CJD case in Saint John prompts letter to patients Canada
CJD case in Saint John prompts letter to patients
Horizon Health Network officials want to reassure patients risk is 'nil'
CBC News Posted: Aug 2, 2012 1:29 PM AT Last Updated: Aug 2, 2012 3:00 PM
Health care officials in Saint John are hoping to meet with nearly 150
surgical patients to reassure them they have not been exposed to
Creutzfeldt-Jakob disease, despite a confirmed case at one of the city's
hospitals in July.
The operating rooms at St. Joseph's Hospital were closed for disinfection
for two days after a patient was diagnosed with CJD, a rare brain disease.
The hospital sent letters to patients who had surgeries prior to that
patient's diagnosis, inviting them to a question-and-answer session on Aug. 7,
said Dr. David Marr, medical director for the Saint John region.
But he contends their risk is "nil."
The disease can only be transferred on brain or neurological tissues and
that couldn't have happened in this case, said Marr.
"There's been no evidence, given the type of surgery that this particular
patient had, and has ever been shown in the literature to result in the
transferring of the disease."
Still, Marr feels the letters and meeting is the right thing to do.
"We felt they deserved to know," he said. "We thought they should know up
front and we felt by taking this head on we would be reassuring to them in the
long-term because in fact we don't believe that there's any risk to patients
here."
The Horizon Health Network did not issue a news release when the patient's
diagnosis was confirmed and patients who were scheduled for surgery during the
two days of disinfection were not given any explanation when their procedures
were cancelled.
The infected patient's condition remains unclear.
CJD is not related to so-called mad cow disease, which is contracted by
eating meat from an infected cow, said Marr.
CJD is a disease caused by protein-like particles called prions. These
attack the brain, killing cells and creating gaps in tissue. The disease is
always fatal. There are two types of CJD — classical and variant.
CANADA
TOO bad Canada’s policy on BSE aka mad cow type disease, and the reporting
there from of completed cases, have ceased to exist on the CFIA site for the
public to follow. you have to request a copy. CFIA ceased giving those copies
out to me. ...
•Request a copy of a completed BSE investigation report for a case after
January 2009
Sunday, May 27, 2012
CANADA PLANS TO IMPRISON ANYONE SPEAKING ABOUT MAD COW or ANY OTHER DISEASE
OUTBREAK, CENSORSHIP IS A TERRIBLE THING
PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD)
in Canada is also on a steady increase. please see ;
> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
Deaths of Definite and Probable CJD
Year Sporadic Iatrogenic Familial GSS FFI vCJD Total
1994 2 0 0 1 0 0 3
1995 3 0 0 0 0 0 3
1996 13 0 0 0 0 0 13
1997 16 0 1 1 0 0 18
1998 22 1 0 1 0 0 24
1999 26 2 2 1 0 0 31
2000 32 0 0 3 0 0 35
2001 27 0 2 1 0 0 30
2002 31 0 2 2 0 1 36
2003 27 1 1 0 0 0 29
2004 42 0 1 0 0 0 43
2005 42 0 0 2 0 0 44
2006 39 0 1 3 1 0 44 2007 35 0 0 4 0 0 39
2008 48 0 1 0 0 0 49
2009 48 0 3 2 0 0 53
2010 34 0 3 0 0 0 37
2011 37 0 2 1 0 1 41
2012 1 0 0 0 0 0 1
Total 525 4 19 22 1 2 573
1. CJDSS began in 1998
2. Data before 1998 are retrospective and partial, data from 1998 to 2008
are complete, and data for 2009 - 2012 are provisional
3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is
pending.
CJD Deaths Reported by CJDSS1, 1994-20122
As of May 31, 2012
CENSORSHIP IS A TERRIBLE THING $$$
Canada has had a COVER-UP policy of mad cow disease since about the 17th
case OR 18th case of mad cow disease. AFTER THAT, all FOIA request were ignored
$$$
THIS proves there is indeed an epidemic of mad cow disease in North
America, and it has been covered up for years and years, if not for decades, and
it’s getting worse $$$
Thursday, February 10, 2011
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011
and how to hide mad cow disease in Canada Current as of: 2011-01-31
Wednesday, August 11, 2010
REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Thursday, August 19, 2010
REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM
ENCEPHALOPATHY (BSE) IN CANADA
Friday, March 4, 2011
Alberta dairy cow found with mad cow disease
please remember a few things, sporadic cjd is not a single strain. sporadic
CJD is multiple strains of CJD from unknown route and source of agent. 85%+ of
all human TSE i.e. sporadic CJD, does NOT happen spontaneously, this is a myth,
one never proven. to date, there has never been a documented spontaneous TSE in
any natural field cases of TSE in any species. all iatrogenic CJD is, is a
sporadic CJD, until the route and source of the iatrogenic event has been
proven. atypical TSE is mounting and spreading. we must make all human TSE
reportable in ALL AGE GROUPS. remember, per the CJD Foundation, in the age group
of 55 years and older, CJD cases jump to one in nine thousand. atypical BSE here
in the USA has been linked to some cases of sporadic CJD. ...
