ANOTHER FAMILIAL CJD Conference The Eleventh Annual CJD Foundation Family
Conference excluding sporadic CJD victims and famlies
Greetings CJD Voice members,
looks like another year goes by, another cjd conference will come and go,
and the sporadic CJD victims and families and friends there from are all left to
fend for themselves again, according to their cjd conference program.
hey, but you will get a free autopsy, one that will change the diagnosis to
assure NO possible link from BSE, CWD, SCRAPIE, typical or atypical TSE human
mad cow type victims will be documented in the USA.
it’s all either a spontaneous sporadic happening from nothing of sorts, or
it’s all familial, with a rise in familial type cjd i.e. vpspr type, and now and
now and now, for the really big shoooow, the familial link, that has no familial
type link i.e. the infamous sporadic FFI or the sporadic GSS, with no familial
type genetic link, but only linked to the infamous only mad cow in the world
that has been documented to date, the infamous atypical h-g-BSE.
hey, but if you want to go find out everything about sporadic CJD, and the
updates on all the routes and sources there from right here in the good old USA,
well then I would skip this CJD Foundation conference too.
now I know all you here on CJD Voice all got your invitations didn’t you?
got all your questions ready don’t you (I assume you still have to submit
them first and get them approved up front before asking them)?
I tell you, there was so much about sporadic CJD in the program, I will
have to come back to read it all.
oh, what about that CJD Questionnaire ???
ANOTHER FAMILIAL CJD Conference The Eleventh Annual CJD Foundation Family
Conference excluding sporadic CJD victims and famlies
1:05 - 1:25 Pierluigi Gambetti, MD U.S. Prion Disease Surveillance and the
Importance of Autopsy; Tests Conducted
SNIP...
9:00 - 9:15 Lori Nusbaum Questionnaire Report Associate Director, The CJD
Foundation Akron, Ohio
Wednesday, March 28, 2012
CJD FOUNDATION CWRU GAMBETTI FAMILIAL FAMILY AFFAIR CONFERENCE 2012
the very importance of autopsy Dr. Gambetti is speaking about, is the one
that will change it from any zoonosis type TSE here in the USA, to a sporadic
CJD.
sporadic CJD in the USA...OUT OF SIGHT, OUT OF MIND $$$ PROBLEM
SOLVED...TSS
Subject: Re: Tracie CJD Foundation
Date: Tue, 5 Nov 2002 15:09:29 -0500
From: "Tracie Kedzierski"
To: "Terry S. Singeltary Sr."
References:
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Terry,
Oh no....I've gone and pissed you off (ha ha)I just find it better to
speak...so that nothing I write is misinterpreted. It is very important to me
that you understand the conflict, the confusion, etc so can I call you or not?
My dime ?
Tracie
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "Tracie Kedzierski" S
ent: Tuesday, November 05, 2002 2:45 PM
Subject: Re: Tracie CJD Foundation
> either mail me your explination or forget the it...TSS
>> Tracie Kedzierski wrote:
>> > Terry,
The only problem is that having it on our message board conflicts with the
information I have on our home page about the surveillance project and the
report form I send out to the families. -----it is confusing. In fact.. I'm
sorry but we (The Foundation) have to pull it off. I need to talk to you about
this and share a number of goals the "new" Foundation has Can I call you? Please
email me your number.... Tracie
> > Original Message -----
> > From: "Terry S. Singeltary Sr." > >
To: "Tracie Kedzierski"
Sent: Tuesday, November 05, 2002 1:34 PM
Subject: Re: Tracie CJD Foundation
hi Tracie,
doing fine, thank you. about the questionnaire? by no means am i trying to
step on Dr Gambetti's toes here. i think there is more to it than just reporting
a case. we _must_ find the source and route of spordic CJDs, and i think a great
deal of it will be from the medical/surgical arena. i just want a questionnaire
made up for _all_ victims of human TSEs in the USA in _every_ state, and i want
it reportable in _every_ state. i am turning the heat up. ****, i'm getting old
and grey, i want to see it done before i die. will be sending this out to many
media and papers and requesting them to turn the heat up on the Gov. you will be
able to keep up with the ones coming through the voice and if i get some that
have not come through the list, i will pass on to Dr. Gambetti if he likes. i
respect Dr. Gambetti very much and would do nothing to hender his work or yours.
i just think that this is too important of a matter not to have one. and i think
by turning the heat up, getting to the media and pressing there buttons a bit,
just might help this get done a bit faster... hope so anyway...
kindest regards,
terry
>>Tracie Kedzierski wrote:> >>> >>>
Hi Terry,
How are you? I'm just curious about your Questionnaire ?
