Saturday, February 07, 2015

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

 


 
Wednesday, January 28, 2015

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

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