and white matter degeneration and widespread prion protein (PrP) deposition.
Lymphoreticular tissue was not available for analysis. Molecular analysis of
PrPSc (the scrapie isoform of PrP) from cerebellar tissue demonstrated a novel
PrPSc type similar to that seen in vCJD (PrPSc type 4). However, this could be
distinguished from the typical vCJD pattern by an altered protease cleavage site
in the presence of the metal ion chelator EDTA.
Conclusions Further studies will be required to characterize the prion
strain seen in this patient and to investigate its etiologic relationship with
bovine spongiform encephalopathy. This case illustrates the importance of
molecular analysis of prion disease, including the use of EDTA to investigate
the metal dependence of protease cleavage patterns of PrPSc.
COMMENT Does the PrPSc typing suggest a BSE-related cause, or can our
findings be accommodated by the spectrum seen in sporadic CJD cases worldwide?
The molecular strain typing of the patient's brain material demonstrated a
novel PrPSc type when compared with our archived cases.21 There is as yet no
internationally agreed-on classification of PrPSc type. Parchi and colleagues23
identified 2 PrPSc types in sporadic CJD. However, Hill et al21 described 3
PrPSc types associated with sporadic and iatrogenic CJD (types 1-3) and PrPSc
type 4 associated with vCJD. The PrPSc type 5 has, to our knowledge, been
observed only in mice expressing human PrP 129V inoculated with vCJD.3,12 Hill
et al21 recently described a novel PrPSc type 6 in sporadic CJD.
The PrPSc type from our case has features similar to PrPSc type 4 (vCJD) in
the predominance of the diglycosylated band; however, it is distinct from PrPSc
type 4 in the dependence of the protease cleavage pattern of PrPSc on metal
ions, suggesting a distinct PrPSc conformation. Unfortunately, only cerebellum
was available for Western blotting in this case, although in vCJD cases from
which whole brain was available we have not found evidence of any regional
variation in PrPSc type. Others have reported coexistence of Gambetti PrPSc type
1 in the brain from patients with vCJD as a minority component.24 It would also
have been interesting to look for peripheral lymphoreticular PrP deposition
because this is prominent in vCJD, but that tissue was not available for
analysis. Transmission of BSE isolates to transgenic mice expressing human PrP
129 valine results in clinical prion disease with undetectable PrPSc; however,
transmission of vCJD isolates to the same mice produces PrPSc type 5 that shares
the same predominance of diglycosylated PrPSc to that of PrPSc type 4, and these
data suggest that the molecular signature of BSE may be preserved after BSE
transmission to PRNP codon 129 VV humans.3,12 Transmission studies of the
current case in transgenic mice are now being undertaken to investigate
transmission characteristics.
We have described a novel PrPSc type that would be designated type 7 by our
classification. A firm connection between novel PrPSc types and BSE cannot be
made on the basis of a single case, and it will be important to see whether
other similar cases occur in the United Kingdom and other BSE-exposed countries
but not elsewhere and to perform detailed transmission studies of prions from
this patient into transgenic and conventional mice to compare with BSE-derived
isolates from cattle and other species. Two other cases of prion disease with
valine homozygosity and atypical features have been reported in the United
Kingdom and the Netherlands. One of these cases was atypical because of very
young onset and a protracted psychiatric history25; the other was notable
because certain clinical and molecular features of the case overlapped with
those of vCJD, including Western blot analysis of autopsied brain showing a
predominance of a diglycosylated PrPSc isoform.26
We recommend keeping an open mind about the etiology of such cases during
the ensuing years. These cases emphasize the importance both of continued
surveillance of prion disease and the further development and refinement of
molecular classification of prion diseases of humans and animals. It will also
be important to assess lymphoreticular involvement in subsequent cases either at
diagnostic tonsil biopsy or at autopsy.
2015
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21
CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from
deer and elk is prohibited for use in feed for ruminant animals. With regards to
feed for non-ruminant animals, under FDA law, CWD positive deer may not be used
for any animal feed or feed ingredients. For elk and deer considered at high
risk for CWD, the FDA recommends that these animals do not enter the animal feed
system.
***However, this recommendation is guidance and not a requirement by law.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
It is clear that the designing scientists must also have shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleys
surprise at the results because all the dose levels right down to 1 gram
triggered infection.
Evidence That Transmissible Mink Encephalopathy Results from Feeding
Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the
farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or
dead dairy cattle...
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to
accord it a very low profile indeed. Dr. A Thiermann showed the picture in the
''Independent'' with cattle being incinerated and thought this was a fanatical
incident to be avoided in the US at all costs. ...
10 years post mad cow feed ban August 1997
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN
COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried,
Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-
contaminated with prohibited bovine meat and bone meal that had been
manufactured on common equipment and labeling did not bear cautionary BSE
statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-
Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M
CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B
DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal,
JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT
Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral,
BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC
LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall #
V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with
commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm
initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross
contaminated with prohibited meat and bone meal and the labeling did not bear
cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
16 years post mad cow feed ban August 1997
2013
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
17 years post mad cow feed ban August 1997
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
Sunday, June 14, 2015
Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain
Specified Risk Materials BSE TSE Prion
*** Monday, October 26, 2015 ***
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015 ***
the OIE BSE TSE Prion policy now, the BSE MRR, legalized the free trading
of the TSE Prion disease, humans and animals have now become expendable.
...
‘’AS i said before, OIE should hang up there jock strap now, since it
appears they will buckle every time a country makes some political hay about
trade protocol, commodities and futures. IF they are not going to be science
based, they should do everyone a favor and dissolve there organization.’’
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries. The
OIE is not responsible for inaccurate publication of country disease status
based on inaccurate information or changes in epidemiological status or other
significant events that were not promptly reported to the Central Bureau,
snip...see ;
*** Thursday, January 14, 2016
*** EMERGING ANIMAL DISEASES Actions Needed to Better Position USDA to
Address Future Risks Report to the Chairman, Committee on Energy and Commerce,
House of Representatives December 2015 GAO-16-132
*** GAO
Sunday, October 18, 2015
World Organisation for Animal Health (OIE) and the Institut Pasteur
Cooperating on animal disease and zoonosis research
Thursday, December 17, 2015
Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738
10 December 2015
Friday, January 1, 2016
South Korea Lifts Ban on Beef, Veal Imports From Canada
US CONGRESS, another failed entity...tss
Tuesday, December 29, 2015
*** Congress repeals country-of-origin labeling rule for beef and pork
December 28, 2015 at 2:21am
*** Australian government assessing risk of importing beef from US, Japan
and the Netherlands
Thursday, December 24, 2015
Infectious disease spread is fueled by international trade
*** you can find some history of the BSE cases in Canada and Klein’s BSE
SSS policy comment here ;
Tuesday, August 12, 2014
MAD COW USDA TSE PRION COVER UP or JUST IGNORANCE, for the record AUGUST
2014
Saturday, December 12, 2015
*** BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION REPORT DECEMBER 14, 2015
Thursday, October 22, 2015
*** Former Ag Secretary Ann Veneman talks women in agriculture and we talk
mad cow disease USDA and what really happened
*** Needless conflict ***
Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b
Published online 16 May 2012
Terry S. Singeltary Sr. said:
I kindly wish to submit the following please ;
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 19–28 February 2013
In response to a Member Country’s detailed justification for listing of
chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2.,
the Code Commission recommended this disease be reconsidered for listing.
