[Federal Register Volume 81, Number 111 (Thursday, June 9, 2016)] [Rules
and Regulations] [Page 37153] From the Federal Register Online via the
Government Publishing Office [www.gpo.gov] [FR Doc No: 2016-13705]
=======================================================================
DEPARTMENT OF HEALTH AND HUMAN SERVICES
Food and Drug Administration
21 CFR Part 14
[Docket No. FDA-2016-N-0001]
Advisory Committee; Transmissible Spongiform Encephalopathies Advisory
Committee; Termination
AGENCY: Food and Drug Administration, HHS.
ACTION: Final rule.
-----------------------------------------------------------------------
SUMMARY: The Food and Drug Administration (FDA) is announcing the
termination of the Transmissible Spongiform Encephalopathies Advisory Committee.
This document removes the Transmissible Spongiform Encephalopathies Advisory
Committee from the Agency's list of standing advisory committees.
DATES: This rule is effective June 9, 2016.
FOR FURTHER INFORMATION CONTACT: Bryan Emery, Division of Scientific
Advisors and Consultants, Food and Drug Administration, 10903 New Hampshire
Ave., Bldg. 71, Rm. 6132, Silver Spring, MD 20993-0002, 240- 402-8054, FAX:
301-595-1307, or bryan.emery@fda.hhs.gov.
SUPPLEMENTARY INFORMATION: The Transmissible Spongiform Encephalopathies
Advisory Committee (the Committee) was established on June 9, 1995 (60 FR 31311,
June 14, 1995; 21 CFR 14.100 erroneously lists the date of establishment as June
21, 1995). The Committee reviews and evaluates available scientific data
concerning the safety of products that may be a risk for transmission of
spongiform encephalopathies having an impact on the public health as determined
by the Commissioner of Food and Drugs. The Committee makes recommendations to
the Commissioner regarding the regulation of such products. In recent years, the
number of issues requiring Committee advice has declined, and the Committee has
met very infrequently. Therefore, the effort and expense of maintaining this
advisory committee is no longer justified. Any relevant Transmissible Spongiform
Encephalopathy issues in the future could be addressed by the Agency's other
advisory committees, such as the Agency's Blood Products Advisory Committee,
with additional augmentation of expertise by appropriate subject matter experts
serving as temporary members on the committee. The Committee is no longer needed
and will be terminated on June 9, 2016. Under 5 U.S.C. 553(b)(3)(B) and (d) and
21 CFR 10.40 (d) and (e), the Agency finds good cause to dispense with notice
and public comment procedures and to proceed to an immediate effective date on
this rule. Notice and public comment and a delayed effective date are
unnecessary and are not in the public interest as this final rule merely removes
the name of the Transmissible Spongiform Encephalopathies Advisory Committee
from the list of standing advisory committees in 21 CFR 14.100. Therefore, the
Agency is amending 21 CFR 14.100(b) as set forth in the regulatory text of this
document.
List of Subjects in 21 CFR Part 14
Administrative practice and procedure, Advisory committees, Color
additives, Drugs, Radiation protection.
Therefore, under the Federal Food, Drug, and Cosmetic Act and under
authority delegated to the Commissioner of Food and Drugs, 21 CFR part 14 is
amended as follows:
PART 14--PUBLIC HEARING BEFORE A PUBLIC ADVISORY COMMITTEE
0 1. The authority citation for part 14 continues to read as follows:
Authority: 5 U.S.C. App. 2; 15 U.S.C. 1451-1461, 21 U.S.C. 41- 50,
141-149, 321-394, 467f, 679, 821, 1034; 28 U.S.C. 2112; 42 U.S.C. 201, 262,
263b, 264; Pub. L. 107-109; Pub. L. 108-155.
Sec. 14.100 [Amended]
0 2. In Sec. 14.100, redesignate paragraph (b)(5) as (b)(4) and remove
paragraph (b)(6).
Dated: June 6, 2016. Jill Hartzler Warner, Associate Commissioner for
Special Medical Programs. [FR Doc. 2016-13705 Filed 6-8-16; 8:45 am] BILLING
CODE 4164-01-P
absolutely a political and corporate move, at a time such as this with TSE
prion disease such as Chronic Wasting Disease CWD TSE Prion spreading from state
to state, BSE mad cow disease surveillance and testing at it’s lowest levels and
a sham anyway, with failure after failure, fraud after fraud, and Scrapie just
being documented again in TEXAS, sporadic CJD now being linked to not only BSE
but Scrapie in sheep and goats now, with CWD in cervids becoming more and more a
risk factor for humans, the FDA et al decides to scuttle the TSEAC. absolutely
insane, imo. ...
