Annual report Creutzfeldt-Jakob disease surveillance in Australia, 2013
Annual report Creutzfeldt-Jakob disease surveillance in Australia,
2013
Commun Dis Intell Q Rep. 2014 Dec 31;38(4):E348-55.
Creutzfeldt-Jakob disease surveillance in Australia, update to December
2013
Genevieve M Klug, Alison Boyd, Shannon Sarros, Christiane Stehmann, Marion
Simpson, Catriona McLean, Colin L Masters, Steven J Collins
Abstract
Nation-wide surveillance of transmissible spongiform encephalopathies
including Creutzfeldt-Jakob disease, is performed by the Australian National
Creutzfeldt-Jakob Disease Registry, based at the University of Melbourne.
Surveillance has been undertaken since 1993. Over this dynamic period in
transmissible spongiform encephalopathy research and understanding, the unit has
evolved and adapted to changes in surveillance practices and requirements, the
emergence of new disease subtypes, improvements in diagnostic capabilities and
the overall heightened awareness and understanding of Creutzfeldt-Jakob disease
and other transmissible spongiform encephalopathies in the health care setting.
In 2013, routine surveillance continued and this brief report provides an update
of the surveillance data collected by the Australian National Creutzfeldt-Jakob
Disease Registry prospectively from 1993 to December 2013, and retrospectively
to 1970. The report highlights the recent multi-national collaborative study
published that has verified the correlation between surveillance intensity and
reported disease incidence.
Commun Dis Intell 2014;38(4):E348–E355.
Keywords: Creutzfeldt-Jakob disease, prion disease, transmissible
spongiform encephalopathy, disease surveillance
Table 2: Classification of Australian National Creutzfeldt-Jakob Disease
Register cases, Australia, 1970 to 2013
Classification Sporadic Familial Iatrogenic Variant CJD Unclassified
Total
Definite 448 49 5* 0 0 502
Probable 241 11 4 0 0 256
Possible 14 0 1 0 0 15
Incomplete 216† 216
Total 703 60 10 0 216 989
* Includes 1 definite iatrogenic case who received pituitary hormone
treatment in Australia but disease onset and death occurred while a resident of
the United Kingdom. This case is not included in statistical analysis since
morbidity and mortality did not occur within Australia.
† includes 136 living cases.
snip...
As of 31 December 2013, there were 989 cases on the register with 757 of
these being classified as probable or definite CJD cases. An additional definite
iatrogenic case who was treated in Australia, and died in the United Kingdom is
included in Table 2; however this case is not classified as an Australian case
due to the location at death and is thereby excluded from the overall
statistical analysis of Australian CJD cases. Since the start of surveillance,
663 suspected prion disease cases have been excluded from the register after
detailed follow-up, with 25 of these being excluded in 2013 (19 after
neuropathological examination).
In 2013, 20 cases were re-classified from incomplete to definite prion
disease, 4 cases to probable and a single case who died in 2002 was
re-classified as possible sporadic CJD, bringing the total number of possible
cases to 15. Fourteen of these cases were sporadic and one was iatrogenic CJD
(Table 2). Of the 216 incomplete cases, 136 are presently alive. In 2013, the
number of incomplete cases under evaluation by the ANCJDR has remained
consistent with the number of incomplete cases in 2012. In contrast, there has
been a 50% reduction in the number of cases excluded from the register and a 35%
reduction in the number of cases classified from incomplete to definite,
probable or possible in 2013 compared with 2012.
snip...
The number of cases classified as definite and probable prion diseases in
2013 (24 cases) is smaller than the number classified in 2012 (39 cases).
Definite case classification declined marginally (16% decrease) in 2013 and
probable case classifications were 70% lower. An explanation for the lower
levels of classifications and exclusion of register cases is in part due to the
inflation of the number of cases classified or excluded in 2012 due to concerted
efforts by the ANCJDR to classify outstanding cases. After an exceptional year
of case classification in 2012, classifications were expected to be lower in
2013 in comparison and return to pre-2012 levels. The ANCJDR aims to maintain a
consistent level of case classification with attention focused on probable case
classification in 2014.