TSE prion disease in species in the USA are multiplying and spreading. CWD
in deer and elk is spreading, and now with more than one strain documented.
scrapie in sheep and goats, and atypical scrapie (Nor-98), has spread from coast
to coast in 5 years, and BSE in cattle mutating to different strains now, with
the USA documenting the c-BSE, atypical h-BSE, atypical h-g-BSE, and the
atypical l-bse (BASE) type, all being documented in the USA now. the partial and
voluntary mad cow feed ban was a joke, and the BSE mad cow surveillance was even
worse. NOW, add all this up to this new strain of sporadic CJD in the USA in
young and old, some of which with long duration. then think all this, all these
TSE, all these prions being consumed one way or the other, ...then think
iatrogenic in all hospital surgical wards, blood donors, tissue donors? one
final thought, IS ALZHEIMER'S TRANSMISSIBLE? is Alzheimer's a TSE ?” see my
report with a few update protocols on TSE prion safety...
Tuesday, July 31, 2012
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob
Disease CJD Greenville Memorial Hospital
Wednesday, June 27, 2012
First US BSE Case Since 2006 Underscores Need for Vigilance
Neurology Today 21 June 2012
PO-028: Oral transmission of L-type bovine spongiform encephalopathy
(L-BSE) in primate model Microcebus murinus
Nadine Mestre-Frances,1 Simon Nicot,2 Sylvie Rouland,1 Anne-Gaëlle
Biacabe,2 Isabelle Quadrio,3 Armand Perret-Liaudet,3 Thierry Baron,2 Jean-Michel
Verdier1 1IN SER M UM2; Montpellier, France; 2Anses; Lyon, France; 3Hopitaux
Civils de Lyon; Lyon, France
An atypical form of bovine spongiform encephalopathy has been identified in
cattle in Europe, North America and Japan and was designed as L-type BSE (L-BSE)
due to the lower apparent molecular mass of the unglycosylated,
protease-resistant prion protein (PrPres) detected by western blot compared with
classical BSE. Experimental evidences from studies in transgenic mice expressing
human PrP and in primate models suggest a higher risk of transmission to humans
of the L-BSE form than for classical BSE agent. However, a major unresolved
issue concerns the potential transmissibility of the L-BSE agent by oral route.
To address this question, we infected mouse lemurs (Microcebus murinus), a
non-human primate model, with L-BSE by intracerebral or oral route.
Four adult lemurs were intracerebrally (IC) inoculated with 5mg of L-BSE
infected brain homogenate of an atypical French BSE case (02-2528). Four young
and four adult animals were fed with 5 mg or 50 mg of infected brain. After
sacrifice, the brain tissues were biochemically and immunocytochemically
investigated for PrPres.
The 4 animals IC inoculated died at 19 and 22 months postinoculation (mpi).
They developed blindness, tremor, abnormal posture, incoordinated movements,
balance loss. Symptoms get worse according to the disease progression, until
severe ataxia. Severe spongiosis was evidenced into the thalamus, the striatum,
the mesencephalon, and the brainstem, whereas into the cortex the vacuolisation
was weaker. Strong deposits of PrPres were detected into the thalamus, the
striatum, and the hippocampus whereas in the cerebral cortex, PrPres was
prominently accumulated in plaques.
The orally inoculated animals showed similar clinical symptoms occurring
between 27 and 34 mpi. Disease was characterized by progressive prostration,
loss of appetite and poor appearance of the fur. Only one adult animal showed
disequilibrium. PrPres was strongly accumulated only in the striatum and
thalamus and weakly into the cortex. No plaques were evidenced. Two animals that
were orally challenged at the age of two years are still alive and healthy 34
months after inoculation. The western blot analysis showed uniform molecular
profiles, irrespective of the route or dose of infection, and included notably a
PrPres form with low apparent molecular mass (~19 kDa) similar to the PrPres in
the original cattle brain. However, the PrPres profile in lemurs was
characterized by a higher proportion of di- and mono-glycosylated species (up to
95% of the total signal) than in the bovine L-BSE inoculum (~80%). In addition,
small amounts of PrPres were detected by western blotting in the spleen of three
animals (one intra-cerebrally inoculated and two fed with 5 mg of cattle
brain).
Here, we demonstrate that the L-BSE agent can be transmitted by oral route
from cattle to young and adult mouse lemurs. In comparison to IC inoculated
animals, orally challenged lemurs were characterized by longer survival periods
as expected with this route of infection.
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...