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3,
Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6,
Pierluigi Gambetti1, Qingzhong Kong1,5,6
1Department of Pathology, 3National Prion Disease Pathology Surveillance
Center, 5Department of Neurology, 6National Center for Regenerative Medicine,
Case Western Reserve University, Cleveland, OH 44106, USA.
4Department of Biological Sciences and Center for Prions and Protein
Folding Diseases, University of Alberta, Edmonton, Alberta, Canada,
2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
Chronic wasting disease (CWD) is a widespread and highly transmissible
prion disease in free-ranging and captive cervid species in North America. The
zoonotic potential of CWD prions is a serious public health concern, but the
susceptibility of human CNS and peripheral organs to CWD prions remains largely
unresolved. We reported earlier that peripheral and CNS infections were detected
in transgenic mice expressing human PrP129M or PrP129V. Here we will present an
update on this project, including evidence for strain dependence and influence
of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of
experimental human CWD prions.
PRION 2016 TOKYO
In Conjunction with Asia Pacific Prion Symposium 2016
PRION 2016 Tokyo
Prion 2016
Prion 2016
Purchase options Price * Issue Purchase USD 198.00
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a.
Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos,
Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT.
Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas.
France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated
bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD)
disease in human. To date, BSE agent is the only recognized zoonotic prion.
Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that
have been circulating for centuries in farmed ruminants there is no apparent
epidemiological link between exposure to ruminant products and the occurrence of
other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).
However, the zoonotic potential of the diversity of circulating TSE agents has
never been systematically assessed. The major issue in experimental assessment
of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the
biological phenomenon that limits TSE agents’ propagation from a species to
another. In the last decade, mice genetically engineered to express normal forms
of the human prion protein has proved essential in studying human prions
pathogenesis and modeling the capacity of TSEs to cross the human species
barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants,
we study their transmission ability in transgenic mice expressing human PrPC
(HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC
(129Met or 129Val) are used to determine the role of the Met129Val dimorphism in
susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to
propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be
susceptible to BSE in sheep or goat to a greater degree than the BSE agent in
cattle and that these agents can convey molecular properties and
neuropathological indistinguishable from vCJD. However homozygous 129V mice are
resistant to all tested BSE derived prions independently of the originating
species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in
HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the
efficiency of transmission at primary passage was low, subsequent passages
resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the
emergence of prion strain phenotypes that showed similar characteristics to
those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie
prions have a zoonotic potential and raise new questions about the possible link
between animal and human prions.
IL-13 Transmission of prions to non human-primates: Implications for human
populations
Jean-Philippe Deslys, Emmanuel E. Comoy
CEW, Institute of Emerging Diseases and Innovative Therapies (iMETI),
Division of Prions and Related Diseases (SEPIA), Fontenay-aux-Roses, France
Prion diseases 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 prion
disease might be zoonotic under appropriate conditions. Contrarily, in the
absence of obvious (epidemiological or experimental) elements supporting a
transmission or genetic predispositions, prion diseases, like the other
proteinopathies, are reputed to occur spontaneously (atypical animal prion
strains, sporadic CJD summing 80 % of human prion cases).
Non-human primate models provided the first evidences supporting the
transmissibility of human prion strains and the zoonotic potential of BSE. Among
them, cynomolgus macaques brought major information for BSE risk assessment for
human health1, according to their phylogenetic proximity to humans and extended
lifetime. We used this model to assess the risk of primary (oral) and secondary
(transfusional) risk of BSE, and also the zoonotic potential of other animal
prion diseases 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' . longer incubation than BSE2. Scrapie, as recently evoked in
humanized mice3, is the third potentially zoonotic prion disease (with BSE and
L-type BSE4), thus questioning the origin of human sporadic cases. We also
observed hidden prions transmitted by blood transfusion in primate which escape
to the classical diagnostic methods and extend the field of healthy carriers. We
will present an updated panorama of our different long-term transmission studies
and discuss the implications on risk assessment of animal prion diseases for
human health and of the status of healthy carrier5.
1. Chen, C. C. & Wang, Y. H. Estimation of the Exposure of the UK
Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake
During the Period 1980 to 1996. PLoS One 9, e94020 (2014).
2. Comoy, E. E. et al. Transmission of scrapie prions to primate after an
extended silent incubation period. Sci Rep 5, 11573 (2015).