Despite the decrease in suspected case notifications in 2012, the incidence
rate in 2012 has been maintained at expected levels (1.1 cases per million per
year). This provides some reassurance that while case notifications have been
lower in 2012, the ANCJDR has maintained the ability to detect the expected
annual number of prion disease cases in the Australian population despite
changes to ANCJDR approaches. No firm conclusions can be made regarding whether
these trends will continue in 2013 as the incidence rates are provisional at the
time of reporting; however the number of definite cases are predicted to be
lower than expected in 2013 due to the suspension of the Queensland autopsy
service.
The proportion of annual TSE cases due to genetic prion disease has
returned to expected levels during 2013. This is pleasing given the concerns in
2012 that genetic prion disease was under-ascertained between 2009 and 2012,
possibly due to the de-centralisation of genetic services to external
laboratories and a disconnect with the ANCJDR regarding genetic testing
outcomes. Processes have been established in order to redress this issue by
genetic services (in conjunction with the CJD support group network), and this
has in part contributed to an increased number of genetic prion disease cases
classified in 2013. While these processes will prove valuable for case
classification in future, the majority of the genetic prion disease identified
in 2013 was classified after case investigation, underscoring the utility and
importance of comprehensive case evaluation by the ANCJDR.
CDI Vol 38 No 4 2014 E351
vpspr ???
Thursday, August 05, 2010 Surveillance of Creutzfeldt-Jakob disease in
Australia: 2010 update
Interestingly, when you have cases of cjd increasing yearly, it's
supposedly due to better surveillance etc. yet here we see, cjd _decreased_ in
2009, and only a few bumps up and down since 2000, pretty much holding the same,
and this is with _better_ surveillance. so, really, the myth that sCJD increases
due to better surveillance, is just that, a myth. sporadic cjd and nvCJD
increased with countries with BSE, and as the feed ban was put into place and
enforcement took hold, BSE cases dropped, along with nvCJD cases and sporadic
CJD cases in BSE countries. interesting is it not. However, I wonder how this
would play out over the next decade or so, if Australia starts importing
products from BSE mad cow Countries ??? something to ponder for sure, down
under. ...TSS
Thursday, August 05, 2010
Surveillance of Creutzfeldt-Jakob disease in Australia: 2010 update
Saturday, November 09, 2013
Surveillance for creutzfeldt-Jakob disease in Australia: update to December
2012
Background of Australian Human Pituitary Hormone Program From 1967 until
1985 2,100 Australians were treated with human pituitary hormones under the
Australian Human Pituitary Hormone Program (AHPHP).
In similar programs in overseas countries the majority of recipients of
human pituitary hormones (hPH) were treated with human growth hormone (hGH) for
short statue. In Australia the Australian Human Pituitary Hormone Program
(AHPHP) treated approximately 1570 woman and about 60 men for infertility using
human pituitary gonadotrophin (hPG). Approximately 660 Australian children were
treated for short statue with human growth hormone (hGH).
Five Australians may so far have developed and died from health-care
associated (iatrogenic) Creutzfeldt-Jakob disease (CJD) after hPH treatment .
The program was suspended in 1985 following CJD deaths of recipients of hGH in
the United States and England.
All those treated with hPH are at low risk of developing CJD. There is no
way of knowing if batches received by recipients were contaminated. To date
there is no test to show if recipients are incubating CJD.
The AHPHP was run under the auspices of the Commonwealth Department of
Health. The hormones were manufactured by the then government-owned Commonwealth
Serum Laboratories in Melbourne.
The AHPHP was conceived and operated by the Human Pituitary Advisory
Committee (HPAC) until its activities ceased in 1985 and the committee was
disbanded.
From 1992 intense media and political pressure followed news of the first
two deaths from iatrogenic CJD as the families demanded an explanation. The then
Minister for Health, Senator Graham Richardson, ordered an independent
inquiry.
Associate Professor Margaret Allars, an administrative law expert from the
University of Sydney conducted the inquiry into the use of Pituitary Derived
Hormones in Australia and Creutzfeldt-Jakob Disease, which reported in June
1994.
