Wednesday, October 09, 2013

WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY, £41,078,281 in compensation

WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY,  £41,078,281 in compensation


CJD


Mr Gray: To ask the Secretary of State for Health (1) if he will make a statement on the commutation policy with regard to relations of deceased sufferers of variant CJD; [169435]


(2) how many claims against his Department made by relations of victims of variant CJD have been settled out of court in the most recent period for which records are available. [169436]



 Dr Poulter: No claims have been settled out of court by the Department in relation to variant Creutzfeldt Jakob disease (vCJD).



 The vCJD Trust, set up by Government in 2000, disburses no-fault compensation to vCJD patients and their families. The latest available figures, 12 September 2013, show that the trust has paid out £41,078,281 in compensation.



 Since March 2012, it is the trust’s policy to increase the basic sum payable to each case, from an initial figure of £120,000, by 2% annually. As of March 2013, the sum payable is £124,848.




enough of the UKBSEnvCJD only theory and the chosen ones crap...enough is enough. it is what it is. it’s the very reason why they are paying these families off, to keep them quite, and the very reason human TSE continues to spread across the globe, and as long as this 3 decade old industry fed science is digested by the very ones that have lost loved ones to human TSE, and attitudes there from, i.e. ONLY ME NVcjd, it will continue to spread. one strain of scrapie, one strain of TSE i.e. c-BSE in cattle there from, nvCJD in humans there from, in one geographical location, when the feeding and rendering practices mirroed that of the UK, with the USA developing the ‘continuous rendering’ technology that supposedly started this mess, and sending it to the UK, for them to start using first, then the USA to follow some 5 years later or so, with the USA awash in animal TSE prion disease in many different species, more so than any other country in the world (excluding zoo animals infected with TSE), all rendered and fed back to food producing animals for human and animal, ...it’s junk science, either ironside was wrong on the 1st 10, or Gambetti is wrong on his first 10, because you can’t have your cake and eat it too...like it or not, the term ‘chosen ones’ is what it is, nvCJD, and the bogus science there from, was chosen by the industry and the government, don’t believe me, just ask vickey rimmer. ...
 

Sent: Monday May 28, 2007
 
Subject: THE BIG LIE SPORADIC CJD AND MAD COW DISEASEs i.e. TSE
 
Terry S. Singeltary Sr.
 
POLICY IN CONFIDENCE; CONFIDENTIAL; CJD IN FARMER WITH BSE COW ie OCCUPATIONAL EXPOSURE
 
Subject: POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
 
POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
 
LIKELY TO ATRACT MEDIA ATTENTION
 
snip...
 
DOES ANYONE BESIDES ME SEE A PATTERN YET ???
 
Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.
 
SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.
 
Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.
 
snip...
 
Sporadic creutzfeldt-jakob disease in two adolescents
 
 
 

see full text sporadic CJD the big lie;
 
Subject: Sporadic creutzfeldt-jakob disease in two adolescents
 
From: "Terry S. Singeltary Sr." <[log in to unmask]>
 
Reply-To: Sustainable Agriculture Network Discussion Group <[log in to unmask]>
 
Date: Mon, 28 May 2007 10:25:25 -0500 Content-Type: text/plain Parts/Attachments: text/plain (946 lines)
 
Subject: Sporadic creutzfeldt-jakob disease in two adolescents (see sCJD, the big lie) Date: May 28, 2007 at 7:58 am PST
 
J Neurol Neurosurg Psychiatry. Published Online First: 23 May 2007. doi:10.1136/jnnp.2006.104570 © 2007 by BMJ Publishing Group Ltd
 
Original articles
 
Sporadic creutzfeldt-jakob disease in two adolescents
 
K Murray 1, D L Ritchie 1, M Bruce 2, C A Young 3, M Doran 3, J W Ironside 4 and R G Will 4* 1 NationalCJD Surveillance Unit, United Kingdom 2 Neuropathogenesis Unit, United Kingdom 3 Walton Centre for Neurology and Neurosurgery, United Kingdom 4 National CJD Surveillance Unit, United Kingdom
 
* To whom correspondence should be addressed. E-mail: [log in to unmask]
 
Accepted 15 April 2007
 
Abstract
 
Background: Sporadic Creutzfeldt-Jakob disease (CJD) is a condition predominantly affecting older age groups, with cases aged less than 45 years rare and an age at onset or death of less than 20 years exceptional.
 