3. Cassard, H. et al. Evidence for zoonotic potential of ovine scrapie
prions. Nat Commun 5, 5821-5830 (2014).
4. Comoy, E. E. et al. Atypical BSE (BASE) transmitted from asymptomatic
aging cattle to a primate. PLoS One 3, e3017 (2008).
5. Gill O. N. et al. Prevalent abnormal prion protein in human appendixes
after bovine spongiform encephalopathy epizootic: large scale survey. BMJ. 347,
f5675 (2013).
Curriculum Vitae
Dr. Deslys co-authored more than one hundred publications in international
scientific journals on main aspects of applied prion research (diagnostic,
decontamination techniques, risk assessment, and therapeutic approaches in
different experimental models) and on underlying pathological mechanisms. He
studied the genetic of the first cases of iatrogenic CJD in France. His work has
led to several patents including the BSE (Bovine Spongiform Encephalopathy)
diagnostic test most widely used worldwide. He also wrote a book on mad cow
disease which can be downloaded here for free (http://www.neuroprion.org/pdf_docs/documentation/madcow_deslys.pdf).
His research group is Associate Laboratory to National Reference Laboratory for
CJD in France and has high security level microbiological installations
(NeuroPrion research platform) with different experimental models (mouse,
hamster, macaque). The primate model of BSE developed by his group with
cynomolgus macaques turned out to mimick remarkably well the human situation and
allows to assess the primary (oral) and secondary (transfusional) risks linked
to animal and human prions even after very long silent incubation periods.
***For several years, his interest has extended to the connections between PrP
and Alzheimer and the prion mechanisms underlying neurodegenerative diseases. He
is coordinating the NeuroPrion international association (initially european
network of excellence now open to all prion researchers).
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer ***
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL
THE WRONG PLACES $$$
*** 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).***
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.***
================
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
*** 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.
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
Wednesday, May 25, 2016
USDA APHIS National Scrapie TSE Prion Eradication Program April 2016
Monthly Report Prion 2016 Tokyo Update
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***
===============
***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.
==============
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.
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
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
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. ...
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...
HUMANS
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER
AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease
Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic
Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of
the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat
derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS
AND FIELD CORRECTIONS: FOODS CLASS II
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 ;
*** 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).
Tuesday, June 07, 2016 Comparison of two US sheep scrapie isolates supports
identification as separate strains
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Tuesday, June 07, 2016
How Did CWD Get Way Down In Medina County, Texas?
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus
Macaque
"BSE-L in North America may have existed for decades"
SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY
CASE INVESTIGATION JULY 2012 CALIFORNIA
Summary Report BSE 2012
Executive Summary
Saturday, August 4, 2012
Final Feed Investigation Summary - California atypical L-type BSE Case -
July 2012
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE
Epidemiological Investigation
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, 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
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012 NIAA
Annual Conference April 11-14, 2011 San Antonio, Texas
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near
Mission, Texas, I believe around Hidalgo county, could this be ground
zero?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide
additional information for the eradication program on the epidemiology of
natural scrapie. The Mission Field Trial Station is located on 450 acres of
pastureland, part of the former Moore Air Force Base, near Mission, Texas. It
was designed to bring previously exposed, and later also unexposed, sheep or
goats to the Station and maintain and breed them under close observation for
extended periods to determine which animals would develop scrapie and define
more closely the natural spread and other epidemiological aspects of the
disease.
The 547 previously exposed sheep brought to the Mission Station beginning
in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were
purchased as field outbreaks occurred, and represented 21 bloodlines in which
scrapie had been diagnosed. Upon arrival at the Station, the sheep were
maintained on pasture, with supplemental feeding as necessary. The station was
divided into 2 areas: (1) a series of pastures and-pens occupied by male animals
only, and (2) a series of pastures and pens occupied by females and young
progeny of both sexes. ...