It just was posted on the Foundation's Message Board without any
introduction... and I was a bit concerned as it may cause some confusion with
the Surveillance Project I'm doing via the Foundation for Dr Gambetti. Could you
let me know?
Tracie
Greetings again Voice,
just what is the _new_ CJD Foundations goals witha CJD Questionnaire that
asks _no_ questions about soure/route of the six variants of sporadic CJDs???
=================================================
i am reminded of a few things deep throat told me years ago;
=================================================
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever
many grains of salt you wish. ...tss)
The most frightening thing I have read all day is the report of Gambetti's
finding of a new strain of sporadic cjd in young people...Dear God, what in the
name of all that is holy is that!!! If the US has different strains of
scrapie.....why????than the UK...then would the same mechanisms that make
different strains of scrapie here make different strains of BSE...if the
patterns are different in sheep and mice for scrapie.....could not the BSE be
different in the cattle, in the mink, in the humans.......
I really think the slides or tissues and everything from these young people
with the new strain of sporadic cjd should be put up to be analyzed by many,
many experts in cjd........bse.....scrapie Scrape the damn slide and put it into
mice.....wait.....chop up the mouse brain and and spinal cord........put into
some more mice.....dammit amplify the thing and start the damned
research.....This is NOT rocket science...we need to use what we know and get
off our butts and move....the whining about how long everything takes.....well
it takes a whole lot longer if you whine for a year and then start the
research!!!
Not sure where I read this but it was a recent press release or something
like that: I thought I would fall out of my chair when I read about how there
was no worry about infectivity from a histopath slide or tissues because they
are preserved in formic acid, or formalin or formaldehyde.....for God's
sake........ Ask any pathologist in the UK what the brain tissues in the
formalin looks like after a year.......it is a big fat sponge...the agent
continues to eat the brain ......you can't make slides anymore because the agent
has never stopped........and the old slides that are stained with Hemolysin and
Eosin......they get holier and holier and degenerate and continue...what you
looked at 6 months ago is not there........Gambetti better be photographing
every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come
of it and there is not a damned thing anyone can do about it. Don't even hint at
it as it will be denied and laughed at.......... USDA is gonna do as little as
possible until there is actually a human case in the USA of the nvcjd........if
you want to move this thing along and shake the earth....then we gotta get the
victims families to make sure whoever is doing the autopsy is credible,
trustworthy, and a saint with the courage of Joan of Arc........I am not
kidding!!!! so, unless we get a human death from EXACTLY the same form with
EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any
action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to
international travel, international food, etc. etc. etc. etc. etc. They will go
so far as to find out if a sex partner had ever traveled to the UK/europe, etc.
etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth.
They have all the cards, all the money, and are willing to threaten and carry
out those threats....and this may be their biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation
from a rather senior person in government here..........knocked me out of my
chair........you must keep pushing. If I was a power person....I would be
demanding that there be a least a million bovine tested as soon as possible and
agressively seeking this disease. The big players are coming out of the woodwork
as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very
dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will
NEVER be found in the US! As for the BSE conference call...I think you did a
great service to freedom of information and making some people feign
integrity...I find it scary to see that most of the "experts" are employed by
the federal government or are supported on the "teat" of federal funds. A scary
picture! I hope there is a confidential panel organized by the new government to
really investigate this thing.
You need to watch your back........but keep picking at them.......like a
buzzard to the bone...you just may get to the truth!!! (You probably have more
support than you know. Too many people are afraid to show you or let anyone else
know. I have heard a few things myself... you ask the questions that everyone
else is too afraid to ask.)
END...TSS
Friday, November 30, 2007
CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION
IN CONFIDENCE
Perceptions of unconventional slow virus in the USA
GAH WELLS
Report of a visit to the U.S.A. April-May 1989
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 fantical incident to be avoided in the USA AT
ALL COSTS.
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except
on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only)
diagnostic criteria CVL 1992
Prion 7:2, 99–108; March/April 2013; © 2013 Landes Bioscience
mini-Rev iew Mini-REVIEW
A closer look at prion strains
Characterization and important implications
Laura Solforosi,†,* Michela Milani,† Nicasio Mancini, Massimo Clementi and
Roberto Burioni
Laboratory of Microbiology and Virology; University Vita-Salute San
Raffaele; Milan, Italy
†These authors contributed equally to this work.