Methods: Data from the systematic study of sporadic CJD in the UK are available from 1970 onwards. Clinical and pathological data are reviewed in order to identify atypical cases, including those at the extremes of the age range of sporadic CJD. Detailed analysis of atypical cases is undertaken and in selected cases laboratory transmission studies are carried out in order to provide information on the characteristics of the infectious agent.
 
Results: In the UK two cases of sporadic CJD in adolescents have been identified, dying aged 16 and 20 years. The first case predated the epidemic of bovine spongiform encephalopathy and the characteristics of the second case, including laboratory transmission studies, are consistent with a diagnosis of sporadic rather than variant CJD.
 
Conclusion: The cases in this report indicate that sporadic CJD can develop at a very young age, that variant CJD is not the only form of CJD occurring in this age group and that neuropathological examination is essential to accurate diagnosis of human prion disease.
 
 

Sent: Monday May 28, 2007
 
Subject: THE BIG LIE SPORADIC CJD AND MAD COW DISEASEs i.e. TSE
 
Terry S. Singeltary Sr.
 
POLICY IN CONFIDENCE; CONFIDENTIAL; CJD IN FARMER WITH BSE COW ie OCCUPATIONAL EXPOSURE
 
Subject: POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
 
POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW
 
LIKELY TO ATRACT MEDIA ATTENTION
 
 
 
 

CONFIRMED CJD IN FARMER WITH BSE COW
 
line to take, sporadic CJD
 
 
 
 
 
 

SECOND CASE CJD IN DAIRY FARMER
 
 
 

CJD IN AN INDIVIDUAL OCCUPATIONALLY EXPOSED TO BSE
 
ii. on page 2 the sentence ''He had drunk pooled milk from the herd which included that from the affected animal'' will mislead the uninformed. It needs to be made clear that milk from a cow which is suspected to be affected with BSE cannot be drunk or added to the bulk milk produced by the rest of the herd.
 
iii. in the final paragraph I suggest that the phrase ''and a causal link with BSE is at most conjectural'' BE DELETED: the first paragraph of the sentence would then stand as a clear statement that the CJD case was likely to have been a CHANCE PHENOMENON.
 
 
 

''DH is aware of a second case of CJD in a dairy farmer who has had BSE in his herd. We cannot comment on the details of the case, but we know of nothing to suggest this is anthing other than a sporadic case of CJD. .........
 
 
 
IN CONFIDENCE
 
SECOND CASE OF CJD IN DAIRY-FARMER
 
IF PRESSED:
 
The numbers concerned are very small, and it is not possible to draw any conclusions from such small numbers. This issue is being considered by the Government's expert advisers....
 
 
 

THE FARMER IS THOUGHT TO HAVE HAD AT LEAST TWO CASES OF BSE IN HIS HERD, which were diagnosed in 1992. The farmer is reported to have asssisted in calving and to have drunk milk from his herd. This does not suggest that this is anything other than a sporadic case of CJD. ...
 
 
 

CONFIDENTIAL
 
CONFIRMED CASE OF CJD IN DAIRY FARMER
 
 
 

3. Neither Dr Will nor the CJD surveillance unit intend to disclose the existence of this case or make any comment at present unless it attracts media attention.
 
snip...
 
HUMAN CASE DETAILS CONFIDENTIAL
 
snip...
 
6. CJD IN FARMERS
 
The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups.
 
These relevant details are:-
 
MEDICAL/PARAMEDICAL/DENTISTRY 7
 
ANIMAL LABORATORY 1
 
PHARMACEUTICAL LABORATORY 0
 
RESEARCH LABORATORY 0
 
FARMERS/VETERINARY SURGEONS 7
 
BUTCHERS/ABATTOIR WORKERS/OCCUPATION INVOLVING DIRECT CONTACT WITH ANIMAL OR CARCASES 5
 
OCCUPATION INVOLVING ANIMAL PRODUCTS 9
 
snip... full text ;
 
 
 

Rocky Mountain oysters, mountain oysters, prairie oysters, Montana tendergroin or swinging sirloin
 
POLICY IN CONFIDENCE
 
CJD AND FARMERS
 
1. The article in the Daily Mail of 12 August again raises the question of a CAUSATIVE LINK BETWEEN BSE AND CJD. This follows the death of a second farmer from CJD...
 
snip...
 
I am, however, concerned about how DH and MAFF would respont to public concern generated if there are further CJD cases among farmers.
 
snip...
 