snip...see full text ;
P.97: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease and distinct from the
scrapie inoculum
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1
1National Animal Disease Center; Ames, IA USA;
2Iowa State University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Title: Scrapie transmits to white-tailed deer by the oral route and has a
molecular profile similar to chronic wasting disease
Authors
item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle,
Robert item West Greenlee, M -
Submitted to: American College of Veterinary Pathologists Meeting
Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015
Publication Date: N/A Technical Abstract: The purpose of this work was to
determine susceptibility of white-tailed deer (WTD) to the agent of sheep
scrapie and to compare the resultant PrPSc to that of the original inoculum and
chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure
(concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All
scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected
in lymphoid tissues at preclinical time points, and deer necropsied after 28
months post-inoculation had clinical signs, spongiform encephalopathy, and
widespread distribution of PrPSc in neural and lymphoid tissues. Western
blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral
cortex had a profile similar to the original scrapie inoculum, whereas WB of
brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile
resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical
scrapie were further passaged to mice expressing cervid prion protein and
intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct
incubation times. Sheep inoculated intranasally with WTD derived scrapie
developed disease, but only after inoculation with the inoculum that had a
scrapie-like profile. The WTD study is ongoing, but deer in both inoculation
groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work
demonstrates that WTD are susceptible to the agent of scrapie, two distinct
molecular profiles of PrPSc are present in the tissues of affected deer, and
inoculum of either profile readily passes to deer.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by
intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and
the disease is likely to continue to spread geographically [10]. However, the
potential that white-tailed deer may be susceptible to sheep scrapie by a
natural route presents an additional confounding factor to halting the spread of
CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie
offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic
areas, but could occur anywhere that sheep with scrapie and susceptible cervids
cohabitate.
This work demonstrates for the first time that white-tailed deer are
susceptible to sheep scrapie by intracerebral inoculation with a high attack
rate and that the disease that results has similarities to CWD. These
experiments will be repeated with a more natural route of inoculation to
determine the likelihood of the potential transmission of sheep scrapie to
white-tailed deer. If scrapie were to occur in white-tailed deer, results of
this study indicate that it would be detected as a TSE, but may be difficult to
differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed
deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture;
Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the
manifestation of CWD and scrapie in WTD after IC inoculation including early and
widespread presence of PrPSc in lymphoid tissues, clinical signs of depression
and weight loss progressing to wasting, and an incubation time of 21-23 months.
Moreover, western blots (WB) done on brain material from the obex region have a
molecular profile similar to CWD and distinct from tissues of the cerebrum or
the scrapie inoculum. However, results of microscopic and IHC examination
indicate that there are differences between the lesions expected in CWD and
those that occur in deer with scrapie: amyloid plaques were not noted in any
sections of brain examined from these deer and the pattern of immunoreactivity
by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to
scrapie.
Deer developed clinical signs of wasting and mental depression and were
necropsied from 28 to 33 months PI. Tissues from these deer were positive for
PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer
exhibited two different molecular profiles: samples from obex resembled CWD
whereas those from cerebrum were similar to the original scrapie inoculum. On
further examination by WB using a panel of antibodies, the tissues from deer
with scrapie exhibit properties differing from tissues either from sheep with
scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are
strongly immunoreactive when probed with mAb P4, however, samples from WTD with
scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4
or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly
immunoreactive and samples from WTD with scrapie are strongly positive. This
work demonstrates that WTD are highly susceptible to sheep scrapie, but on first
passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were
susceptible to scrapie.
White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection
Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion
Research Unit, National Animal Disease Center, USDA-ARS
Interspecies transmission studies afford the opportunity to better
understand the potential host range and origins of prion diseases. Previous
experiments demonstrated that white-tailed deer are susceptible to sheep-derived
scrapie by intracranial inoculation. The purpose of this study was to determine
susceptibility of white-tailed deer to scrapie after a natural route of
exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal
(1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep
clinically affected with scrapie. Non-inoculated deer were maintained as
negative controls. All deer were observed daily for clinical signs. Deer were
euthanized and necropsied when neurologic disease was evident, and tissues were
examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and
western blot (WB). One animal was euthanized 15 months post-inoculation (MPI)
due to an injury. At that time, examination of obex and lymphoid tissues by IHC
was positive, but WB of obex and colliculus were negative. Remaining deer
developed clinical signs of wasting and mental depression and were necropsied
from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and
WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal
and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work
demonstrates for the first time that white-tailed deer are susceptible to sheep
scrapie by potential natural routes of inoculation. In-depth analysis of tissues
will be done to determine similarities between scrapie in deer after
intracranial and oral/intranasal inoculation and chronic wasting disease
resulting from similar routes of inoculation.