Keywords: cellular prion protein (PrPC), scrapie prion protein (PrPSc),
transmissible spongiform encephalopathies (TSEs), prion strains, strain
mutation, variant Creutzfeldt-Jakob disease, sporadic Creutzfeldt-Jakob
disease
Abbreviations: PrPC, cellular prion protein; PrPSc, scrapie prion protein;
TSEs, transmissible spongiform encephalopathies; TME, transmissible mink
encephalopathy; CJD, Creutzfeldt-Jakob disease; sCJD, sporadic CJD; vCJD,
variant CJD; FFI, fatal familial insomnia; BSE, bovine spongiform
encephalopathy; CWD, chronic wasting disease; PK, proteinase K; SAF,
scrapie-associated fibrils; CNS, central nervous system; WB, western blot; PE,
phosphatidylethanolamine; sPMCA, serial protein misfolding cyclic amplification;
CPA, cell panel assay
Prions are infectious proteins that are responsible for transmissible
spongiform encephalopathies (TSEs) and consist primarily of scrapie prion
protein (PrPSc), a pathogenic isoform of the host-encoded cellular prion protein
(PrPC). The absence of nucleic acids as essential components of the infectious
prions is the most striking feature associated to these diseases. Additionally,
different prion strains have been isolated from animal diseases despite the lack
of DNA or RNA molecules. Mounting evidence suggests that prion-strain-specific
features segregate with different PrPSc conformational and aggregation states.
Strains are of practical relevance in prion diseases as they can
drastically differ in many aspects, such as incubation period, PrPSc biochemical
profile (e.g., electrophoretic mobility and glycoform ratio) and distribution of
brain lesions. Importantly, such different features are maintained after
inoculation of a prion strain into genetically identical hosts and are
relatively stable across serial passages.
This review focuses on the characterization of prion strains and on the
wide range of important implications that the study of prion strains involves.
Introduction
Transmissible spongiform encephalopathies (TSEs) or prion diseases, such as
Creutzfeldt-Jakob disease (CJD) in human, bovine spongiform encephalopathy (BSE)
in cattle, chronic wasting disease (CWD) in cervids and scrapie in sheep, are a
group of fatal neurodegenerative disorders. The major neuropathological
hallmarks of TSEs are extensive spongiosis, neuronal cell loss in the central
nervous system, gliosis,1 and deposition of amyloid plaques.2
Prions are infectious proteins that are responsible for transmissible
spongiform encephalopathies (TSEs) and consist primarily of scrapie prion
protein (PrPSc), a pathogenic isoform of the host-encoded cellular prion protein
(PrPC). The absence of nucleic acids as essential components of the infectious
prions is the most striking feature associated to these diseases. Additionally,
different prion strains have been isolated from animal diseases despite the lack
of DNA or RNA molecules. Mounting evidence suggests that prion-strain-specific
features segregate with different PrPSc conformational and aggregation states.
Strains are of practical relevance in prion diseases as they can
drastically differ in many aspects, such as incubation period, PrPSc biochemical
profile (e.g., electrophoretic mobility and glycoform ratio) and distribution of
brain lesions. Importantly, such different features are maintained after
inoculation of a prion strain into genetically identical hosts and are
relatively stable across serial passages.
This review focuses on the characterization of prion strains and on the
wide range of important implications that the study of prion strains involves.
...
snip...
This classification arises from the hypothesis that if the polymorphism 129
can modulate the phenotype of the familial prion diseases (fCJD and FFI, as
explained earlier in this review), then probably it can modulate also that of
sporadic prion diseases, justifying their heterogeneity. According to this
hypothesis, the cases affected by sCJD were divided into six groups according to
the genotype of the polymorphism in position 129 and the type of PrPSc. Then,
the phenotypes of every group were analyzed to evaluate the homogeneity within
every group. The results have permitted a molecular sub-classification of the
sCJD.90,91 However, this classification seems not to be sufficient to explain
the complexity of the sporadic form of CJD. In fact, in some molecular subtypes,
additional variants have been reported, such as MM or VV patients with amyloid
plaques, which are absent in the majority of patients with these genotypes.44
Moreover, among patients belonging to the same subgroup, important phenotypic
differences can be found, such as, for instance, the extent of neuronal loss or
PrPSc deposition differences.92
Even at the biochemical level the complexity is higher: indeed, aside from
the migratory differences of the PrPSc of types 1 and 2, there are other
properties that could be important during the propagation of the strain, like
the presence of other fragments derived from differential cleavage at the C- and
N-terminus of the protein, which probably coincide with the presence of other
forms of PrPSc with different resistance to PK digestion.44 All these molecular
classifications are based upon the principle that in all CNS districts the type
of PrPSc is the same, but there are pieces of evidence pointing to the fact that
different types of PrPSc can be found in different brain areas.64,93 The first
evidence of the presence of more than one form of PrPSc in the brain of a sCJD
patient was reported by Puoti in 1999.94 These different types of PrPSc can be
found to coexist in the same brain region or they can infect distinct districts.