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ;
chronic wasting disease cwd 2012 cdc report
Tuesday, July 17, 2012
O.I.E. BSE, CWD, SCRAPIE, TSE PRION DISEASE Final Report of the 80th
General Session, 20 - 25 May 2012
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
***The pathology features of Nor98 in the cerebellum of the affected sheep
showed similarities with those of sporadic Creutzfeldt-Jakob disease in
humans.
*** Intriguingly, these conclusions suggest that some pathological features
of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
*** These observations support the view that a truly infectious TSE agent,
unrecognized until recently, infects sheep and goat flocks and may have
important implications in terms of scrapie control and public health.
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
12/10/76
AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON
SCRAPIE
Office Note CHAIRMAN: PROFESSOR PETER WILDY
snip...
A The Present Position with respect to Scrapie A] The Problem Scrapie is a
natural disease of sheep and goats. It is a slow and inexorably progressive
degenerative disorder of the nervous system and it ia fatal. It is enzootic in
the United Kingdom but not in all countries. The field problem has been reviewed
by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in
Britain for a variety of reasons but the disease causes serious financial loss;
it is estimated that it cost Swaledale breeders alone $l.7 M during the five
years 1971-1975. A further inestimable loss arises from the closure of certain
export markets, in particular those of the United States, to British sheep. It
is clear that scrapie in sheep is important commercially and for that reason
alone effective measures to control it should be devised as quickly as possible.
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates.
One particularly lurid speculation (Gajdusek 1977) conjectures that the
agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible
encephalopathy of mink are varieties of a single "virus". The U.S. Department of
Agriculture concluded that it could "no longer justify or permit scrapie-blood
line and scrapie-exposed sheep and goats to be processed for human or animal
food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by
the finding that some strains of scrapie produce lesions identical to the once
which characterise the human dementias" Whether true or not. the hypothesis that
these agents might be transmissible to man raises two considerations. First, the
safety of laboratory personnel requires prompt attention. Second, action such as
the "scorched meat" policy of USDA makes the solution of the acrapie problem
urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Tuesday, June 26, 2012
Creutzfeldt Jakob Disease Human TSE report update North America, Canada,
Mexico, and USDA PRION UNIT as of May 18, 2012
type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the
rise in Canada and the USA
Wednesday, August 01, 2012
Behavioural and Psychiatric Features of the Human Prion Diseases:
Experience in 368 Prospectively Studied Patients
Scottish TSE Network November Symposium Announcement Event: 12 November
2012
Chair: Prof Hugh Perry, University of Southampton, Southampton UK
Location: The Roslin Institute Building Auditorium
If you would like to book a place at this event, please let Gila Holliman
know.
Cost: £125.
Title: Is Alzheimer’s Disease a transmissible disease?
Speakers:
Session 1:
Prof Bob Will, National CJD Surveillance Unit, Edinburgh UK
Prof James Ironside, National CJD Surveillance Unit, Edinburgh UK
Prof Lary Walker, Emory School of Medicine, Atlanta USA
Session 2:
Prof Mathias Jucker, Hertie Institute for Clinical Brain Research,
Stuttgart Germany
Prof William Van Nostrand, Stony Brook University, Stony Brook USA
Dr Claudio Soto, University of Texas Medical School, Houston USA
Session 3:
Dr Fabrizio Tagliavini, Instituto Neurologico Carlo Besta, Milan Italy
Prof Pedro Piccardo, Food and Drug Administration, Washington DC USA
Dr Bruce Chesebro, National Institutes of Health, Missoula USA
From: Terry S. Singeltary Sr. Sent: Wednesday, May 16, 2012 3:29 PM To:
BSE-L@LISTS.AEGEE.ORG
Subject: [BSE-L] Alzheimer’s disease and Transmissible Spongiform
Encephalopathy prion disease, Iatrogenic, what if ?
Proposal ID: 29403
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both disease, and it’s variants, in many cases are merely
names of the people that first discovered them. Both diseases are incurable and
debilitating brain disease, that are in the end, 100% fatal, with the
incubation/clinical period of the Alzheimer’s disease being longer than the TSE
prion disease. Symptoms are very similar, and pathology is very similar. I
propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation
disease, and that Alzheimer’s is Transmissible, and is a threat to the public
via the many Iatrogenic routes and sources. It was said long ago that the only
thing that disputes this, is Alzheimer’s disease transmissibility, or the lack
of. today, there is enough documented science (some confidential), that shows
that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and
or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and
one that needs to be addressed immediately.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around
1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you
can take the ash and mix it with saline and inject that ash into a mouse, and
the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still
Infectious after Biodiesel Production as well. the TSE prion agent also survives
Simulated Wastewater Treatment Processes. IN fact, you should also know that the
TSE Prion agent will survive in the environment for years, if not decades. you
can bury it and it will not go away. TSE prion agent is capable of infected your
water table i.e. Detection of protease-resistant cervid prion protein in water
from a CWD-endemic area. it’s not your ordinary pathogen you can just cook it
out and be done with. that’s what’s so worrisome about Iatrogenic mode of
transmission, a simple autoclave will not kill this TSE prion agent.