The inquiry report made a number of recommendations concerning the care of
recipients, the establishment of support services and the formation of a
ministerial advisory council.
Recipients of hPH now live with a health status of being at “low risk” of
CJD. Current infection control guidelines refer to “low risk” patients.
Recipients and their families also live with anxiety linked to the threat of
contracting a disease which can lie dormant for decades and for which there is
no test, treatment or cure.
Tuesday, November 23, 2010
Prosecutors call for prison terms for CJD growth hormone doctors
Tuesday, May 04, 2010
Review of the Human Pituitary Trust Account and CJD Issue 20 January
2010
Creutzfeldt-Jakob Disease, CJD Support Group for short statured children of
the 1970's and 1980's. Recommendations for Unapproved/Unregistered recipiants
wonder how Michael is doing today ??? hope is all well...
Mr. Michael O'Meara
Senator Bernardi Senator for South Australia Michael O’Meara 120 Port Road
P.O. Box 250 Hindmarsh SA 5007 Kinglake 3763 24th February 24, 2009
Dear Senator Bernardi
Re; Senate Committee Inquiry on Men’s Health
It is with regret that the 60 page submission I was preparing for this
inquiry was lost in the recent Kinglake Bushfire, along with all other property
and possessions of mine, and I now submit an abbreviated submission. Under such
personal adversity, I believe this submission falls within the Terms of
Reference.
Its is with pleasure that this submission be accepted in accordance with
your Notice Of Motion (276) published in November 2008, some 5 months after a
Private Member Motion was read in the House of Representatives. The Member for
McEwen (Ms Fran Bailey) read a very emotional speech in the House (Committee
Room) on 16th June 2008, supported by the Member for Moore, (Dr Mal Washer) and
further with bipartisan support by the Rudd Government - expressed by the
Members of Page, (Ms Janelle Saffin) and Dobell, (Mr. Craig Thomson)
It is with my pleasure that I submit the following Submission on behalf of
myself and all other (then) boys and men treated with Human Pituitary Hormones,
unofficially, and not recorded, under the Australian Human Pituitary Hormone
Program, and who have suffered, with both short term and long term side effects
to the male endocrine system as a result of such Human Experimentation, and with
such side effects that are irreversible.
Approved Recipients of Human Growth Hormone or Human Pituitary
Gonadotrohpin were subjected to a Senate Inquiry in 1993, known as “The Allars
Inquiry”, however – unapproved and/or “Off Program” recipients who were not
included in the Allars Inquiry, and whom were not disclosed to the Department of
Health and Aging, who are at the same risk of CJD, and were never advised of
their risk, particularly unrecorded recipients of hPG at Prince Henry’s Hospital
in Melbourne – hundreds of males. The Senate now records (1998) the “Allars
Inquiry” was misled.
It is these Males who were “overtreated” with Human Pituitary
Gonadotrophin1, who were “overstimulated” through invivo experimentation, with
batches varying2 and causing dire consequences to physical, mental and
reproductive health - those who were exposed to anabolic steroids (a
carcinogenic) as a Growth Promotant with severe side effects. Particular
Recommendations were presented and submitted to The Minister for Heath by
Professor Margaret Allars in 1994, and further explored by the Senate Affairs
Reference Committee in 1998. Of these numerous recommendations, I draw
particular reference to Recommendation 5 m stating
That the settlement offer should not preclude a plaintiff making any future
claim in relation to: (a) Other physical illnesses contracted by recipients
which may be related to long term side effects of HPH treatment3 This submission
is dedicated to the Infant boys, Toddlers boys, Prepubescent boys, Teenage boys,
Young, Middle Aged and Elderly Men aged 2 to 101 – who were treated under such
experimental Programs, exposed to Endocrine Disruptors during the 1970’s,
particularly those whom were castrated and sterilized by the Australian
Government and/or representatives engaged under the Health Act 1958. Such
Section with the Act has since been repealed so that the “experimental nature”
of “The Program” cannot happen again - following the “Allars Inquiry”. This does
not repeal or repair the ongoing side effects. In particular, I dedicate this
submission to the memory of the child who lost his life under these experimental
programs at Prince Henry’s Hospital during the 1970’s4.