Such co-infection influences the vacuolization and the amyloid aggregates
formation.95 Even the ratio between the different glycoforms is determined in a
regionspecific manner according to the type of PrPSc (1 or 2) and the genotype
of codon 129.
The high degree of phenotypic heterogeneity characterizing sCJD90 can lead
to the conclusion that transmission studies will probably identify a broad panel
of different prions with a great divergence between strains. However, quite
surprisingly, many of the recent studies focusing on the characterization of
sCJD subtypes have shown that there is a strong tendency to converge to a
limited number of strains. This aspect can find an explanation considering the
selection conditions, already described in this review, mediated by the
environment in which the prion replicates and by the differences in the amino
acid sequence of the PrPC. In particular, studies with bank voles96 and mice97
lead to results that support the idea that there are two principal strains
responsible of the sCJD, M1 and V2, and two potential strains, M2 and V1, which
need further studies to be confirmed.
Different is the case of vCJD. vCJD has been observed in 12 different
countries, but in every registered case the same clinical and pathological
characteristics have been found.39 In particular, the PrPSc responsible of the
vCJD shows a peculiar WB profile, with the unglycosylated form of the
protease-resistant PrPSc of 19 kDa (type 2) and a higher representation of the
diglycosilated PrPSc (PrPSc 2B) compared with sCJD.39 Nevertheless, using
specific antibodies against type 1 PrPSc, a small amount of PrPSc type 1 with a
high percentage of diglycosilated form can be detected in association with PrPSc
2B.98 The 2B type is a useful marker for identifying the replication of BSE
prions also in other species, including non-human primates.99 In addition,
unlike sporadic and genetic CJD, in vCJD the same biological marker (2B type)
has been found in all the analyzed brain areas.100 This strong biochemical and
pathological homogeneity is in agreement with the hypothesis of the existence of
a unique strain. However, unexpectedly, typization experiments of the strains in
different transgenic models have given divergent results. In one of these
studies, in a context of homotropic transmission, transgenic mice expressing
high levels of human PrPC-M129 were inoculated with vCJD isolates coming from
France and from the UK.101 All of the French isolates propagated as vCJD, with
abundant amyloid plaques and presence of PrPSc 2B.102 Instead, the isolates from
the UK led to the propagation of either vCJD or sCJD.103 In particular, the
incubation time was shorter and the lesion profile was different compared with
the one obtained with the propagation of the classical vCJD strain. Moreover,
early replication of the typical agent of the vCJD in lymphoid tissues was
detected, indicating that both strains were present in the inoculum.
This new strain with phenotypical features that were similar to sCJD was
found to be of type 1 and the transmission in transgenic mice expressing the
bovine PrPC failed, unlike the vCJD classical strain (Type 2B).26 The idea that
the infection of vCJD contains a minor component of sCJD prions is supported by
many pieces of evidence such as the presence of this prion strain at the first
passage or the persistence of both types of PrPSc through serial passages in
mice.98 In conclusion, although vCJD is one of the most standardized phenotypes
among the prion human diseases characterized by a typical form of PrPSc, the
transmission studies of vCJD have shown the great potential of divergence of
prions, contrary to the results obtained from the studies of sCJD. This data
challenge our ability to recognize the pathologies that can derive from the
divergence of the BSE strains when they infect humans, both at the pathological
and at the biochemical level.