OIE CWD TSE PRION TO HUMANS RISK FACTORS STILL IGNORED
REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS
COMMISSION Paris, 17–26 September 2013
Item 5 Criteria for listing diseases (Chapter 1.2.)
Comments were received from Australia, EU, Japan, New Zealand, Switzerland,
Thailand and AU-IBAR The Code Commission noted a Member Country’s comment
suggesting that greater clarity was needed for the term ‘significant morbidity
and mortality’. As noted in the February 2013 report, the Code Commission
considered that the structured process of listing diseases, first by an expert
group whose conclusions are documented and circulated for Member Countries’
review and comment, then consideration by the World Assembly of Delegates before
final adoption, is sufficiently rigorous and transparent.
link updated ;
Monday, May 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing
*** Singeltary submission ;
*** Program Standards: Chronic Wasting Disease Herd Certification Program
and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411 ***
see attachments PDF @ bottom of submission...tss
SCRAPIE TO HUMANS RISK FACTORS STILL IGNORED
***This information will have a scientific impact since it is the first
study that demonstrates the transmission of scrapie to a non-human primate with
a close genetic relationship to humans. This information is especially useful to
regulatory officials and those involved with risk assessment of the potential
transmission of animal prion diseases to humans.
***This observation strengthens the questioning of the harmlessness of
scrapie to humans, at a time when protective measures for human and animal
health are being dismantled and reduced as c-BSE is considered controlled and
being eradicated. Our results underscore the importance of precautionary and
protective measures and the necessity for long-term experimental transmission
studies to assess the zoonotic potential of other animal prion strains.
Monday, November 16, 2015
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
98 | Veterinary Record | January 24, 2015
EDITORIAL
Scrapie: a particularly persistent pathogen
Cristina Acín
Resistant prions in the environment have been the sword of Damocles for
scrapie control and eradication. Attempts to establish which physical and
chemical agents could be applied to inactivate or moderate scrapie infectivity
were initiated in the 1960s and 1970s,with the first study of this type focusing
on the effect of heat treatment in reducing prion infectivity (Hunter and
Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate
the prion protein are based on the method developed by Kimberlin and
collaborators (1983). This procedure consists of treatment with 20,000 parts per
million free chlorine solution, for a minimum of one hour, of all surfaces that
need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so
on). Despite this, veterinarians and farmers may still ask a range of questions,
such as ‘Is there an official procedure published somewhere?’ and ‘Is there an
international organisation which recommends and defines the exact method of
scrapie decontamination that must be applied?’
From a European perspective, it is difficult to find a treatment that could
be applied, especially in relation to the disinfection of surfaces in lambing
pens of affected flocks. A 999/2001 EU regulation on controlling spongiform
encephalopathies (European Parliament and Council 2001) did not specify a
particular decontamination measure to be used when an outbreak of scrapie is
diagnosed. There is only a brief recommendation in Annex VII concerning the
control and eradication of transmissible spongiform encephalopathies (TSE
s).
Chapter B of the regulation explains the measures that must be applied if
new caprine animals are to be introduced to a holding where a scrapie outbreak
has previously been diagnosed. In that case, the statement indicates that
caprine animals can be introduced ‘provided that a cleaning and disinfection of
all animal housing on the premises has been carried out following
destocking’.
Issues around cleaning and disinfection are common in prion prevention
recommendations, but relevant authorities, veterinarians and farmers may have
difficulties in finding the specific protocol which applies. The European Food
and Safety Authority (EFSA ) published a detailed report about the efficacy of
certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and
even a formulation of copper or iron metal ions in combination with hydrogen
peroxide, against prions (EFSA 2009). The report was based on scientific
evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006,
Solassol and others 2006) but unfortunately the decontamination measures were
not assessed under outbreak conditions.
The EFSA Panel on Biological Hazards recently published its conclusions on
the scrapie situation in the EU after 10 years of monitoring and control of the
disease in sheep and goats (EFSA 2014), and one of the most interesting findings
was the Icelandic experience regarding the effect of disinfection in scrapie
control. The Icelandic plan consisted of: culling scrapie-affected sheep or the
whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of
stables, sheds, barns and equipment with high pressure washing followed by
cleaning with 500 parts per million of hypochlorite; drying and treatment with
300 ppm of iodophor; and restocking was not permitted for at least two years.
Even when all of these measures were implemented, scrapie recurred on several
farms, indicating that the infectious agent survived for years in the
environment, even as many as 16 years after restocking (Georgsson and others
2006).
In the rest of the countries considered in the EFSA (2014) report,
recommendations for disinfection measures were not specifically defined at the
government level. In the report, the only recommendation that is made for sheep
is repopulation with sheep with scrapie-resistant genotypes. This reduces the
risk of scrapie recurrence but it is difficult to know its effect on the
infection.
Until the EFSA was established (in May 2003), scientific opinions about TSE
s were provided by the Scientific Steering Committee (SSC) of the EC, whose
advice regarding inactivation procedures focused on treating animal waste at
high temperatures (150°C for three hours) and high pressure alkaline hydrolysis
(SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory
Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe
working and the prevention of TSE infection. Annex C of the ACDP report
established that sodium hypochlorite was considered to be effective, but only if
20,000 ppm of available chlorine was present for at least one hour, which has
practical limitations such as the release of chlorine gas, corrosion,
incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its
active chemicals and the stability of dilutions (ACDP 2009).
In an international context, the World Organisation for Animal Health (OIE)
does not recommend a specific disinfection protocol for prion agents in its
Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General
recommendations on disinfection and disinsection (OIE 2014), focuses on
foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on
prion disinfection. Nevertheless, the last update published by the OIE on bovine
spongiform encephalopathy (OIE 2012) indicates that few effective
decontamination techniques are available to inactivate the agent on surfaces,
and recommends the removal of all organic material and the use of sodium
hydroxide, or a sodium hypochlorite solution containing 2 per cent available
chlorine, for more than one hour at 20ºC.
The World Health Organization outlines guidelines for the control of TSE s,
and also emphasises the importance of mechanically cleaning surfaces before
disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO
1999).
Finally, the relevant agencies in both Canada and the USA suggest that the
best treatments for surfaces potentially contaminated with prions are sodium
hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution,
while most commercial household bleaches contain 5.25 per cent sodium
hypochlorite. It is therefore recommended to dilute one part 5.25 per cent
bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency
2013).
So what should we do about disinfection against prions? First, it is
suggested that a single protocol be created by international authorities to
homogenise inactivation procedures and enable their application in all
scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available
chlorine seems to be the procedure used in most countries, as noted in a paper
summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015).
But are we totally sure of its effectiveness as a preventive measure in a
scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease
be needed?
What we can conclude is that, if we want to fight prion diseases, and
specifically classical scrapie, we must focus on the accuracy of diagnosis,
monitoring and surveillance; appropriate animal identification and control of
movements; and, in the end, have homogeneous and suitable protocols to
decontaminate and disinfect lambing barns, sheds and equipment available to
veterinarians and farmers. Finally, further investigations into the resistance
of prion proteins in the diversity of environmental surfaces are required.
References
snip...
98 | Veterinary Record | January 24, 2015
*** These results suggest that AA fibrils are relatively heat stable and
that similar to prions, autoclaving at 135 °C is required to destroy the
pathogenicity of AA fibrils.