4. Unwelcome, though it maybe to the Tyrrell Committee, I think they must be asked at their next meeting to give further thought to what they might advise the Department and MAFF if ANOTHER FARMER (or TWO) DEVELOPS CJD. OR, if a butcher or abattoir worker develops the disease.
 
5. Although the Committee were given plenty of advance warning about the second farmer, they may NOT BE SO FORTUNATE NEXT TIME ROUND. Some Contingency planning on the Committee's response to a further case of CJD in a farmer seems essential. At the same time the Committee should consider if there is SPECIAL RISK TO FARMERS, FOR EXAMPLE THEIR HISTORICAL HABIT OF CHEWING CATTLE NUTS, that might be implicated. .....(oh my GOD...tss)
 
 
 

Ministers will note from this that experts are of the view, that there is unlikely to be a direct link between the cases of BSE, and the occurance of CJD in the farmer.
 
(NOTE CJD increasing over 3 years. ...TSS)
 
 
 

'AGE AT ONSET' is therefore likely to be a reflection of particulary aetiological factors, about which, for sporadic CJD at least, much is yet unknown. IT has therefore been suggested that examination of the f/d i/p of other groups with TSE's, and comparison with that of CJD subsets might help to elucidate aetiological mechanisms for sporadic CJD in particular; i.e. ALMOST A REVERSAL OF THE ORIGINAL UNDERTAKING.
 
 
 

OCCUPATIONAL EXPOSURE TO BSE AND CJD
 
2. The Tyrrell Committee met on 7 October and the significance of the two cases of CJD reported in dairy farmers who had BSE-affected animals on their farms was discussed at some length, AS WERE THE IMPLICATIONS OF A THIRD (OR FORTH) similar case.
 
3. The Committee were unable to identify any possible risk factors over and above those that they had already considered, both in general and with particular of TASTING THE FEED does continue but there was no consensus about the value of advising farmers to discontinue this practice. Feed currently in use does not pose a risk because of the ruminant-ruminant feed ban.
 
 
 

MRC
 
STRAIN CHARACTERISATION OF THE CREUTZFELDT-JAKOB DISEASE AGENT BY TRANSMISSION TO MICE
 
In view of the CONCERN that exposue to BSE OR SCRAPIE MAY POSE A RISK TO HUMANS, it is proposed investigate the relationship between sporadic creutzfeldt-jakob disease.....
 
 
 

OCCUPATIONAL EXPOSURE TO BSE AND CJD
 
3. While Committee may have no leads to pursue on why farmers might be at increased risk, I hope they understand the urgency with which they will need to respond if or when a THIRD FARMER DEVELOPS CJD.
 
 
 

INCREASE IN SPORADIC CJD
 
 

occupational
 
 
 

Dealler
 
 
 
 
 
 
 
 

STACKING THE DECK AGAINST SPORADIC CJD AND SOUND SCIENCE
 
APPOINTMENTS IN CONFIDENCE
 
MEMBERSHIP TO SEAC
 
snip...
 
I have informed Dr Tyrrell that we have now written to Dr Hueston to invite him to serve on the Committee and he was very pleased to hear this. He was also in favour of our idea of having a deputy Chairman who could take any emergency meetings eg IF THERE WERE TO BE ANOTHER CJD CASE IN AGRICULTURE. I suggested that either Dr. WIll or Dr Kimberlin were likely candidates and he thought that this was about right. He felt that on balance he would prefer Dr Will who he thought took a more cautious line and was LESS DOGMATIC. .....
 
 
 

BUYING THE BEST JUNK SCIENCE YOU CAN FROM THE USA VIA DR. HUESTON
 
 
 

CHANGING SCIENCE TO FIT YOUR INDUSTRY NEEDS COVER-UP IN FULL MODE NOW
 

PROBLEM
 
7. The main findings in the case-control study were STATISTICALLY SIGNIFICANT ASSOCIATIONS BETWEEN CONSUMPTION OF VEAL OR VENISON AND THE DEVELOPMENT OF CJD (INCREASED RISKS OF 2-13x).
 
IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)
 
 
 

A REVISED VERSION WHERE THE FOLLOWING WAS MADE TO BE REMOVED FROM SCIENTIFIC FINDINGS. ...TSS
 
''This year's findings show a number of associations but the strongest is for veal.''
 
A BIG LINE WAS DRAWN THROUGH THAT SENTENCE TO BE REMOVED DUE TO THE FOLLOWING. THIS IS THE NEXT SENTENCE ;
 
''This is of considerable concern given recent developments. In particular, Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.''
 