Please accept my gratitude with appreciation with your efforts in this
forthcoming Inquiry.
Yours Faithfully
Michael O’Meara
PDF 159KB
see also ;
Michael was recruited into the growth hormone clinic at Prince Henry's
Hospital in 1972 when he was just 10 years old. He was subjected to deep sleep
therapy in April 1972. At this time he was administered the human growth hormone
using products from cadavers. It has since been found that some of this material
was contaminated, with a number of young recipients subsequently contracting and
dying of the deadly Creutzfeldt-Jakob disease, or CJD.
also, I always remember this old study here, fascinating to me, just how
little, and how long, yet still deadly for some, why ?
J Neurol Neurosurg Psychiatry 2002;72:792-793 doi:10.1136/jnnp.72.6.792
Short report
Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth
hormone
E A Croes1, G Roks1,*, G H Jansen3, P C G Nijssen2, C M van Duijn1
+ Author Affiliations 1Genetic Epidemiology Unit, Department of
Epidemiology and Biostatistics, Erasmus University Medical Centre Rotterdam, PO
Box 1738, 3000 DR Rotterdam, Netherlands 2Department of Neurology, St Elisabeth
Hospital, PO Box 90151, 5000 LC Tilburg, Netherlands 3Department of Pathology,
University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht,
Netherlands
Correspondence to: Professor C M van Duijn, Genetic Epidemiology Unit,
Department of Epidemiology and Biostatistics, Erasmus University Medical Centre
Rotterdam, PO Box 1738, 3000 DR Rotterdam, Netherlands; vanduijn@epib.fgg.eur.nl
Received 27 December 2001 Accepted 12 March 2002 Revised 1 March 2002
Abstract
A 47 year old man is described who developed pathology proven
Creutzfeldt-Jakob disease (CJD) 38 years after receiving a low dose of human
derived growth hormone (hGH) as part of a diagnostic procedure. The patient
presented with a cerebellar syndrome, which is compatible with iatrogenic CJD.
This is the longest incubation period described so far for iatrogenic CJD.
Furthermore, this is the first report of CJD after diagnostic use of hGH. Since
the patient was one of the first in the world to receive hGH, other cases of
iatrogenic CJD can be expected in the coming years.
snip...
An incubation period as long as 38 years had never been reported for
iatrogenic CJD. Huillard d'Aignaux et al7 studied the incubation period in 55
patients with hGH related CJD in a cohort of 1361 French hGH recipients. The
median incubation period was between 9 and 10 years. Under the most pessimistic
model, the upper limit of the 95% confidence interval varied between 17 and 20
years. Although the infecting dose cannot be quantified, it can be speculated
that the long incubation period in our patient is partly explained by the
administration of a limited amount of hGH. This hypothesis is supported by
experimental models, in which higher infecting doses usually produce shorter
incubation periods.6 Since our patient was one of the first in the world to
receive hGH, this case indicates that still more patients with iatrogenic CJD
can be expected in the coming years. Another implication of our study is that
CJD can develop even after a low dose of hGH. This case once more testifies that
worldwide close monitoring of any form of iatrogenic CJD is mandatory.
SHORT REPORT
Creutzfeldt-Jakob disease 38 years after diagnostic use of human growth
hormone
the warning shots fired over the bow of the boat that were never heard ;
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...
NON-LICENSED HUMAN TISSUE DEVICES WERE NOT COMMERCIALLY AVAILABLE
snip...
I was quite prepared to believe in unofficial pituitary hormones, also in
the 1970's, whether as described by Dr. Little, or in other circumstances, for
animal use.
snip...
The fact that there were jars of pituitaries (or extract) around on shelves
is attested by the still potent 1943 pituitaries, described in Stockell Hartree
et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the
trouble to collect them, they were not lightly thrown out...