*** These findings may contribute to the prevention of AA fibril
transmission through food materials to different animals and especially to
humans.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
PL1
Using in vitro prion replication for high sensitive detection of prions and
prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders,
Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the
ability to selfpropagate to spread disease between cells, organs and in some
cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m
encephalopathies (TSEs), prions are mostly composed by a misfolded form of the
prion protein (PrPSc), which propagates by transmitting its misfolding to the
normal prion protein (PrPC). The availability of a procedure to replicate prions
in the laboratory may be important to study the mechanism of prion and
prion-like spreading and to develop high sensitive detection of small quantities
of misfolded proteins in biological fluids, tissues and environmental samples.
Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient
methodology to mimic prion replication in the test tube. PMCA is a platform
technology that may enable amplification of any prion-like misfolded protein
aggregating through a seeding/nucleation process. In TSEs, PMCA is able to
detect the equivalent of one single molecule of infectious PrPSc and propagate
prions that maintain high infectivity, strain properties and species
specificity. Using PMCA we have been able to detect PrPSc in blood and urine of
experimentally infected animals and humans affected by vCJD with high
sensitivity and specificity. Recently, we have expanded the principles of PMCA
to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in
Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to
study the utility of this technology to detect Aβ and α-syn aggregates in
samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental
prion contamination on the horizontal spreading of TSEs. These experiments have
focused on the study of the interaction of prions with plants and
environmentally relevant surfaces. Our results show that plants (both leaves and
roots) bind tightly to prions present in brain extracts and excreta (urine and
feces) and retain even small quantities of PrPSc for long periods of time.
Strikingly, ingestion of prioncontaminated leaves and roots produced disease
with a 100% attack rate and an incubation period not substantially longer than
feeding animals directly with scrapie brain homogenate. Furthermore, plants can
uptake prions from contaminated soil and transport them to different parts of
the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety
of environmentally relevant surfaces, including stones, wood, metals, plastic,
glass, cement, etc. Prion contaminated surfaces efficiently transmit prion
disease when these materials were directly injected into the brain of animals
and strikingly when the contaminated surfaces were just placed in the animal
cage. These findings demonstrate that environmental materials can efficiently
bind infectious prions and act as carriers of infectivity, suggesting that they
may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental
questions of prion propagation and has broad applications in research areas
including the food industry, blood bank safety and human and veterinary disease
diagnosis.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4,
Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge,
Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency
Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and
Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary
Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School
of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington,
UK
Classical scrapie is an environmentally transmissible prion disease of
sheep and goats. Prions can persist and remain potentially infectious in the
environment for many years and thus pose a risk of infecting animals after
re-stocking. In vitro studies using serial protein misfolding cyclic
amplification (sPMCA) have suggested that objects on a scrapie affected sheep
farm could contribute to disease transmission. This in vivo study aimed to
determine the role of field furniture (water troughs, feeding troughs, fencing,
and other objects that sheep may rub against) used by a scrapie-infected sheep
flock as a vector for disease transmission to scrapie-free lambs with the prion
protein genotype VRQ/VRQ, which is associated with high susceptibility to
classical scrapie. When the field furniture was placed in clean accommodation,
sheep became infected when exposed to either a water trough (four out of five)
or to objects used for rubbing (four out of seven). This field furniture had
been used by the scrapie-infected flock 8 weeks earlier and had previously been
shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of
23) through exposure to contaminated field furniture placed within pasture not
used by scrapie-infected sheep for 40 months, even though swabs from this
furniture tested negative by PMCA. This infection rate decreased (1 out of 12)
on the same paddock after replacement with clean field furniture. Twelve grazing
sheep exposed to field furniture not in contact with scrapie-infected sheep for
18 months remained scrapie free. The findings of this study highlight the role
of field furniture used by scrapie-infected sheep to act as a reservoir for
disease re-introduction although infectivity declines considerably if the field
furniture has not been in contact with scrapie-infected sheep for several
months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental
contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it
has been reported in naïve, supposedly previously unexposed sheep placed in
pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the
vector for disease transmission is not known, soil is likely to be an important
reservoir for prions (2) where – based on studies in rodents – prions can adhere
to minerals as a biologically active form (21) and remain infectious for more
than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in
mule deer housed in paddocks used by infected deer 2 years earlier, which was
assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was
greater through exposure to contaminated wooden, plastic, and metal surfaces via
water or food troughs, fencing, and hurdles than through grazing. Drinking from
a water trough used by the scrapie flock was sufficient to cause infection in
sheep in a clean building. Exposure to fences and other objects used for rubbing
also led to infection, which supported the hypothesis that skin may be a vector
for disease transmission (9). The risk of these objects to cause infection was
further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid
tissue after grazing on one of the paddocks, which contained metal hurdles, a
metal lamb creep and a water trough in contact with the scrapie flock up to 8
weeks earlier, whereas no infection had been demonstrated previously in sheep
grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate
dropped significantly to 8% of 12 sheep, with soil of the paddock as the most
likely source of infection caused by shedding of prions from the
scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field
furniture sufficient to cause infection was dependent on two factors: stage of
incubation period and time of last use by scrapie-infected sheep. Drinking from
a water trough that had been used by scrapie sheep in the predominantly
pre-clinical phase did not appear to cause infection, whereas infection was
shown in sheep drinking from the water trough used by scrapie sheep in the later
stage of the disease. It is possible that contamination occurred through
shedding of prions in saliva, which may have contaminated the surface of the
water trough and subsequently the water when it was refilled. Contamination
appeared to be sufficient to cause infection only if the trough was in contact
with sheep that included clinical cases. Indeed, there is an increased risk of
bodily fluid infectivity with disease progression in scrapie (24) and CWD (25)
based on PrPSc detection by sPMCA. Although ultraviolet light and heat under
natural conditions do not inactivate prions (26), furniture in contact with the
scrapie flock, which was assumed to be sufficiently contaminated to cause
infection, did not act as vector for disease if not used for 18 months, which
suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for
infectivity measurements by bioassay in sheep or mice. In this reported study,
however, the levels of PrPSc present in the environment were below the limit of
detection of the sPMCA method, yet were still sufficient to cause infection of
in-contact animals. In the present study, the outdoor objects were removed from
the infected flock 8 weeks prior to sampling and were positive by sPMCA at very
low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive
reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay
could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo
formation of infectious prions have been reported (27, 28). This is in contrast
to our previous study where we demonstrated that outdoor objects that had been
in contact with the scrapie-infected flock up to 20 days prior to sampling
harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions
(12)] and was significantly more positive by the assay compared to analogous
samples from the scrapie-free farm. This discrepancy could be due to the use of
a different sPMCA substrate between the studies that may alter the efficiency of
amplification of the environmental PrPSc. In addition, the present study had a
longer timeframe between the objects being in contact with the infected flock
and sampling, which may affect the levels of extractable PrPSc. Alternatively,
there may be potentially patchy contamination of this furniture with PrPSc,
which may have been missed by swabbing. The failure of sPMCA to detect
CWD-associated PrP in saliva from clinically affected deer despite confirmation
of infectivity in saliva-inoculated transgenic mice was associated with as yet
unidentified inhibitors in saliva (29), and it is possible that the sensitivity
of sPMCA is affected by other substances in the tested material. In addition,
sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more
difficult from furniture exposed to weather, which is supported by the
observation that PrPSc was detected by sPMCA more frequently in indoor than
outdoor furniture (12). A recent experimental study has demonstrated that
repeated cycles of drying and wetting of prion-contaminated soil, equivalent to
what is expected under natural weathering conditions, could reduce PMCA
amplification efficiency and extend the incubation period in hamsters inoculated
with soil samples (30). This seems to apply also to this study even though the
reduction in infectivity was more dramatic in the sPMCA assays than in the sheep
model. Sheep were not kept until clinical end-point, which would have enabled us
to compare incubation periods, but the lack of infection in sheep exposed to
furniture that had not been in contact with scrapie sheep for a longer time
period supports the hypothesis that prion degradation and subsequent loss of
infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of
furniture that had been in contact with scrapie-infected animals should be
recommended, particularly since cleaning and decontamination may not effectively
remove scrapie infectivity (31), even though infectivity declines considerably
if the pasture and the field furniture have not been in contact with
scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in
furniture that was subjected to weathering, even though exposure led to
infection in sheep, this method may not always be reliable in predicting the
risk of scrapie infection through environmental contamination. These results
suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the
detection of environmentally associated scrapie, and suggest that extremely low
levels of scrapie contamination are able to cause infection in susceptible sheep
genotypes.
