flatfish
03-13-2007, 01:12 PM
Subject: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES)
Date: March 13, 2007 at 8:15 am PST
Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans
Lessons From 2 Highly Suspicious but Negative Cases
C. Alan Anderson, MD; Patrick Bosque, MD; Christopher M. Filley, MD; David B. Arciniegas, MD; B. K. Kleinschmidt-DeMasters, MD; W. John Pape, BS; Kenneth L. Tyler, MD
Arch Neurol. 2007;64:439-441.
Objective To describe 2 patients with rapidly progressive dementia and risk factors for exposure to chronic wasting disease (CWD) in whom extensive testing negated the possible transmission of CWD.
Design/Methods We describe the evaluation of 2 young adults with initial exposure histories and clinical presentations that suggested the possibility of CWD transmission to humans.
Patients A 52-year-old woman with possible laboratory exposure to CWD and a 25-year-old man who had consumed meat from a CWD endemic area.
Interventions Clinical evaluation, neuropathological examination, and genetic testing.
Results Neuropathological and genetic assessment in the 2 patients proved the diagnoses of early-onset Alzheimer disease and a rare genetic prion disease.
Conclusion No convincing cases of CWD transmission to humans have been detected in our surveillance program.
Author Affiliations: Departments of Neurology (Drs Anderson, Bosque, Filley, Arciniegas, Kleinschmidt-DeMasters, and Tyler), Psychiatry (Drs Anderson, Filley, and Arciniegas), Pathology (Dr Kleinschmidt-DeMasters), Medicine (Dr Tyler), Microbiology (Dr Tyler), and Immunology (Dr Tyler); University of Colorado School of Medicine, Denver; Denver Veterans Affairs Medical Center, Denver (Drs Anderson, Filley, Arciniegas, and Tyler); Denver Health Medical Center, Denver (Dr Bosque); and Colorado Department of Public Health and Environment, Denver (Mr Pape).
http://archneur.ama-assn.org/cgi/content/abstract/64/3/439?ct
> Results Neuropathological and genetic assessment in the 2 patients proved the
> diagnoses of early-onset Alzheimer disease and a rare genetic prion disease
very interesting, and something to ponder here for sure ;
AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
and i think this would apply to CWD to humans as well.
> rare genetic prion disease
would be interesting to know the exact genetic TSE they are speaking of. GSS, FFI, Familial/Genetic CJD, and or the sporadic FFI that is not genetic, and don't ask me why ??? does not make sense to me either. it's either genetic or not. like i have said many times, the diagnostic criteria differentiating the different human and animal TSE is missing something. but if you have a strain of genetic/familial TSE i.e. FFI, and then you classify a sub-type of that strain that use to be gentic to sporadic, then you have either gone back to sCJD, or the complete damn diagnostic criteria is wrong. you just have well named the damn thing ;
Parchi-Capellari-Chin-Schwarz-Schecter-Butts-Hudkins-Burns-Powers-Gambetti-DISEASE.
TSS
Subject: Alzheimer-type neuropathology in a 28-year old patient with iatrogenic CJD after dural grafting
Date: March 9, 2007 at 9:15 am PST
HUMAN-04
Alzheimer-type neuropathology in a 28-year old patient with iatrogenic
Creutzfeldt-Jakob disease after dural grafting
M Preusser1, T Stroebel1, E Gelpi1, 2, M Eiler3, G Broessner4, E Schmutzhard4, H Budka1, 2
1 Institute of Neurology, Medical University Vienna, Austria; 2 Austrian Reference Centre for Human Prion Diseases
(OERPE), General Hospital Vienna, Austria; 3 Department of Neurology, LKH Rankweil, Austria; 4 Department of
Neurology, Medical University Innsbruck, Austria
We report the autopsy case of a 28-year old male patient who had received a cadaverous dura
mater graft after a traumatic open skull fracture with tearing of dura at the age of 5 years. A
clinical suspicion of Creutzfeldt-Jakob disease (CJD) was confirmed by a brain biopsy 5 months
prior to death and by autopsy, thus warranting the diagnosis of iatrogenic CJD (iCJD) according
to WHO criteria. Immunohistochemistry showed widespread cortical depositions of diseaseassociated
prion protein (PrPsc) in a synaptic pattern and western blot analysis identified PrPsc of
type 2A according to Parchi et al. Surprisingly, we found Alzheimer-type senile plaques and
cerebral amyloid angiopathy in widespread areas of the brain. Plaque-type and vascular amyloid
was immunohistochemically identified as deposits of beta-A4 peptide. CERAD criteria for
diagnosis of definite Alzheimer´s disease (AD) were met in the absence of neurofibrillar tangles
or alpha-synuclein immunoreactive inclusions. There was no family history of AD, CJD, or any
other neurological disease, and genetic analysis showed no disease-specific mutations of the
prion protein, presenilin 1 and 2, or amyloid precursor protein genes. This case represents 1. the
iCJD case with the longest incubation time after dural grafting reported so far, 2. the youngest
documented patient with concomitant CJD and Alzheimer-type neuropathology to date, 3. the
first description of Alzheimer type-changes in iCJD, and 4. the second case of iCJD in Austria.