see full text ;
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was
detected in a Mule Deer
Saturday, April 02, 2016
TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER
BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE
Friday, February 26, 2016
TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease
CWD TSE Prion
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed
Herd with Testing of Exposed Animals
Wednesday, July 01, 2015
TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18,
2015
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014
UPDATE 2015
Thursday, May 02, 2013
*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY
TEXTING
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West
Texas
Wednesday, February 10, 2016
*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD
***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of
$298,770 for 228 white-tailed deer killed on farm ***
http://chronic-wasting-disease.blogspot.com/2016/01/wisconsin-captive-cwd-lotto-pays-out.html
Sunday, May 08, 2016
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE
ABYSS UPDATE
http://chronic-wasting-disease.blogspot.com/2016/05/wisconsin-chronic-wasting-disease-cwd.html
Tuesday, May 03, 2016
Arkansas Chronic Wasting Disease CWD TSE Prion and Elk Restoration Project
and Hunkering Down in the BSE Situation Room USDA 1998
Monday, April 25, 2016
Arkansas AGFC Phase 2 sampling reveals CWD positive deer in Madison and
Pope counties
Tuesday, April 19, 2016
Arkansas First Phase of CWD sampling reveals 23 percent prevalence rate in
focal area With 82 Confirmed to Date
http://chronic-wasting-disease.blogspot.com/2016/04/arkansas-first-phase-of-cwd-sampling.html
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL
CONTROL MEASURES
Friday, April 22, 2016
Missouri MDC finds seven new cases of ChronicWasting Disease CWD during
past‐season testing
Friday, April 22, 2016
COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING
PROGRAM IS MINIMAL AND LIMITED
KANSAS CWD CASES ALARMING
Wednesday, March 02, 2016 Kansas Chronic Wasting Disease CWD TSE Prion 52
cases 2015 updated report 'ALARMING'
Tuesday, February 02, 2016
Illinois six out of 19 deer samples tested positive for CWD in the Oswego
zone of Kendall County
*** SEE CWD HIGH INFECTION RATE MAPS FOR COLORADO ! ***
I could go on, for more see ;
Thursday, March 31, 2016
*** Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016
***
Saturday, May 28, 2016
Infection and detection of PrPCWD in soil from CWD infected farm in Korea
Prion 2016 Tokyo
Saturday, May 28, 2016
TPWD gives in to Breeders again and postponed their decision regarding
proposed changes to state regulations for managing CWD allowing the TSE Prion to
spread further
Thursday, April 14, 2016
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
Saturday, April 23, 2016
v-CJD prion distribution in the tissues of patients at preclinical and
clinical stage of the disease
Saturday, April 16, 2016
*** APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on
Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission
***
SPONTANEOUS TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW
TYPE DISEASE ???
*** We describe the transmission of spongiform encephalopathy in a
non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie.
Because of this extended incubation period in a facility in which other prion
diseases are under study, we are obliged to consider two alternative
possibilities that might explain its occurrence. We first considered the
possibility of a sporadic origin (like CJD in humans). Such an event is
extremely improbable because the inoculated animal was 14 years old when the
clinical signs appeared, i.e. about 40% through the expected natural lifetime of
this species, compared to a peak age incidence of 60–65 years in human sporadic
CJD, or about 80% through their expected lifetimes.
***Moreover, sporadic disease has never been observed in breeding colonies
or primate research laboratories, most notably among hundreds of animals over
several decades of study at the National Institutes of Health25, and in nearly
twenty older animals continuously housed in our own facility.***
>>> Moreover, sporadic disease has never been observed in breeding
colonies or primate research laboratories, most notably among hundreds of
animals over several decades of study at the National Institutes of Health25,
and in nearly twenty older animals continuously housed in our own facility.
<<<
Monday, May 09, 2016
A comparison of classical and H-type bovine spongiform encephalopathy
associated with E211K prion protein polymorphism in wild type and EK211 cattle
following intracranial inoculation
*** Singeltary reply ; Molecular, Biochemical and Genetic
Characteristics of BSE in Canada Singeltary reply ;
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
Discussion: The C, L and H type BSE cases in Canada exhibit molecular
characteristics similar to those described for classical and atypical BSE cases
from Europe and Japan.
*** This supports the theory that the importation of BSE contaminated
feedstuff is the source of C-type BSE in Canada.
*** It also suggests a similar cause or source for atypical BSE in these
countries. ***
see page 17 6 of 201 pages...tss
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer
and Elk in Animal Feed Singeltary Submission
Saturday, May 28, 2016
Infection and detection of PrPCWD in soil from CWD infected farm in Korea
Prion 2016 Tokyo
Saturday, April 9, 2016
The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion
disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer
(Rangifer tarandus tarandus)
Department for Environment, Food and Rural Affairs
Saturday, May 28, 2016
TPWD gives in to Breeders again and postponed their decision regarding
proposed changes to state regulations for managing CWD allowing the TSE Prion to
spread further
*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary
Sr. Submission ***
Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats
snip...
please see file attachment for full submission and recent science and my
deep concerns on the TSE Prion disease... No documents available.