Conclusion
The discovery of prions has led to new interpretations of the pathogenetic
mechanism of protein misfolding diseases. Indeed, the common thought was that a
protein misfolding disease could only be caused by a mutation in the primary
sequence of an endogenous protein, but the discovery of prions changed this
view. In fact, it was demonstrated that a seed of misfolded protein can arise
from an exogenous infectious protein, which is able to act as a template or as a
catalyst for the formation of new aberrant protein.5,6 Importantly, new evidence
shows how processes similar to those described for prions could be implicated in
the propagation of misfolded proteins of other neurodegenerative pathologies
like Alzheimer disease, Parkinson disease, Huntington disease and amyotrophic
lateral sclerosis.104,105
Certainly, one of the most puzzling aspects in the prion field is the
existence of different strains of an infectious protein. Nevertheless, such
diversity can be accommodated within the protein-only hypothesis, as several
robust pieces of experimental evidence indicate that strain-specificity is
encoded at the level of the different conformations that the pathogenic protein
can adopt. The identification of factors and mechanisms influencing the
generation of new prion strains or the selection, from a conformationally
heterogeneous PrPSc population, of the most suitable prion conformation in a
specific environment, represents an important milestone toward the understanding
of the mechanisms of prion strain diversity, which can have fundamental clinical
and therapeutic implications. Although considerable advances have been made in
the understanding of the phenomenon of prion strains, many pieces of information
are still missing, foremost among them the definitive evidence for the
structural nature of the differences between prion strains.
Thursday, February 21, 2013
National Prion Disease Pathology Surveillance Center Cases Examined January
16, 2013
16 YEAR OLD SPORADIC FFI ?
Monday, January 14, 2013
Gambetti et al USA Prion Unit change another highly suspect USA mad cow
victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes
along with this BSe
Monday, December 31, 2012
Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State,
2006–2011-2012
Tuesday, December 25, 2012
CREUTZFELDT JAKOB TSE PRION DISEASE HUMANS END OF YEAR REVIEW DECEMBER 25,
2012
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, June 13, 2012
MEXICO IS UNDER or MIS DIAGNOSING CREUTZFELDT JAKOB DISEASE AND OTHER PRION
DISEASE SOME WITH POSSIBLE nvCJD
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion
poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank
voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1
Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan
Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome,
Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna,
Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently
described “sporadic”neurodegenerative disease involving prion protein
aggregation, which has clinical similarities with non-Alzheimer dementias, such
as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in
Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the
prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is
the electrophoretic pattern of PrPSc after digestion with proteinase K (PK).
After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern
similar to that described in GSS cases. The clinical and pathological features
of VPSPr raised the question of the correct classification of VPSPr among prion
diseases or other forms of neurodegenerative disorders. Here we report
preliminary data on the transmissibility and pathological features of VPSPr
cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic
lines of bank voles, carrying either methionine or isoleucine at codon 109 of
the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases
selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical
diagnosis in voles was confirmed by brain pathological assessment and western
blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission
in BvM109. Overall, 3 voles were positive with survival time between 290 and 588
d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form
of the typical PrP27–30, which was indistinguishable to that previously observed
in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until
now. Overall, 5 voles were positive with survival time between 281 and 596
d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like
PrPSc electrophoretic pattern, characterized by low molecular weight PrPres.
These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative
with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus
and the N-terminus. Second passages are in progress from these first successful
transmissions.
Conclusions. Preliminary results from transmission studies in bank voles
strongly support the notion that VPSPr is a transmissible prion disease.
Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of
voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and
animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion
diseases might be wider than expected and raises crucial questions about the
epidemiology and strain properties of these new forms. We are investigating this
latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
Wednesday, March 28, 2012
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion
poker goes up again $
Wednesday, March 20, 2013
GAO-13-244, Mar 18, 2013 Dietary Supplements FDA May Have Opportunities to
Expand Its Use of Reported Health Problems to Oversee Product
From: Terry S. Singeltary Sr.
Sent: Tuesday, March 19, 2013 2:46 PM
To: gomezj@gao.gov
Wednesday, February 20, 2013
World Organization for Animal Health Recommends United States' BSE Risk
Status Be Upgraded
Statement from Agriculture Secretary Tom Vilsack:
Thursday, February 14, 2013
The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and
TSE prion disease
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
Sunday, April 18, 2010
SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible
Spongiform Encephalopathies of Small Ruminants, France, 2002-2009
Volume 17, Number 1 January 2011
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform
encephalopathy following passage in sheep
Monday, April 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5-May 2011
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
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, March 18, 2013
PROCEEDINGS ONE HUNDRED AND FIFTEENTH ANNUAL MEETING of the UNITED STATES
ANIMAL HEALTH ASSOCIATION September 29 – October 5, 2011
TSS