Despite the young patient age, the Alzheimer-type changes may be an incidental finding, possibly
related to the childhood trauma.
249 of 411 pages...tss
http://www.tse-forum.de/tse_forum/deutsch/oeffentlich/bilder/Abstract_BookFINAL_nov2.pdf
some other things to ponder ;
Alzheimer's and Transmissible Spongiform Encephalopathies
*******************************.com/showthread.php?t=13175
------------------------------------------------------------
Comments sent via JAMA Feedback Page
------------------------------------------------------------
NAME: Terry S. Singeltary Sr.
E-MAIL: flounder9@verizon.net
------------------------------------------------------------
COMMENTS:
I wish to submit the following ;
HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory
TSEs have been rampant in the USA for decades in many
species, and they all have been rendered and fed back
to animals for human/animal consumption. I propose that
the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the
continued belief of the UKBSEnvCJD only theory in 2005.
With all the science to date refuting it, to continue
to validate this myth, will only spread this TSE agent
through a multitude of potential routes and sources
i.e. consumption, surgical, blood, medical, cosmetics
etc. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE
Tranmissible Spongiform Encephalopathy is far from an
exact science, but there is enough proven science to
date that this myth should be put to rest once and for
all, and that we move forward with a new classification
for human and animal TSE that would properly identify
the infected species, the source species, and then the
route. This would further have to be broken down to
strain of species and then the route of transmission
would further have to be broken down. Accumulation and
Transmission are key to the threshold from subclinical
to clinical disease, and of that, I even believe that
physical and or blunt trauma may play a role of onset
of clinical symptoms in some cases, but key to all
this, is to stop the amplification and transmission of
this agent, the spreading of, no matter what strain.
BUT, to continue with this myth that the U.K. strain of
BSE one strain in cows, and the nv/v CJD, one strain in
humans, and that all the rest of human TSE is one
single strain i.e. sporadic CJD (when to date there are
6 different phenotypes of sCJD), and that no other
animal TSE transmits to humans, to continue with this
masquerade will only continue to spread, expose, and
kill, who knows how many more in the years and decades
to come. ONE was enough for me, My Mom, hvCJD, DOD
12/14/97 confirmed, which is nothing more than another
mans name added to CJD, like CJD itself, Jakob and
Creutzfeldt, or Gerstmann-Straussler-Scheinker
syndrome, just another CJD or human TSE, named after
another human. WE are only kidding ourselves with the
current diagnostic criteria for human and animal TSE,
especially differentiating between the nvCJD vs the
sporadic CJD strains and then the GSS strains and also
the FFI fatal familial insomnia strains or the ones
that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of
the human and animal TSEs are paramount in all variants
of all TSE. There must be a proper classification that
will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive
testing coming about, I only hope that my proposal will
some day be taken seriously.