Keywords: classical scrapie, prion, transmissible spongiform
encephalopathy, sheep, field furniture, reservoir, serial protein misfolding
cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier
Andréoletti1, Affiliations Contributions Corresponding author Journal name:
Nature Communications Volume: 5, Article number: 5821 DOI:
doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014
Published 16 December 2014 Article tools Citation Reprints Rights &
permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Monday, January 4, 2016
Long live the OIE, or time to close the doors on a failed entity?
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL
DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
Subject: Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using
Population Monitoring and Capture-Recapture Data
To date, we are unaware of a study that documents a decrease in CWD
prevalence over time in mule deer, white-tailed deer or elk. We briefly consider
three plausible explanations for our findings: a) that natural oscillations
occur in CWD outbreaks; b) that the outbreak has peaked and is declining to a
lower endemic level; or c) that previous management actions were more successful
at suppressing the outbreak than originally believed.
Sharp & Pastor [41] illustrated that CWD outbreaks may play out as a
series of reoccurring epidemics characterized by either stable limit cycles or
oscillations that may dampen or amplify as a function of deer density. If this
is the case, we would expect today’s declining deer population to feedback on
conditions–lowering transmission rates leading to reduced CWD effects and a
growing population. Increasing abundance would support higher transmission
rates, deer decline, and oscillations of CWD prevalence and deer. Alternatively,
Almberg et al. [21] (see also [22–24,41,42]) suggested that CWD outbreaks could
reach endemic equilibrium characterized by coexistence of a smaller deer
population and CWD. Under these scenarios, population prevalence would reach a
lower, constant level after a period of high prevalence and deer decline.
Although neither of the foregoing scenarios can be dismissed completely,
invoking them ignores the extensive management of this deer population that
occurred in the years between the two time points we chose as the basis for our
analyses. Management aimed to reduce CWD transmission between 2000 and 2005,
which included a combination of (crude and unpopular) focal culling and a
broader increase in female harvest, decreased overall deer abundance by about
25%. Analyses carried out shortly after suggested that reductions in deer
density had made little impact on CWD prevalence [10]. However, our current
findings suggest that these management actions may indeed have attenuated the
outbreak. Observed dynamics over the last decade closely approximate those
predicted from models by Wild et al. [42] that included a substantial amount of
selective predation on CWD-infected individuals. That harvest could be a source
of selective mortality is supported by an early notion that CWD-infected deer
might be more vulnerable to harvest [43], just as infected deer also appear to
be more vulnerable to vehicle collisions and predation [20,33,44]. This offers
the possibility that hunting could be used as a more tightly controlled
substitute for predation in studies of system responses with CWD and perhaps
other similar diseases.
The protracted time-scale of the CWD outbreak is much longer than the
timespan of our research, which limits our ability to identify the true
explanation of our findings. Nonetheless, our research suggests that, at least
for the foreseeable future (e.g., decades), mule deer populations sharing the
overall survival and infection probabilities estimated from our analyses may
persist but likely will not thrive where CWD becomes established as an endemic
infectious disease.
‘’Nonetheless, our research suggests that, at least for the foreseeable
future (e.g., decades), mule deer populations sharing the overall survival and
infection probabilities estimated from our analyses may persist but likely will
not thrive where CWD becomes established as an endemic infectious disease. ‘’
*** Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using
Population Monitoring and Capture-Recapture Data
‘’Mountain lions prey selectively on CWD infected deer [33] and CWD could
result in an abundance of vulnerable prey, thereby enhancing mountain lion
survival and reproduction [20].’’
please see ;
‘’preliminary results suggesting that bobcats (Lynx rufus) may be
susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting
disease agent.’’
references on Feline Spongiform Encephalopathy FSE toward the bottom, see
;
Assessing Transmissible Spongiform Encephalopathy Species Barriers with an
In Vitro Prion Protein Conversion Assay
Friday, January 01, 2016
Bayesian Modeling of Prion Disease Dynamics in Mule Deer Using Population
Monitoring and Capture-Recapture Data
Saturday, December 12, 2015
CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015
Wednesday, December 30, 2015
Michigan Deer suspected positive for CWD found in Watertown Township; Jan.
12 public meeting set
http://chronic-wasting-disease.blogspot.com/2015/12/michigan-deer-suspected-positive-for.html
Tuesday, December 29, 2015
TEXAS MONTHLY CHRONIC WASTING DISEASE CWD JANUARY 2016 DEER BREEDERS STILL
DON'T GET IT $
Chronic Wasting Unease
The emergence of a deadly disease has wildlife officials and deer breeders
eyeing each other suspiciously.
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for
scrapie transmission
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the
intra- and cross-species transmission of AA amyloidosis ***
Friday, December 04, 2015
Iatrogenic and sporadic Creutzfeldt-Jakob disease in two sisters without
mutation in the prion protein gene
*** Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ???
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
INSULIN
Do we know what bovine materials are used in which
products, both as the active ingredient and in production? Bovine
active
ingredients in human products include insulin, vasopressin, bone,
immune
globulins, fibrin, dermal collagen, albumin. Bovine serum albumin and
fetal calf serum must be used in preparation of very many products.
For
each of these products would any “BSE agent” be destroyed or
eliminated
in processing? If not, and the product is administered parenterally
or
topically into an open wound, might there be a risk? [For oral
products, there would only be a trivially increased load on top of
that
taken in food in omnivores/carnivores including man. But for some
herbivores, this might allow the agent to be introduced into yet
another
species].
--------------------------
Medicines and medical devises;
please see why as follows ;
"The fact that certain medicinal products could be injected directly into
the body (most commonly intramuscularly) meant that in theory they would pose a
greater risk than beef products in food."
Infectivity of bovine materials used in medicinal products and the
importance of inoculation route
3.221 The risk from infectivity present in medicinal products was
considered by the Southwood Working Party. They noted that ‘the greatest risk .
. . would be from the parenteral injection of material derived from bovine brain
or lymphoid tissue’.538 (As described previously, it was generally accepted that
the oral route was considerably less efficient than the parenteral
route.539)
3.222 In reality, different routes exist within the parenteral category –
intracerebral, intraperitoneal, intramuscular, intravenous, intraspinal and
subcutaneous. Experiments in 1978 looking at several of these routes found the
efficiency between them to vary. Intracerebral and intraspinal were generally
the most efficient, followed by intravenous, intraperitoneal and then
subcutaneous.540 The fact that certain medicinal products could be injected
directly into the body (most commonly intramuscularly) meant that in theory they
would pose a greater risk than beef products in food.