YOU can see the beginning of the ukbsenvCJD only theory beginning to unfold now. full text of this ukbsenvcjd only conspiracy can be seen here. ...TSS
 
POLICY RESTRICTED
 
 
 

BRITISH DEER FARMERS ASSOCIATION
 
OCTOBER 1994
 
Dear Mr Elmhirst,
 
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
 
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
 
The Surveillance Unit is completely independent outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
 
snip...
 
The statistical results regarding the consumption of venison was put into perspective in the body of the report and was NOT MENTIONED AT ALL IN THE PRESS RELEASE. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of VENISON was highlighted only by the media i.e. in the News at one television programme.
 
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of Venison, would increase, and quite possibly GIVE DAMAGING CREDENCE, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
 
 

see buttered and watered down report here that caters to industry instead of human safety...TSS
 
 


SEE WHERE THIS ;
 
''This year's findings show a number of associations but the strongest is for veal.''
 
WENT TO THIS;
 
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and increased risk of CJD. When some account was taken of possible confounding, the association between veal eating and risk of CJD emerged as the strongest of these associations statistically. These findings concerning dietary history are particulary difficult to interpret for two reasons.
 
1. .........BSeee...........TSS
 
2. .........BSeee...........TSS
 
(I.E. BSeee = bull sh!t encephalopathy or government cover-up i.e. God save the industry at all cost, including human health. ...TSS)
 
THUS, the reported veal eating habits of confirmed CJD cases appear virtually identical to suspect cases later judged not to have the disease. This provides good circumstantial evidence to support the hypothesis that the apparent association between veal consumption and CJD is due to recall bias. Analysis of other apparent dietary risk factors for CJD, including venison, has provided similar evidence of recall bias.
 
snip...
 
In summary, the analysis of the dietary case-control study demonstrates a strong association between a lifetime history of veal consumption and the risk of developing Creutzfeldt-Jakob disease. HOWEVER this result may well be due to recall bias and analysis of clinical and molecular bilogical features does not provide supportive evidence for the hypothesis that veal eating is a risk factor for CJD. ...
 
snip...
 
MORE OF THIS BSeee CAN BE READ IN THE FINAL GOVERNMENT DICTATED CJD REPORT OF 1994
 
 


BSE SCIENTIST WAS 'CENSORED'
 
He says that when he worked at MAFF, ''the way it was structurally set up was not that science would drive the politics, but that the politics will drive the science. And that's wrong.''
 
 
 

11/3/96 DGRC alerts DTI Ministers and CSA to discovery of nvCJD on basis of letter from MRC Chief Executive dated 11/3/96
 
BIRTH OF THE UKBSEnvCJD ONLY THEORY, the birth of the 'BIG LIE' begins. ...tss
 
 
 
 
REPORT OF 16 YEAR OLD GIRL WITH CJD
 
5. This case may raise fears of a link between BSE and CJD. Current advice is that there is no scientific evidence of a link between BSE in cattle and CJD in humans. Furthermore advice from the Spongiform Encephalopathy Advisory Committee is that they are satisified that all necessary safeguards are in place to minimise further spread of spongiform encephalopathies in animals and to prevent any risk of transmission to humans. ...
 
 
 

To ask the Secretary of State for Health, how many people under the age of 20 years in each of the last five years have suffered from Creutzfeldt-Jakob disease; and of these how many had not had any growth treatment previously.
 
SUGGESTED REPLY
 
We are not aware of any people under the age of 20 in the UK suffering from Creutzfeldt-Jakob Disease in the last five years.
 
 
 

STATEMENT FROM HOSPITAL
 
 
 

As we discussed, a general line could be added, _if pressed_, to the line you have already received, as follows;
 
"We are confident that no-one from the CJD Surveillance Unit would discuss with any patient's relatives matters relating to BSE or to contact with the press"...(_and consider adding_..."in the way that has been reported."
 
 
 

PREPARING FOR THE STORM 'LINE TO TAKE'
 
 Handling
 
4. In addition, Channel 4 is due to broadcast "Dispatches" (made by Fulcrum Productions) tomorrow evening, 26 January. The programme will cover the above issues. Paragraph 2 of a letter from Fulcrum (at D) includes transcript of an interview recorded for the programme with the teenage girl's relative. A copy of the reply from Dr Will, head of the CJD Surveillance Unit, to Fulcrum is also enclosed. The points Dr will makes are fully endorsed by the Department. It is worth noting that Dr Will had earlier spent a considerable amount of time briefing Fulcrum on the CJD Surveillance Unit's activities and on general CJD issues.
 