Thursday, October 7, 2010
Australia first documented case of atypical scrapie confirmed
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions
Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves
Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle
Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia
Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1,
Affiliations Contributions Corresponding author Journal name: Nature
Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821
Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014
Article tools Citation Reprints Rights & permissions Article metrics
Abstract
Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant
Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie
prions remains unknown. Mice genetically engineered to overexpress the human
prion protein (tgHu) have emerged as highly relevant models for gauging the
capacity of prions to transmit to humans. These models can propagate human
prions without any apparent transmission barrier and have been used used to
confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie
prions transmit to several tgHu mice models with an efficiency comparable to
that of cattle BSE. The serial transmission of different scrapie isolates in
these mice led to the propagation of prions that are phenotypically identical to
those causing sporadic CJD (sCJD) in humans. These results demonstrate that
scrapie prions have a zoonotic potential and raise new questions about the
possible link between animal and human prions.
Subject terms: Biological sciences• Medical research At a glance
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01 Most doctors believe that sCJD is caused by a prion protein
deforming by chance into a killer. But Singeltary thinks otherwise. He is one of
a number of campaigners who say that some sCJD, like the variant CJD related to
BSE, is caused by eating meat from infected animals. Their suspicions have
focused on sheep carrying scrapie, a BSE-like disease that is widespread in
flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb...
2001
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep
infected with scrapie?
28 Mar 01
Like lambs to the slaughter
31 March 2001
by Debora MacKenzie Magazine issue 2284.
FOUR years ago, Terry Singeltary watched his mother die horribly from a
degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary
was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded
an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Most doctors believe that sCJD is caused by a prion protein deforming by
chance into a killer. But Singeltary thinks otherwise. He is one of a number of
campaigners who say that some sCJD, like the variant CJD related to BSE, is
caused by eating meat from infected animals. Their suspicions have focused on
sheep carrying scrapie, a BSE-like disease that is widespread in flocks across
Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight
to the campaigners' fears. To their complete surprise, the researchers found
that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by
some strains of scrapie," says team member Jean-Philippe Deslys of the French
Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses,
south-west of Paris. Hans Kretschmar of the University of Göttingen, who
coordinates CJD surveillance in Germany, is so concerned by the findings that he
now wants to trawl back through past sCJD cases to see if any might have been
caused by eating infected mutton or lamb.
Scrapie has been around for centuries and until now there has been no
evidence that it poses a risk to human health. But if the French finding means
that scrapie can cause sCJD in people, countries around the world may have
overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD. They
injected the brains of macaque monkeys with brain from BSE cattle, and from
French and British vCJD patients. The brain damage and clinical symptoms in the
monkeys were the same for all three. Mice injected with the original sets of
brain tissue or with infected monkey brain also developed the same
symptoms.
As a control experiment, the team also injected mice with brain tissue from
people and animals with other prion diseases: a French case of sCJD; a French
patient who caught sCJD from human-derived growth hormone; sheep with a French
strain of scrapie; and mice carrying a prion derived from an American scrapie
strain. As expected, they all affected the brain in a different way from BSE and
vCJD. But while the American strain of scrapie caused different damage from
sCJD, the French strain produced exactly the same pathology.
"The main evidence that scrapie does not affect humans has been
epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute
for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not
there are many sheep, and in countries such as New Zealand with no scrapie." In
the only previous comparisons of sCJD and scrapie in mice, Bruce found they were
dissimilar.
But there are more than 20 strains of scrapie, and six of sCJD. "You would
not necessarily see a relationship between the two with epidemiology if only
some strains affect only some people," says Deslys. Bruce is cautious about the
mouse results, but agrees they require further investigation. Other trials of
scrapie and sCJD in mice, she says, are in progress.
People can have three different genetic variations of the human prion
protein, and each type of protein can fold up two different ways. Kretschmar has
found that these six combinations correspond to six clinical types of sCJD: each
type of normal prion produces a particular pathology when it spontaneously
deforms to produce sCJD.
But if these proteins deform because of infection with a disease-causing
prion, the relationship between pathology and prion type should be different, as
it is in vCJD. "If we look at brain samples from sporadic CJD cases and find
some that do not fit the pattern," says Kretschmar, "that could mean they were
caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence
elsewhere. Singeltary and other US activists think that some of these people
died after eating contaminated meat or "nutritional" pills containing dried
animal brain. Governments will have a hard time facing activists like Singeltary
if it turns out that some sCJD isn't as spontaneous as doctors have
insisted.