3.223 Various cattle tissues were of relevance to medicinal products,
including insulin, heparin, surgical catgut sutures and serum. The consideration
given to these materials prior to March 1996 is addressed in vol. 7: Medicines
and Cosmetics.
533 SEAC 22/5 534 Wells, G. (1998) Preliminary Observations on the
Pathogenesis of Experimental Bovine Spongiform Encephalopathy (BSE): An Update,
Veterinary Record, 142, 103 535 Wells, G., Hawkins, S., Green, P., Spencer, Y.,
Dexter, I. and Dawson, D. (1999) Limited Detection of Sternal Bone Marrow
Infectivity in the Clinical Phase of Experimental Bovine Spongiform
Encephalopathy (BSE), Veterinary Record, 144, 292–4 536 Scott, M.R., Will, R.,
Ironside, J., Nguyen, H.-O., Tremblay, P., DeArmond, S.J. and Prusiner, S.B.
(1999) Compelling Transgenetic Evidence for Transmission of Bovine Spongiform
Encephalopathy Prions to Humans, Proceedings of the National Academy of Sciences
of the USA, 96, 15137–42 537 Scott, M.R., Safar, J., Telling, G., Nguyen, H.-O.,
Groth, D., Torchia, M., Kochler, R., Tremblay, P., Walther, D., Cohen, F.,
DeArmond, S. and Prusiner, S. (1997) Identification of a Prion Protein Epitope
Modulating Transmission of Bovine Spongiform Encephalopathy Prions to Transgenic
Mice, Proceedings of the National Academy of Sciences of the United States of
America, 94, 14279–84 538 IBD1 tab 2 para. 5.3.3 539 Kimberlin, R. and Walker,
C. (1989) Pathogenesis of Scrapie in Mice after Intragastric Infection, Virus
Research, 12, 213–20; Diringer, H., Beekes, M. and Oberdieck, U. (1994) The
Nature of the Scrapie Agent: The Virus Theory, Annals of The New York Academy of
Science, 724, 246–58; Prusiner, S., Cochran, S. and Alpers, S. (1985)
Transmission of Scrapie in Hamsters, Journal of Infectious Diseases, 152, 971–8
540 Kimberlin, R.H. and Walker, C.A. (1978) Pathogenesis of Mouse Scrapie:
Effect of Route of Inoculation on Infectivity Titres and Dose-Response Curves,
Journal of Comparative Pathology, 88, 39–47
COMMERCIAL IN CONFIDENCE
NOT FOR PUBLICATION
COMMITTEE ON SAFETY OF MEDICINES
WORKING PARTY ON BOVINE SPONGIFORM ENCEPHALOPATHY
3. Products for injection using bovine tissue
This category includes tissue derived products, other than from brain or
lymphoid tissue and excludes bovine blood.
3.1 Bovine Pancreas
3.1.1 Insulin
The following companies hold licences for bovine insulin.
Source Country
Denmark
USA
USA
Denmark, Sweden, USA, Italy, Canada, Portugal, Netherlands
In 1988 a sample consignment from UK was used. UK source material is no
longer used.
Comment
There are no bovine insulins manufctured from UK sourced material.
Bovine insulin is not widely prescribed, but has a niche in the market for
diabetics unable to tolerate other products.
3.1.2 Glucagon
bovine pancreas from USA.
as for insulin - Scandinavia, USA, Italy, Canada, Portugal and
Netherlands.
3.1.3
Miscellaneous products containing Bovine Pancreas
3.1.3.1 Zonulysin (Chymotrypsin) - sourced from Canada
3.1.3.2 Streptokinase - culture medium, containing bovine muscle and
pancreas are used in process - all sourced from Germany
3.1.3.3 Fibrinogen + Desoxyribonuclease - bovine pancreas sourced from
Canada and S Africa.
3.2. Vaccines using Bovine Products in process
snip...see full text ;
USDA allows diseased animals into human food supply
Mon, 14 Aug 2000. Information provided by Terry S. Singeltary Sr. Farm
Sanctuary web site
In Confidence - Perceptions of unconventional slow virus diseases of
animals in the USA - Report of a visit to the USA - April-May 1989 - G A H Wells
[head of England's main veterinary lab -- webmaster]
2. Meeting with USDA, BSE Task Force
MAD COW DISEASE BSE CJD CHILDREN VACCINES
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
TIP740203/l 0424 CONFIDENTIAL
Subject: Louping-ill vaccine documents from November 23rd, 1946
Date: Sat, 9 Sep 2000 17:44:57 -0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946
NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND
ANNUAL CONGRESS, 1946
snip...
As a result of this experience a large-scale transmision experiment
involving the ue of 788 sheep was commenced in 1938 on a farm specially taken
for the purpose by the Animal Diseases Research Association with funds provided
by the Agricultural Research Council. The experiment was designed to determine
the nature of the infective agent and the pathogenesis of the disease. It is
only possible here to give a summary of the result which showed that (1) saline
suspensions of brain and spinal cord tissue of sheep affected with scrapie were
infective to normal sheep when inoculatted intracerebrally or subcutaneously;
(2) the incubation period after intracerebral inoculation was seven months and
upwards and only 60 percent of the inoculated sheep developed scrapie during a
period of four and a half years; (3) the incubation period after subcutaneous
inoculation was 15 months and upwards and only about 30 percent of the
inoculated sheep developed the disease during the four and a half years: (4) the
infective agent was of small size and probably a filtrable virus.
The prolonged incubative period of the disease and the remarkable
resistance of the causal agent to formalin are features of distinct interest. It
still remains to determine if a biological test can be devised to detect
infected animals so that they can be killed for food before they develop
clinical symptoms and to explore the possibilities of producing an immunity to
the disease.
==================================================================
Greetings List Members,
pretty disturbing document. now, what would stop this from happening with
the vaccineCJD in children???
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
Subject: Re: VACCINES/CHILDREN/TSE'S -- 'CONFIDENTIAL'
From: tom
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 6 Sep 2000 18:20:09 -0800
Content-Type: text/plain
Parts/Attachments: text/plain (110 lines)
Reply
######### Bovine Spongiform Encephalopathy #########
Just when I was thinking the Internet had reached a terminal condition of
shallow pages and broken links, some young people come along and invent a really
effective Internet search engine: http://www.google.com/ This works quite well
to search the entire http://www.mad-cow.org
site (or find 393 web sites such as GenBank that link to it, or 936 sites that
cite it in text) back to 1996 as well as the BSE Inquiry http://www.bse.org.uk/
Thus for louping ill (unnecessary cites suppressed):
http://www.bse.org.uk/witness/htm/stat537.htm
Witness Statements 537 - Coulthard
29.Pituitary FSH from pigs has been used in the USA prior to its use in
the UK and much more extensively there and Canada.... 30.Thousands of embryos
were exported from this country to the USA prior to the ban being imposed... 42.
No cow pituitaries were used in the preparation of FSH [follicular stimulating
hormone] products compared with the case of louping ill vaccine for
scrapie.