Conclusions
There should be a Global Congressional Science round table event (one of
scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics let science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already. what’s the use of science progressing human life to
the century mark, if your brain does not work?
combined cannot exceed 350 Words
shortened to proper word count ;
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease
have both been around a long time, and was discovered in or around the same time
frame, early 1900’s. Both diseases are incurable and debilitating brain disease,
that are in the end, 100% fatal, with the incubation/clinical period of the
Alzheimer’s disease being longer (most of the time) than the TSE prion disease.
Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals,
transmission studies, and observations of loved ones and friends that have died
from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant
Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long
incubation disease, and that Alzheimer’s is Transmissible, and is a threat to
the public via the many Iatrogenic routes and sources. It was said long ago that
the only thing that disputes this, is Alzheimer’s disease transmissibility, or
the lack of. The likelihood of many victims of Alzheimer’s disease from the many
different Iatrogenic routes and modes of transmission as with the TSE prion
disease.
Conclusions
There should be a Global Congressional Science round table event set up
immediately to address these concerns from the many potential routes and sources
of the TSE prion disease, including Alzheimer’s disease, and a emergency global
doctrine put into effect to help combat the spread of Alzheimer’s disease via
the medical, surgical, dental, tissue, and blood arena’s. All human and animal
TSE prion disease, including Alzheimer’s should be made reportable in every
state, and Internationally, WITH NO age restrictions. Until a proven method of
decontamination and autoclaving is proven, and put forth in use universally, in
all hospitals and medical, surgical arena’s, or the TSE prion agent will
continue to spread. IF we wait until science and corporate politicians wait
until politics lets science _prove_ this once and for all, and set forth
regulations there from, we will all be exposed to the TSE Prion agents, if that
has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
source references
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob
disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds
for considering a similar pathogenesis for AD and the spongiform virus
encephalopathies. However, the crux of the comparison rests squarely on results
of attempts to transmit AD to experimental animals, and these results have not
as yet validated a common etiology. Investigations of the biologic similarities
between AD and the spongiform virus encephalopathies proceed in several
laboratories, and our own observation of inoculated animals will be continued in
the hope that incubation periods for AD may be even longer than those of CJD.
BSE101/1 0136
IN CONFIDENCE
CMO
From: Dr J S Metters DCMO
4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
From: Dr. A Wight Date: 5 January 1993
Copies:
Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
Wednesday, January 5, 2011
ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions
David W. Colby1,* and Stanley B. Prusiner1,2
Tuesday, October 4, 2011
Molecular Psychiatry
advance online publication 4 October 2011; doi: 10.1038/mp.2011.120
De novo induction of amyloid-ß deposition in vivo
Our results suggest that some of the typical brain abnormalities associated
with AD can be induced by a prion-like mechanism of disease transmission through
propagation of protein misfolding. These findings may have broad implications
for understanding the molecular mechanisms responsible for the initiation of AD,
and may contribute to the development of new strategies for disease prevention
and intervention. Keywords: amyloid; prion; protein misfolding; disease
transmission
see more here ;
Wednesday, September 21, 2011
PrioNet Canada researchers in Vancouver confirm prion-like properties in
Amyotrophic Lateral Sclerosis (ALS)
snip...end
Thank You for accepting my submission
# 29403, Alzheimer’s disease and Transmissible Spongiform Encephalopathy
prion disease, Iatrogenic, what if ? and the opportunity to present it, at the
Alzheimer’s Association International Conference 2012 (AAIC), as a poster
presentation. However, with great sadness, I must regretfully decline the
invitation due to a medical reasons, and traveling to Canada, of which is not
possible. ...
Thank You,
With Kindest Regards,
I am sincerely,
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net
From:
Sent: Saturday, April 07, 2012 8:20 PM
To: Terry S. Singeltary Sr.
Subject: RE: re-submission
Dear Terry,
Yes, your proposal was accepted as a poster presentation. Please decline
the invitation if appropriate.
Best Regards,
______________________________________
Alzheimer’s Association – National Office 225 North Michigan Avenue – Floor
17 Chicago, Illinois 60601
=============snip...end...source reference...# 29403==========
Wednesday, May 16, 2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
TSS
==============JUNE 2012 UPDATE TSE USA=====================
Tuesday, July 31, 2012
11 patients may have been exposed to fatal disease Creutzfeldt-Jakob
Disease CJD Greenville Memorial Hospital
layperson
Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
2:41 PM
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