My name is Terry S. Singeltary Sr. and I am no
scientist, no doctor and have no PhDs, but have been
independently researching human and animal TSEs since
the death of my Mother to the Heidenhain Variant of
Creutzfeldt Jakob Disease on December 14, 1997
'confirmed'. ...TSS
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
CONTINUED
Date: March 13, 2007 at 8:15 am PST
Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans
Lessons From 2 Highly Suspicious but Negative Cases
C. Alan Anderson, MD; Patrick Bosque, MD; Christopher M. Filley, MD; David B. Arciniegas, MD; B. K. Kleinschmidt-DeMasters, MD; W. John Pape, BS; Kenneth L. Tyler, MD
Arch Neurol. 2007;64:439-441.
Objective To describe 2 patients with rapidly progressive dementia and risk factors for exposure to chronic wasting disease (CWD) in whom extensive testing negated the possible transmission of CWD.
Design/Methods We describe the evaluation of 2 young adults with initial exposure histories and clinical presentations that suggested the possibility of CWD transmission to humans.
Patients A 52-year-old woman with possible laboratory exposure to CWD and a 25-year-old man who had consumed meat from a CWD endemic area.
Interventions Clinical evaluation, neuropathological examination, and genetic testing.
Results Neuropathological and genetic assessment in the 2 patients proved the diagnoses of early-onset Alzheimer disease and a rare genetic prion disease.
Conclusion No convincing cases of CWD transmission to humans have been detected in our surveillance program.
Author Affiliations: Departments of Neurology (Drs Anderson, Bosque, Filley, Arciniegas, Kleinschmidt-DeMasters, and Tyler), Psychiatry (Drs Anderson, Filley, and Arciniegas), Pathology (Dr Kleinschmidt-DeMasters), Medicine (Dr Tyler), Microbiology (Dr Tyler), and Immunology (Dr Tyler); University of Colorado School of Medicine, Denver; Denver Veterans Affairs Medical Center, Denver (Drs Anderson, Filley, Arciniegas, and Tyler); Denver Health Medical Center, Denver (Dr Bosque); and Colorado Department of Public Health and Environment, Denver (Mr Pape).
http://archneur.ama-assn.org/cgi/content/abstract/64/3/439?ct
> Results Neuropathological and genetic assessment in the 2 patients proved the
> diagnoses of early-onset Alzheimer disease and a rare genetic prion disease
very interesting, and something to ponder here for sure ;
AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
and i think this would apply to CWD to humans as well.
> rare genetic prion disease
would be interesting to know the exact genetic TSE they are speaking of. GSS, FFI, Familial/Genetic CJD, and or the sporadic FFI that is not genetic, and don't ask me why ??? does not make sense to me either. it's either genetic or not. like i have said many times, the diagnostic criteria differentiating the different human and animal TSE is missing something. but if you have a strain of genetic/familial TSE i.e. FFI, and then you classify a sub-type of that strain that use to be gentic to sporadic, then you have either gone back to sCJD, or the complete damn diagnostic criteria is wrong. you just have well named the damn thing ;
Parchi-Capellari-Chin-Schwarz-Schecter-Butts-Hudkins-Burns-Powers-Gambetti-DISEASE.
TSS
Subject: Alzheimer-type neuropathology in a 28-year old patient with iatrogenic CJD after dural grafting
Date: March 9, 2007 at 9:15 am PST
HUMAN-04
Alzheimer-type neuropathology in a 28-year old patient with iatrogenic
Creutzfeldt-Jakob disease after dural grafting
M Preusser1, T Stroebel1, E Gelpi1, 2, M Eiler3, G Broessner4, E Schmutzhard4, H Budka1, 2
1 Institute of Neurology, Medical University Vienna, Austria; 2 Austrian Reference Centre for Human Prion Diseases
(OERPE), General Hospital Vienna, Austria; 3 Department of Neurology, LKH Rankweil, Austria; 4 Department of
Neurology, Medical University Innsbruck, Austria
We report the autopsy case of a 28-year old male patient who had received a cadaverous dura
mater graft after a traumatic open skull fracture with tearing of dura at the age of 5 years. A
clinical suspicion of Creutzfeldt-Jakob disease (CJD) was confirmed by a brain biopsy 5 months
prior to death and by autopsy, thus warranting the diagnosis of iatrogenic CJD (iCJD) according
to WHO criteria. Immunohistochemistry showed widespread cortical depositions of diseaseassociated
prion protein (PrPsc) in a synaptic pattern and western blot analysis identified PrPsc of
type 2A according to Parchi et al. Surprisingly, we found Alzheimer-type senile plaques and
cerebral amyloid angiopathy in widespread areas of the brain. Plaque-type and vascular amyloid
was immunohistochemically identified as deposits of beta-A4 peptide. CERAD criteria for
diagnosis of definite Alzheimer´s disease (AD) were met in the absence of neurofibrillar tangles
or alpha-synuclein immunoreactive inclusions. There was no family history of AD, CJD, or any
other neurological disease, and genetic analysis showed no disease-specific mutations of the
prion protein, presenilin 1 and 2, or amyloid precursor protein genes. This case represents 1. the
iCJD case with the longest incubation time after dural grafting reported so far, 2. the youngest
documented patient with concomitant CJD and Alzheimer-type neuropathology to date, 3. the
first description of Alzheimer type-changes in iCJD, and 4. the second case of iCJD in Austria.