In the 1930's: 18,000 UK sheep were inoculated against louping ill, a
brain inflammatory illness spread by ticks. Despite formalin-treatment of the
inoculated agent, the procedure gave rise to 1,500 cases of scrapie. Louping is
a Scottish word for fleeing or leaping, related to loping. In humans, louping
ill is called Russian spring-summer encephalitis, a meningo-encephalitis with
muscular tremors and spasms followed by varying degrees of paralysis.... [John
Lanchester 2 Dec 96 New Yorker]
In what the story calls a grand historical irony, this landmark series of
experiments was being confirmed at the same time in England as a result of an
outbreak of scrapie in several hundred sheep that had been immunized against
louping ill with a vaccine prepared from tissue from the brain, spinal cord, and
spleen of sheep that were belatedly discovered to have been exposed to natural
scrapie infection.[6.Gordon WS. Advances in veterinary research. Vet Rec 1946;
58: 516-520] The transmissible nature of the scrapie agent was thus established
beyond any doubt. [P Brown, 1755 and All That: A Historical Primer of TSE.
We need to look at the full text of the article and its cites to see how
they actually made the vaccine, whether they exported vaccine-infected sheep to
Canada and the US, and what became of the vaccinated flocks. Perhaps there is
still sample available, Moredun Institute is still around.
Gordon WS. Advances in veterinary research. Vet Rec 1946; 58: 516-520 (not
covered by Medline) Gordon, Bronlee and Wilson 1939 [full cite is available only
in a letter we don't have)
Terry was reading Draft Factual Account 17 http://www.bse.org.uk/dfa/dfa17.htm
236. Mrs Alderman replied on 3 June 1988, listing products containing
bovine insulin and noting there were two rabies vaccines listed but the species
used in manufacture was not shown.[282] 237. On 6 June 1988 Mr Lawrence wrote to
Sir Richard Southwood and enclosed some brief answers to the questions that had
been tabled at the meeting on 19 May.[283] In relation to Q6, which asked ŒWhat
is meat and other material from scrapie infected sheep used for - does it
include pet food and material for biological products?¹ Part of the answer
stated: ...
There has been one instance of inadvertant [sic] transmission of the
scrapie agent to sheep through louping ill vaccine (Gordon, Bronlee and Wilson
1939). One of the three batches of vaccine made in 1935 at the Moredun Institute
contained the scrapie agent resulting in 7% of the recipients of the 18, 000
doses in the batch developing scrapie. This vaccine was made from
formalin-inactivated sheep brain, and brought to the attention of research
workers that formalin, at a concentration of 0.35% for at least 3 months, which
inactivated conventional viruses, did not totally inactivate the scrapie agent.
---------------------------- 4. Questions we might want to have answered are:
the highest risk would be from parenterals prepared from brain (eg rabies
vaccine). Any species in which transmissible spongiform encephalopathies have
been described would be suspect (“natural” infections in sheep, goats, cattle,
deer, mink, but can be transmitted to hamster, mouse, guinea-pig etc). Are
sterilisation processes adequate for the most resistant strain of scrapie agent
or for CJD agent? Should companies be asked to include investigation for
inclusion of scrapie agent (eg mouse innoculation [sic]) in at least some
batches? If BSE behaves like scrapie, then we might expect other nervous tissue,
spleen, lymph nodes and placenta to be contaminated. Infection has been
described in other tissues too, eg gut wall, and we can not [sic] be sure blood
is free. Do we know what bovine materials are used in which products, both as
the active ingredient and in production? Bovine active ingredients in human
products include insulin, vasopressin, bone, immune globulins, fibrin, dermal
collagen, albumin. Bovine serum albumin and fetal calf serum must be used in
preparation of very many products. For each of these products would any “BSE
agent” be destroyed or eliminated in processing? If not, and the product is
administered parenterally or topically into an open wound, might there be a
risk? [For oral products, there would only be a trivially increased load on top
of that taken in food in omnivores/carnivores including man. But for some
herbivores, this might allow the agent to be introduced into yet another
species]. -------------------------- Medicines and medical devises;
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
############
Friday, March 25, 2011
Detection of Prion Protein in Urine-Derived Injectable Fertility Products
by a Targeted Proteomic Approach
SNIP...PLEASE SEE MORE HERE ;
Wednesday, January 28, 2015
BOVINE HEPARIN POSITION STATEMENT ON THE REINTRODUCTION and POTENTIAL BSE
TSE PRION RISK FACTORS THEREFROM
Tuesday, December 30, 2014
TSEAC USA Reason For Recalls Blood products, collected from a donors
considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were
distributed END OF YEAR REPORT 2014
Tuesday, April 21, 2015
Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING
SCHEDULED FOR June 1, 2015
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES ADVISORY COMMITTEE MEETING
Thursday, June 2, 1999
CHAIRMAN BROWN: My name is Dr. Paul Brown.
Welcome to the FDA traveling road show. We are asked yet once more by the
FDA to consider a question of theoretical risk in the absence of sufficient
knowledge on which to base any firm conclusion. The issue before us today is
that of excluding categories of American blood donors who have either visited or
resided for longer periods of time in Great Britain. The issue is sufficiently
delicate, as you see that we have been moved outside the Beltway.
(Laughter.)
snip...
see all here ;
Saturday, April 18, 2015
*** vCJD TEXAS CDC Emerging Infectious Diseases May 2015 Baylor College of
Medicine Neuroscience 2014 case of human form of “mad cow disease” highlights
need for continued surveillance
>>> Variant CJD and blood transfusion: are there additional cases?
TSE Prion and blood transfusion: will there be additional cases? this
should be the concern. ...TSS
Thursday, March 26, 2015
Variant CJD and blood transfusion: are there additional cases?
Vox Sanguinis (2014) 107, 220–225 ORIGINAL PAPER © 2014 International
Society of Blood Transfusion DOI: 10.1111/vox.12161
Tuesday, December 30, 2014
TSEAC USA Reason For Recalls Blood products, collected from a donors
considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were
distributed END OF YEAR REPORT 2014
Sunday, March 09, 2014
A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of
Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
Sunday, June 9, 2013
TSEAC March 14, 2013: Transmissible Spongiform Encephalopathies Advisory
Committee Meeting Webcast
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 ;
2001 Singeltary Submission to FDA on blood related risk factors from TSE
prion aka mad cow type disease
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 08,2001 3:03 PM freas ...
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Transmissible Spongiform Encephalopthy TSE Prion Disease
*** Kuru Video
Kuru: The Science and The Sorcery
*** Scrapie Video
*** Human Mad Cow Video
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
2014
***Moreover, L-BSE has been transmitted more easily to transgenic mice
overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.
***It has been suggested that some sporadic CJD subtypes in humans may
result from an exposure to the L-BSE agent.
*** Lending support to this hypothesis, pathological and biochemical
similarities have been observed between L-BSE and an sCJD subtype (MV genotype
at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and
another sCJD subtype (MM genotype) [15].
snip...
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...
*** Creutzfeldt-Jakob Disease Public Health Crisis VIDEO
Tuesday, May 26, 2015
*** Minimise transmission risk of CJD and vCJD in healthcare settings
***
Last updated 15 May 2015
Monday, November 23, 2015
1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
Tuesday, August 18, 2009
BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009
Friday, October 23, 2015
CJD FOUNDATION CREUTZFELDT JAKOB DISEASE TSE PRION QUESTIONNAIRE UPDATE
OCTOBER 2015
Saturday, December 12, 2015
CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015
Thursday, September 10, 2015
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015
Friday, November 13, 2015
No evidence of asymptomatic variant CJD infection in immunodeficiency
patients treated with UK-sourced immunoglobulin ?