5. The implication of a cover-up with respect to the diagnosis in this case and possible links with BSE cannot be substantiated. ...
 
 
 

BARONESS CUMBERLEGE TRYING TO MANIPULATE THE MEDIA
 
 
 

MAD COW MEAL DESTROYED MY DAUGHTERS LIFE
 
A TEENAGE GIRL may have caught the human form of MAD COW DISEASE by eating a contaminated burger it was claimed last night.
 
VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).
 
 
 

GIVE ME BACK MY LIFE
 
 
 

HUSH UP! GOVERNMENT TOLD GRAN: ''YOU MUST THINK OF THE ECONOMY''
 
 
 

WHY IS MY GIRL DYING ? '' IT WAS LIKE SOMEBODY OLD INSIDE A YOUNG PERSON'S BODY
 
 
 

I have interviewed Mrs Rimmer at my constituency surgery
 
IF there is nothing to hide, why is there so much SECRECY? WHY is the Government and other Bodies trying to stop any CHANCE OF PEOPLE CONNECTING THE TWO DISEASES. The B.S.E. problem is obvious, but if the correct measures are taken, surely the problem could be contained, however, as it stands the lack of investigation and interest of the possibility of B.S.E. and C.J.D. being linked is open for speculation and surely someone has to account for peoples lives! WHY is so much trouble being taken to convice people that B.S.E. and C.J.D. are not linked? Guilty Conscience perhaps ? - or cover up?
 
HOUSE OF COMMONS
 
FROM BARRY JONES, M.P.
 
22 FEBRUARY 1994
 
 
 

Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.
 
(now story changes that biopsy shows she does not have CJD...tss)
 
 

 
now story changes to ;
 
Advice
 
7. The Parliamentary Secretary is invited to note the recent statements made on __________ and the present position which remains that CJD cannot be confirmed, in this case at this stage.
 
 

 
 
 
3. The Medical Director at ___________________ Hospital advised the Department on 6 June that the results of ___________________ brain biopsy had been received and that it showed NO EVIDENCE OF CJD. ______________ Hospital subsequently issued a statement to the press to this effect and this was publicised widely in the press (doc 1). News coverage which followed suggested that the statement made by ________________ Hospital had been misleading (doc 2). Enquires have been made of the Medical Director at _______________ Hospital who has CONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WAS ISSUED IN ERROR. The facts are that two pathology reports on the same piece of brain tissue were recieved. The first report indicated that CJD was unlikely, The second report indicated that CJD was possible, PERHAPS EVEN LIKELY, but that no definitive diagnosis could be made before a post mortem was undertaken.
 
 
 

more industry fed science ;
 
 
 
 
 
 
 
 
(ONLY PROBLEM IS, VICKY RIMMER, 16, DID NOT DIE FROM nvCJD, SHE DIED FROM SPORADIC CJD, the same damn thing. ...TSS)
 
 
Friday, 27 April, 2001, 17:44 GMT 18:44 UK Inquest uncertainty over CJD death
 
Victoria Rimmer, CJD victim
 
Victoria Rimmer was diagnosed with CJD at the age of 15
 
 
Victoria Rimmer, CJD victim
 
 
 
Relatives have expressed disappointment after a coroner ruled that a girl was likely to have died of a form of CJD unrelated to BSE-infected cattle. Following an inquest into the death of 20-year-old Vicky Rimmer from Deeside - who had lain in a coma for four-and-a-half years - Coroner John Hughes said the evidence was unclear but suggested she died from sporadic CJD.
 
 Sporadic CJD has not been linked to BSE-infected cattle and normally affects people in their sixties.
 
Grandmother Beryl Rimmer, 61, who had looked Vicky since she was a small child, had been pressing for a verdict of new variant CJD which is related to cattle.
 
She told North East Wales Coroner's Court in Flint how she first noticed symptoms in her granddaughter - believed to be the youngest person in Wales to have died of the disease - when she was 16.
 
From that point on, she said turned from the "perfect teenage daughter" into a moody and depressed wreck.
 
"Vicky was always full of life, she was sports mad and animal mad," she said.
 
'Staggering'
 
"Her health was excellent until March 1993. She was always tall and slim but ate everything in sight, but she started losing weight and started to look anorexic.
 