AttachmentsView All (1) scrapie-usa-blogspot-com View Attachment:
Tuesday, May 31, 2016
Priority Interim Position Paper PROTECTING THE FOOD CHAIN FROM PRIONS
Perspectives
Sunday, May 1, 2016
*** Center for Biologics Evaluation and Research 25th Meeting of: The
Transmissible Spongiform Encephalopathies Advisory Committee June 1, 2015
Transcript ***
FOOD AND DRUG ADMINISTRATION
Freas, William
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Monday, January 08,2001 3:03 PM
TO: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To
Scientific Advisors and Consultants Staff January 2001 Meeting (short
version)
CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific
Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and
Consultants Staff 2001 Advisory Committee (short version).
I understand the reason of having to shorten my submission, but only hope
that you add it to a copy of the long version, for members to take and read at
their pleasure, (if cost is problem, bill me, address below). So when they
realize some time in the near future of the 'real' risks i speak of from
human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk
of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt
here:
remember AIDS/HIV, 'no problem to heterosexuals in the U.S.? no need to go
into that, you know of this blunder:
DO NOT make these same stupid mistakes again with human/animal TSE's aka
MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD
as well (both cases confirmed). I have seen many deaths, from many diseases. I
have never seen anything as CJD, I still see my Mom laying helpless, jerking
tremendously, and screaming "God, what's wrong with me, why can't I stop this".
I still see this, and will never forget. Approximately 10 weeks from 1st of
symptoms to death. This is what drives me. I have learned more in 3 years about
not only human/animal TSE's but the cattle/rendering/feeding industry/government
than i ever wished to.
I think you are all aware of CJD vs vCJD, but i don't think you all know
the facts of human/animal TSE's as a whole, they are all very very similar, and
are all tied to the same thing, GREED and MAN.
I am beginning to think that the endless attempt to track down and ban,
potential victims from known BSE Countries from giving blood will be futile. You
would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT
SWIFTLY to find blood test for TSE's, whether it be blood test, urine test,
.eyelid test, anything at whatever cost, we need a test FAST.
DO NOT let the incubation time period of these TSEs fool you.
To think of Scrapie as the prime agent to compare CJD, but yet overlook the
Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by
scrapie from a vaccine made of scrapie infected sheep brains, would be foolish.
I acquired this full text version of the event which was recorded in the Annual
Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the
BVA and the URL is posted in my (long version).
U.S.A. should make all human/animal TSE's notifiable at all ages, with
requirements for a thorough surveillance and post-mortem examinations free of
charge, if you are serious about eradicating this horrible disease in man and
animal.
There is histopathology reports describing o florid plaques" in CJD victims
in the USA and some of these victims are getting younger. I have copies of such
autopsies, there has to be more. PLUS, sub-clinical human TSE's will most
definitely be a problem.
THEN think of vaccineCJD in children and the bovine tissues used in the
manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS
-- Brown et al. 97 (7): 3418 scrapie agent live at 600*C
Then think of the CONFIDENTIAL documents of what was known of human/animal
TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to
hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's
from the polio vaccine, (one taken orally i think?), but yet neglect to act on
the other potential TSE vaccines (inoculations, the most effective mode to
transmit TSEs) of which thousands of doses were kept and used, to deplete
stockpile, again would be foolish.
--Oral polio; up to 1988, foetal calf serum was used from UK and New
Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large
stocks are held.
--Rubella; bulk was made before 1979 from foetal calf serum from UK and New
Zealand. None has been made as there are some 15 years stock.
--Diphtheria; UK bovine beef muscle and ox heart is used but since the end
of 1988 this has been sourced from Eire. There are 1,250 litres of stock.
--Tetanus; this involves bovine material from the UK mainly Scottish. There
are 21,000 litres of stock.
--Pertussis; uses bovine material from the UK. There are 63,000 litres of
stock. --They consider that to switch to a non-UK source will take a minimum of
6-18 months and to switch to a non-bovine source will take a minimum of five
years.
3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are
sourced from the USA and the company believes that US material only is
used.
89/2.14/2.1
============
BSE3/1 0251
4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there
are 440,000 units of stock. They have also got MMR using bovine serum from the
UK.
5. XXXXXXXXXXX have influenza, rubella, measles,' MMR vaccines likely to be
used in children. Of those they think that only MMR contains bovine material
which is probably a French origin.
6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. hese
use veal material, some of which has come from the UK and has been ade by
XXXXXXXXXXX (see above).