Deslys's work on macaques also provides further proof that the human
disease vCJD is caused by BSE. And the experiments showed that vCJD is much more
virulent to primates than BSE, even when injected into the bloodstream rather
than the brain. This, says Deslys, means that there is an even bigger risk than
we thought that vCJD can be passed from one patient to another through
contaminated blood transfusions and surgical instruments.
Friday, January 30, 2015
*** Scrapie: a particularly persistent pathogen ***
price of prion poker goes up again with this study. I strongly urge the
United States FDA et al to revisit their failed ruminant mad cow feed ban, where
still to this day, the feed ban does NOT include cervids. ...
Saturday, January 31, 2015
European red deer (Cervus elaphus elaphus) are susceptible to Bovine
Spongiform Encephalopathy BSE by Oral Alimentary route
Sunday, December 28, 2014
CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA
USAHA INC DECEMBER 28, 2014
CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD
$$$
CWD, spreading it around...
Tuesday, January 06, 2015
APHIS Provides Additional Information on Chronic Wasting Disease (CWD)
Indemnity Requests January 5, 2015 05:26 PM EST
ruminant feed ban for cervids in the United States ?
Posted by flounder on 31 Jan 2015 at 20:14 GMT
*** Singeltary reply ;
Molecular, Biochemical and Genetic Characteristics of BSE in Canada
Saturday, January 31, 2015
RAPID ADVICE 17-2014 : Evaluation of the risk for public health of casings
in countries with a “negligible risk status for BSE” and on the risk of
modification of the list of specified risk materials (SRM) with regard to BSE
Saturday, January 24, 2015
Bovine Spongiform Encephalopathy: Atypical Pros and Cons
*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD
strains, TSE prion aka Mad Cow Disease United States of America Update December
14, 2014 Report ***
UPDATE* NOVEMBER 16, 2014 vpspr, sgss, sffi, TSE, an iatrogenic by-product
of gss, ffi, familial type prion disease, what it ???
Friday, January 10, 2014
Greetings again Friends, Neighbors, and Colleagues,
I would kindly like to follow up on ‘vpspr, sgss, sffi, TSE, an iatrogenic
by-product of gss, ffi, familial type prion disease, what it ???’ ran across an
old paper from 1984, that some might find interest in, and I will update the
link with this old science paper from 1984, a 2010 paper from Japan, and some
information on scrapie transmission. The paper from Japan first, then the 1984
paper, and then the scrapie transmission studies.
***The occurrence of contact cases raises the possibility that transmission
in families may be effected by an unusually virulent strain of the agent.
From: Terry S. Singeltary Sr.
Sent: Saturday, November 15, 2014 9:29 PM
To: Terry S. Singeltary Sr.
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL
1984
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
R. G. WILL
1984
snip...
Friday, January 10, 2014
*** vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial
type prion disease, what it ??? ***
Sunday, April 06, 2014
SPORADIC CJD and the potential for zoonotic transmission there from, either
directly or indirectly via friendly fire iatrogenic mode, evidence to date
Thursday, January 22, 2015
Transmission properties of atypical Creutzfeldt-Jakob disease: a clue to
disease etiology?
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
BOVINE HEPARIN POSITION STATEMENT ON THE REINTRODUCTION and POTENTIAL BSE TSE PRION RISK FACTORS THEREFROM http://transmissiblespongiformencephalopathy.blogspot.com/2015/01/bovine-heparin-position-statement-on.html
Friday, February 06, 2015
Evaluation of the protection of primates transfused with variant
Creutzfeldt-Jakob disease–infected blood products filtered with prion removal
devices: a 5-year update
Saturday, December 13, 2014
*** Terry S. Singeltary Sr. Publications TSE prion disease Peer Review
***
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
snip...
Terry S. Singeltary Sr. Bacliff, Texas USA 77518
posted by Terry S. Singeltary Sr. at
9:06 PM
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