P.85: Improving Creutzfeldt-Jakob disease incidence estimates by
incorporating results of neuropathological analyses, United States,
2003–2011
Ryan Maddox1, Marissa Person1, Arialdi Minino2, Janis Blevins3, Lawrence
Schonberger1, and Ermias Belay1
1National Center for Emerging and Zoonotic Infectious Diseases; Centers for
Disease Control and Prevention, Atlanta GA USA; 2National Center for Health
Statistics; Centers for Disease Control and Prevention; Hyattsville, MD USA;
3National Prion Disease Pathology Surveillance Center; Case Western Reserve
University; Cleveland, OH USA
Introduction. The incidence of invariably fatal prion diseases such as
Creutzfeldt-Jakob disease (CJD) can be estimated by analyzing death certificate
data, but there are limitations.
Methods. Prion disease decedents were identified from the US national
multiple cause-ofdeath data and the National Prion Disease Pathology
Surveillance Center (NPDPSC) database for 2003–2011. Due to limited personal
identifying information, an algorithm was constructed to determine likely
decedent matches between the 2 databases. NPDPSC decedents with a positive prion
disease autopsy or biopsy result or genetic mutation for whom no match was found
in the multiple cause-of-death data were added as cases for incidence
calculations; those with negative neuropathology results but Prion 2015 Poster
Abstracts S55 with a death certificate indicating prion disease were removed.
The resulting average annual age-adjusted incidence was then calculated.
Results. A total of 2986 decedents were identified as having prion disease
indicated as a cause of death in the multiple cause-of-death data; 469
additional NPDPSC decedents were identified with positive neuropathology and/or
genetic findings, while 140 decedents with death certificates indicating prion
disease had negative neuropathology results. Incorporating the matched data, the
average annual ageadjusted incidence of CJD in the United States was 1.2 per
million.
Conclusion. Analysis of multiple cause-of death data is an efficient means
of conducting CJD surveillance. However, not all decedents are captured as the
death certificate may not list the diagnosis; conversely, a CJD diagnosis on the
certificate may be contradicted by neuropathology results. Incorporating
findings from NPDPSC neuropathological and genetic analyses produces an estimate
closer to the true incidence of the disease.
spontaneous atypical BSE ???
don’t let anyone fool you. spontaneous TSE prion disease is a hoax in
natural cases, never proven.
all one has to do is look at France. France is having one hell of an
epidemic of atypical BSE, probably why they stopped testing for BSE, problem
solved $$$ same as the USA, that’s why they stopped testing for BSE mad cow
disease in numbers they could find any with, after those atypical BSE cases
started showing up. shut down the testing to numbers set up by OIE that are so
low, you could only by accident find a case of BSE aka mad cow disease. and this
brilliant idea by the WHO et al, to change the name of mad cow disease, thinking
that might change things is preposterous. it’s all about money now folks, when
the OIE, USDA and everyone else went along and made the TSE prion disease aka
mad cow type disease a legal trading commodity by the BSE MRR policy, I would
say everyone bit off more then they can chew, and they will just have to digest
those TSE Prions coming from North America, and like it, and just prey you don’t
get a mad cow type disease i.e. Transmissible Spongiform Encephalopathy TSE
prion disease in the decades to come, and or pass it to some other poor soul via
the iatrogenic medical surgical tissue friendly fire mode of transmission i.e.
second hand transmission. it’s real folks, just not documented much, due to lack
of trace back efforts. all iatrogenic cjd is, is sporadic cjd, until the
iatrogenic event is tracked down and documented, and put into the academic and
public domain, which very seldom happens. ...
As of December 2011, around 60 atypical BSE cases have currently been
reported in 13 countries, *** with over one third in France.
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many
spontaneous events of mad cow disease $$$
so 20 cases of atypical BSE in France, compared to the remaining 40 cases
in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+
cases per country, besides Frances 20 cases. you cannot explain this away with
any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
19 May 2010 at 21:21 GMT
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
snip...see link ;
Saturday, May 09, 2015
Expression of genes involved in the T cell signalling pathway in
circulating immune cells of cattle 24 months following oral challenge with
Bovine Amyloidotic Spongiform Encephalopathy (BASE)
Saturday, January 9, 2016
***Transmission of sheep-bovine spongiform encephalopathy to pigs Research
article
IN CONFIDENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY 1. CMO should be aware that
a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has
after 15 months developed an illness, now confirmed as a spongiform
encephalopathy. This is the first ever description of such a disease in a pig,
although it seems there ar no previous attempts at experimental inoculation with
animal material. The Southwood group had thought igs would not be susceptible.
Most pigs are slaughtered when a few weeks old but there have been no reports of
relevant neurological illness in breeding sows or other elderly pigs.
...see full text ;
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since
so few are allowed to reach adulthood this has not been recognised through
clinical disease. ...
snip...
CONFIDENTIAL EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
PLEASE NOTE, these old BSE Inquiry links take a while to open with the
wayback machine, so be patient. ...tss Title: Experimental Intracerebral and
Oral Inoculation of Scrapie to Swine: Preliminary Report In the United States,
feeding of ruminant by-products to ruminants is prohibited, but feeding of
ruminant materials to swine and poultry still occurs. The potential for swine to
have access to scrapie-contaminated feedstuffs exists, but the potential for
swine to serve as a host for replication/accumulation of the agent of scrapie is
unknown. The purpose of this study was to perform oral and intracerebral
inoculation of the U.S. scrapie agent to determine the potential of swine as a
host for the scrapie agent and their clinical susceptibility.
snip...
IN CONFIDENCE EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY 1. CMO should
be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain
suspension has after 15 months developed an illness, now confirmed as a
spongiform encephalopathy. This is the first ever description of such a disease
in a pig, although it seems there ar no previous attempts at experimental
inoculation with animal material. The Southwood group had thought pigs would not
be susceptible. Most pigs are slaughtered when a few weeks old but there have
been no reports of relevant neurological illness in breeding sows or other
elderly pigs. ...see full text ;
we cannot rule out the possibility that unrecognised subclinical spongiform
encephalopathy could be present in British pigs though there is no evidence for
this: only with parenteral/implantable pharmaceuticals/devices is the
theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of
papers relating to this experimental finding to prevent premature release of the
information. ...
3. It is particularly important that this information is not passed outside
the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly
mentioned at all. ...
***Our records show that while some use is made of porcine materials in
medicinal products, the only products which would appear to be in a
hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for
which the source material comes from outside the United Kingdom, namely America
China Sweden France and Germany. The products are manufactured by Ferring and
Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon,
makes use of porcine skin - which is not considered to be a ''high risk''
tissue, but one of its uses is described in the data sheet as ''in dural
replacement''. This product is sourced from the United Kingdom.....
snip...
It was not until . . . August 1990, that the result from the pig persuaded
both SEAC and us to change our view and to take out of pig rations any residual
infectivity that might have arisen from the SBOs.
4.303 The minutes of the meeting record that: It was very difficult to draw
conclusions from one experimental result for what may happen in the field.