I have documents of imports from known BSE Countries, of ferments, whole
blood, antiallergenic preparations,
2
human blood plasma, normal human blood sera, human immune blood sera, fetal
bovine serum, and other blood fractions not elsewhere specified or included,
imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us
not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate.
This tissue was considered to be of greatest risk of containing BSE and
consequently transmitting the disease.
ANNEX 6
MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO
BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL
How much of this was used in the U.S.?
Please do not keep making the same mistakes; 'Absence of evidence is not
evidence of absence'.
What are the U.S. rules for importing and manufacturing vaccines, medicines
and medical devices?
Does the U.S.A. allow sourcing of raw material of ruminants from the
U.S.A.?
U.S. cattle, what kind of guarantee can you give for serum or tissue donor
herds? . The U.S. rendering system would easily amplify T.S.E.'s:
Have we increased the stability of the system (improved heat treatments)
since the EU SSC report on the U.S.A. was published in july 2000?
What is done to avoid cross-contaminations in the U.S.A.?
How can the U.S. control absence of cross-contaminations of animal TSE's
when pig and horse MBM and even deer and elk are allowed in ruminant feed, as
well as bovine blood? I sadly think of the rendering and feeding policy before
the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police
horse, to the circus elephant, i will not mention all the scrapie infected
sheep. I am surprised that we have not included man 'aka soyent green'. It is a
disgusting industry and nothing more than greed fuels it.
When will the U.S.. start real surveillance of the U.S. bovine population
(not passive, this will not work)?
When will U.S. start removing SRMs?
Have they stopped the use of pneumatic stunners in the U.S.?
If so, will we stop it in all U.S. abattoirs or only in those abattoirs
exporting to Europe?
If not, WHY NOT?
same questions for removal of SRM in the U.S.A., or just for export?
If not, WHY NOT?
How do we now sterilize surgical/dental instruments in the U.S.A.?
Where have we been sourcing surgical catgut?
(i have copies of imports to U.S., and it would floor you) hen will
re-usable surgical instruments be banned?
'Unregulated "foods" such as 'nutritional supplements' containing various
extracts from ruminants, whether imported or derived from
3
US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or
at least very seriously regulated. (neighbors Mom, whom also died from CJD, had
been taking bovine based supplement, which contained brain, eye, and many other
bovine/ovine tissues for years, 'IPLEX').
What is the use of banning blood or tissue donors from Germany, France,
etc... when the U.S.A. continues exposing cattle, sheep and people to SRM,
refuses to have a serious feed ban, refuses to do systematic
BSE-surveillance?
The FDA should feel responsible for the safety of what people eat, prohibit
the most dangerous foods, not only prohibit a few more donors - the FDA should
be responsible for the safe sourcing of medical devices, not only rely on
banning donors "from Europe", The 'real' risks are here in the U.S. as well, and
nave been for some time.
We must not forget the studies that have proven infectivity in blood from
TSE's.
The Lancet, November 9, 1985
Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat
from two patients. We also transmitted the disease from, whole blood samples of
a patient (and of mice) infected with CJD.l Brain, Cornea, and urine from this
patient were also infectious, and the clinicopathological findings2 are
summarised as follows.
snip...
Samples,were taken aseptically at necropsy. 10% crude homogenates of brain
and cornea in saline, whole blood (after crushing a clot), and untreated CSF and
urine were innoculated intracerebrally into CFl strain mice (20 ul per animal).
Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and
sometimes tremor after long incubation periods. Tissues obtained after the
animal died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes, consisting of
severe spongiform changes, glial proliferation, and a moderate loss of nerve
cells. A few mice inoculated with brain tissue or urine had the same amyloid
plaques found in patients and animals with CJD.3
snip...
Department of Neuropathology,. Neurological Institute, Faculty of Medicine,
Kyushu University, Fukuoka812, Japan JUN TATEISHI
(full text-long version)
and
CWD and transmission to man will be no different than other TSE's.
"Clearly, it is premature to draw firm conclusions about CWD passing
naturally into humans, cattle and sheep, but the present results suggest that
CWD transmissions to humans would be as limited by PrP incompatibility as
transmissions of BSE or sheep scrapie to humans. Although there is no evidence
that sheep scrapie has affected humans, it is likely that BSE has
4
caused variant CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the presumably large
number of people exposed to BSE infectivity, the susceptibility of humans may
still be very low compared with cattle, which would be consistent with the
relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent to take
reasonable measures to limit exposure of humans (as well as sheep and cattle) to
CWD infectivity as has been recommended for other animal TSEs,"
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4,
P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B.