Despite the young patient age, the Alzheimer-type changes may be an incidental finding, possibly
related to the childhood trauma.
249 of 411 pages...tss
http://www.tse-forum.de/tse_forum/deutsch/oeffentlich/bilder/Abstract_BookFINAL_nov2.pdf
some other things to ponder ;
Alzheimer's and Transmissible Spongiform Encephalopathies
*******************************.com/showthread.php?t=13175
------------------------------------------------------------
Comments sent via JAMA Feedback Page
------------------------------------------------------------
NAME: Terry S. Singeltary Sr.
E-MAIL: flounder9@verizon.net
------------------------------------------------------------
COMMENTS:
I wish to submit the following ;
HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory
TSEs have been rampant in the USA for decades in many
species, and they all have been rendered and fed back
to animals for human/animal consumption. I propose that
the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the
continued belief of the UKBSEnvCJD only theory in 2005.
With all the science to date refuting it, to continue
to validate this myth, will only spread this TSE agent
through a multitude of potential routes and sources
i.e. consumption, surgical, blood, medical, cosmetics
etc. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE
Tranmissible Spongiform Encephalopathy is far from an
exact science, but there is enough proven science to
date that this myth should be put to rest once and for
all, and that we move forward with a new classification
for human and animal TSE that would properly identify
the infected species, the source species, and then the
route. This would further have to be broken down to
strain of species and then the route of transmission
would further have to be broken down. Accumulation and
Transmission are key to the threshold from subclinical
to clinical disease, and of that, I even believe that
physical and or blunt trauma may play a role of onset
of clinical symptoms in some cases, but key to all
this, is to stop the amplification and transmission of
this agent, the spreading of, no matter what strain.
BUT, to continue with this myth that the U.K. strain of
BSE one strain in cows, and the nv/v CJD, one strain in
humans, and that all the rest of human TSE is one
single strain i.e. sporadic CJD (when to date there are
6 different phenotypes of sCJD), and that no other
animal TSE transmits to humans, to continue with this
masquerade will only continue to spread, expose, and
kill, who knows how many more in the years and decades
to come. ONE was enough for me, My Mom, hvCJD, DOD
12/14/97 confirmed, which is nothing more than another
mans name added to CJD, like CJD itself, Jakob and
Creutzfeldt, or Gerstmann-Straussler-Scheinker
syndrome, just another CJD or human TSE, named after
another human. WE are only kidding ourselves with the
current diagnostic criteria for human and animal TSE,
especially differentiating between the nvCJD vs the
sporadic CJD strains and then the GSS strains and also
the FFI fatal familial insomnia strains or the ones
that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of
the human and animal TSEs are paramount in all variants
of all TSE. There must be a proper classification that
will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive
testing coming about, I only hope that my proposal will
some day be taken seriously.
My name is Terry S. Singeltary Sr. and I am no
scientist, no doctor and have no PhDs, but have been
independently researching human and animal TSEs since
the death of my Mother to the Heidenhain Variant of
Creutzfeldt Jakob Disease on December 14, 1997
'confirmed'. ...TSS
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
CONTINUED