However it would be prudent to exclude specified bovine offals from the pig
diet. Although any relationship between BSE and the finding of a spongiform
encephalopathy in cats had yet to be demonstrated, the fact that this had
occurred suggested that a cautious view should be taken of those species which
might be susceptible. The 'specified offals' of bovines should therefore be
excluded from the feed of all species. 17
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles, Links
Click here to read
The neuropathology of experimental bovine spongiform encephalopathy in the
pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA. Veterinary Laboratories Agency
Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy. The lesions consisted principally
of severe neuropil vacuolation affecting most areas of the brain, but mainly the
forebrain. In addition, some vacuolar change was identified in the rostral
colliculi and hypothalamic areas of normal control pigs. PrP accumulations were
detected immunocytochemically in the brains of BSE-infected animals. PrP
accumulation was sparse in many areas and its density was not obviously related
to the degree of vacuolation. The patterns of PrP immunolabelling in control
pigs differed strikingly from those in the infected animals. PMID: 10684682
[PubMed - indexed for MEDLINE]
Transgenic mice expressing porcine prion protein resistant to classical
scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical
scrapie.
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation snip... In the US, feeding of ruminant by-products to ruminants is
prohibited, but feeding of ruminant materials to swine, mink and poultry still
occurs. Although unlikely, the potential for swine to have access to
TSE-contaminated feedstuffs exists.
snip...
Wednesday, July 06, 2011
Swine Are Susceptible to Chronic Wasting Disease by Intracerebral
Inoculation (see tonnage of mad cow feed in commerce USA...tss)
In an experimental study of the transmissibility of BSE to the pig, seven
of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral
inoculation with a homogenate of bovine brain from natural BSE cases developed
lesions typical of spongiform encephalopathy.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?holding=npg&cmd=Retrieve&db=PubMed&list_uids=10684682&dopt=Abstract
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report
Title: Experimental Intracerebral and Oral Inoculation of Scrapie to Swine: Preliminary Report
In the United States, feeding of ruminant by-products to ruminants is
prohibited, but feeding of ruminant materials to swine and poultry still occurs.
The potential for swine to have access to scrapie-contaminated feedstuffs
exists, but the potential for swine to serve as a host for
replication/accumulation of the agent of scrapie is unknown. The purpose of this
study was to perform oral and intracerebral inoculation of the U.S. scrapie
agent to determine the potential of swine as a host for the scrapie agent and
their clinical susceptibility. snip... snip... In the United States, feeding of
ruminant by-products to ruminants is prohibited, but feeding of ruminant
materials to swine and poultry still occurs. The potential for swine to have
access to scrapie-contaminated feedstuffs exists, but the potential for swine to
serve as a host for replication/accumulation of the agent of scrapie is unknown.
The purpose of this study was to perform oral and intracerebral inoculation of
the U.S. scrapie agent to determine the potential of swine as a host for the
scrapie agent and their clinical susceptibility.
see full text and more transmission studies here ;
snip... see full text ;
Thursday, November 10, 2011
National Meat Association v. Harris Docket No., 10-224 DEADSTOCK DOWNER
PIGS AND PORCINE SPONGIFORM ENCEPHALOPATHY PSE Court Likely to Overturn Calif.
Law on Livestock
Friday, April 20, 2012
Ultrastructural findings in pigs experimentally infected with bovine
spongiform encephalopathy agent
Wednesday, July 29, 2015
Porcine Prion Protein Amyloid or mad pig disease PSE
The Pathological Protein:
Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
Philip Yam
''Answering critics like Terry Singeltary, who feels that the US
undercounts CJD, Schonberger _conceded_ that the current surveillance system has
errors but stated that most of the errors will be confined to the older
population''....end
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
2 January 2000
British Medical Journal
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999
British Medical Journal
vCJD in the USA * BSE in U.S.
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America. Now scientists in France have stumbled across new
evidence that adds weight to the campaigners' fears. To their complete surprise,
the researchers found that one strain of scrapie causes the same brain damage in
mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
07 02:27 AM
Terry S. Singeltary Sr. said:
re-Evidence for human transmission of amyloid-? pathology and cerebral
amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26
April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated
online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and
the newspaper articles.
***snip...see full text ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO
PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report them in
their proper context. 'This hopefully will avoid misunderstanding and possible
distortion by the media to portray the results as having more greater
significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the researchers have demonstrated the transmission of a pathological process
from two cases one of severe Alzheimer's disease the other of
Gerstmann-Straussler disease to marmosets. However they have not demonstrated
the transmission of either clinical condition as the "animals were behaving
normally when killed". As the report emphasises the unanswered question is
whether the disease condition would have revealed itself if the marmosets had
lived longer. They are planning further research to see if the conditions, as
opposed to the partial pathological process, is transmissible.
what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of
things highly unusual. However it could be argued that the results reveal a
potential risk, in that brain tissue from these two patients has been shown to
transmit a pathological process. Should therefore brain tissue from such cases
be regarded as potentially infective? Pathologists, morticians, neuro surgeons
and those assisting at neuro surgical procedures and others coming into contact
with "raw" human brain tissue could in theory be at risk. However, on a priori
grounds given the highly specific route of transmission in these experiments
that risk must be negligible if the usual precautions for handling brain tissue
are observed.
1
92/11.4/1.1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral injection. If other prion diseases can be transmitted in this way
it is little surprise that some pathological findings observed in GSS were also
transmissible to a marmoset. But the transmission of features of Alzheimer's
pathology is a different matter, given the much greater frequency of this
disease and raises the unanswered question whether some cases are the result of
a transmissible prion. The only tenable public line will be that "more research
is required’’ before that hypothesis could be evaluated. The possibility on a
transmissible prion remains open. In the meantime MRC needs carefully to
consider the range and sequence of studies needed to follow through from the
preliminary observations in these two cases. Not a particularly comfortable
message, but until we know more about the causation of Alzheimer's disease the
total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH
832 llllYc!eS 2 92/11.4/1.2
>>> The only tenable public line will be that "more research is
required’’ <<<
>>> possibility on a transmissible prion remains
open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is
"more research is required’’ enough time for evaluation ?
Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
Wednesday, January 13, 2016
ALS-Causing Mutations Significantly Perturb the Self-Assembly and
Interaction with Nucleic Acid of the Intrinsically Disordered Prion-Like Domain
of TDP-43
Research Article
Wednesday, January 13, 2016
An efficient procedure for removal and inactivation of alpha-synuclein
assemblies from laboratory materials
***>>>An efficient procedure for removal and inactivation of
alpha-synuclein assemblies from laboratory materials<<<***
***>>> This retrospective study, however, does not definitively
exclude the possibility that a-synucleinopathy can transmit between humans.
<<<***
An efficient procedure for removal and inactivation of alpha-synuclein
assemblies from laboratory materials ???
Thursday, January 14, 2016
*** Preventable Tragedies: Superbugs and How Ineffective Monitoring of
Medical Device Safety Fails Patients REPORT
*** how can it be, HOW CAN IT BE $$$ not a word about CJD GSS FFI VPSPR TSE
Prions that I saw...absolutely crazy, WE ARE MISSING THE BIGGER PICTURE!
*** how many victims that will never be reported ???
BSE INQUIRY DFAs
Sunday, May 18, 2008
BSE Inquiry DRAFT FACTUAL ACCOUNT DFA
BSE Inquiry DRAFT FACTUAL ACCOUNTS DFA's
Sunday, May 18, 2008
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Sunday, May 18, 2008
MAD COW DISEASE BSE CJD CHILDREN VACCINES
Terry S. Singeltary Sr.