Caughey1,7
or more recently transmission of BSE to sheep via whole blood Research
letters Volume 356, Number 9234 16 September 2000
Transmission of BSE by blood transfusion in sheep
Lancet 2000; 356: 999 – 1000
F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock
See Commentary
"We have shown that it is possible to transmit bovine spongiform
encephalopathy (BSE) to a sheep by transfusion with whole blood taken from
another sheep during the symptom-free phase of an experimental BSE infection.
BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by
the same infectious agent, and the sheep-BSE experimental model has a similar
pathogenesis to that of human vCJD. Although UK blood transfusions are
leucodepleted--a possible protective measure against any risk from blood
transmission-- this report suggests that blood donated by symptom-free
vCJD-infected human beings may represent a risk of spread of vCJD infection
among the human population of the UK."
"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD)
is caused by the same agent that causes bovine spongiform encephalopathy (BSE)
in cattle1 has raised concerns that blood from human beings in the symptom-free
stages of vCJD could transmit infection to recipients of blood transfusions
(full text long version)"
and...
"The large number of cases (1040), temporal clustering of the outbreaks (15
in the first 6 months of 1997), the high in-flock incidence, and the exceptional
involvement of goats (390 cases), suggested an accidental infection. The source
of the epidemic might have been TSE-contaminated meat and bonemeal, but eight
flocks had never been fed any commercial feedstuff. Infection might have risen
from the use of a formol-inactivated vaccine against contagious agalactia
prepared by a single laboratory with brain and mammary gland homogenates of
sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the
donor sheep have not been found, it is possible that one or more of them were
harbouring the
5
infectious agent. Between 1995 and 1996, this vaccine was given
subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these
animals the disease appeared between 23 and 35 months after vaccination. No
information is available for herd 13 because it was made up of stolen animals.
Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine,
thus suggesting a naturally occurring disease.’’ (again, full text long
version).
IN SHORT, please do under estimate this data and or human/animal TSE's
including CWD in the U.S.A.
A few last words, please.
The cattle industry would love to have us turn our focus to CWD and forget
about our own home grown TSE in Bovines. This would be easy to do. Marsh's work
was from downer cattle feed, NOT downer deer/elk feed. This has been
proven.
DO NOT MAKE THAT MISTAKE.
There should be NO LESS THAN 1,000,000 tests for BSE/TSE ' in 2001 for
U.S.A. French are testing 20,000 a week. The tests are available. Why wait until
we stumble across a case from passive surveillance, by then it is to late. IF we
want the truth, this is a must???
United States Total ,Bovine Brain Submissions by State,
May 10 ,1990 thru October 31, 2000
Total 11,700
FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???
with same feeding and rendering practices as that of U.K. for years and
years, same scrapie infected sheep used in feed, for years and years, 950
scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known
to date. (hmmm, i am thinking why there is not a variant scrapie, that is
totally different than all the rest)? just being sarcastic.
with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need
to reconsider that blood meal etc. 'TOTAL BAN')
AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied
to this environmental death sentence. "PROVE IT". It's just not true. The
'CHOSEN ONES' are not the only ones dying because of this man-made death
sentence. When making regulations for human health from human/animal TSEs, you
had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic
CJD with the 'prehistoric' testing available to date. This could be a deadly
mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death,
and hvCJD is the fastest. Could it just be a higher titre of infectivity, or
route or source, or all three?
Last, but not least. The illegal/legal harvesting of body parts and tissues
will come back to haunt you. Maybe not morally, but due to NO background checks
and human TSEs, again it will continue to spread.
Stupidity, Ignorance and Greed is what fuels this disease. You must stop
all of this, and ACT AT ONCE...
Sent: Monday, January 08,2001 3:03 PM
TO: freas@CBS5055530.CBER.FDA.GOV
FDA CJD BSE TSE Prion Scientific Advisors and Consultants Staff January
2001 Meeting Singeltary Submission
2001 FDA CJD TSE Prion Singeltary Submission
Thursday, April 14, 2016
Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD
Sunday, January 17, 2016
Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease
Alzheimer-type brain pathology may be transmitted by grafts of dura mater
26/01/2016
Tuesday, April 21, 2015
Transmissible Spongiform Encephalopathy Advisory Committee TSEAC MEETING
SCHEDULED FOR June 1, 2015
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
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 ;
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.
Terry S. Singeltary Sr.
No comments:
Post a Comment