"She started falling, like you see cows with BSE staggering on television...
 
"She couldn't understand and said "What's happening to me mum?'
 
scientist at work
 
Experts are still investigating CJD
 
According to Professor James Ironside of the National CJD Surveillance Unit, Miss Rimmer's case was "unique" and tests showed signs of both vCJD and new variant CJD.
 
"Our understanding of the case is not complete. It is one of the most unusual and difficult cases I have ever come across," he explained.
 
"The characteristics of the disease suffered by Miss Rimmer do not fall neatly into any category.
 
"The investigations that we have performed so far would indicate that this case, unique as it is, has more similarities to sporadic CJD than to new variant."
 
Neurological damage
 
Miss Rimmer was initially admitted to Wrexham Maelor Hospital in August 1993.
 
Shortly after being moved to the Walton Neurological Centre in Liverpool, she fell into a coma. Never regaining consciousness, she died in November 1997.
 
At the time of her death, the inquest was told that her brain was so damaged as to look like that "of a 90-year-old who had undergone severe neurological damage".
 
After tests had been carried out, Mrs Rimmer told the coroner, a doctor had told her Vicky had spongiform encephalopathies.
 
Not sure what it meant, she told Vicky's GP who said: "That's mad cow disease."
 
 I think the way I was treated was unbelievable Beryl Rimmer When she pressed doctors at the hospital, she said she was told not to go to the press as it "could damage the economy".
 
"I think the way I was treated was unbelievable," Mrs Rimmer said.
 
Coroner John Hughes explained the reason for the four year delay to the inquest was because Beryl Rimmer wanted both the results of an inquiry into BSE and medical tests into CJD to be made public before any hearing.
 
Mr Hughes returned a verdict of death by natural causes and concluded that Miss Rimmer died of bronchial pneumonia caused by CJD.
 
"I ask you to recognise that I take this step simply on the weight of evidence before the court," he said.
 
He went on to say that "new knowledge can confound us all" and said if new evidence came to light he would petition the Home Secretary to have the inquest reopened.
 
 
 
 

2013 USA
 
 
Monday, September 02, 2013

 Atypical BSE: role of the E211K prion polymorphism

 Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES


Location: Virus and Prion Research Unit

http://bse-atypical.blogspot.com/2013/09/atypical-bse-role-of-e211k-prion.html



Sunday, September 1, 2013


Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy


We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)


snip...


***Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.


http://transmissiblespongiformencephalopathy.blogspot.com/2013/09/evaluation-of-zoonotic-potential-of.html



Sunday, August 11, 2013

Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013

Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010

http://creutzfeldt-jakob-disease.blogspot.com/2013/08/creutzfeldt-jakob-disease-cjd-cases.html



Tuesday, September 24, 2013


NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/nordion-us-inc-and-bioaxone-biosciences.html



Atypical BSE in Cattle


To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.


In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.



This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.


 http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2




Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip...


EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.


snip...



http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1



http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf



Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.

***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.

Second threat

snip...


http://www.neuroprion.org/en/np-neuroprion.html



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.)



 http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html




U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001


Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001


http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html




Prion2013


Oral.05: Contaminated blood products induce a highly atypical prion disease devoid of PrPres in primates


Emmanuel Corney,1 Nina Jaffre,1 Jacqueline Mikol,1 Valerie Durand,1 Christelle Jas-Duval,1,2 Sophie Luccantoni-Freire,1 Evelyne Correia,1 Nathalie Lescoutra-Etcheqaray,3 Nathalie Streichenberqer,4 Stephane Haik,5 Chryslain Sumian,3 Paul Brown1 and Jean-Philippe Deslys1


1Commissariat a l'Energie Atomique; Institute of Emerging Diseases and Innovative Therapies (iMETI); Division of Prions and Related Diseases (SEPIA); Fontenay-aux- Roses, France; 2EFS·Nord de France; Lille, France; 3MacoPharm; Tourcoing, France; 4Hospices Civils de Lyon; Prion Unit; Neurobiology Department; Bron, France; 5Inserm; U 975·CNRS; UMR 7225 - Universite Pierre et Marie Curie; Paris, France


Background, Concerns about the blood-borne risk of prion infection have been confirmed by the occurrence in the UK of four transfusion-related infections of vCJD and an apparently silent infection in an hemophiliac patient. Asymptomatic incubation periods in prion diseases can extend over decades in humans. We present here unexpected results of experiments evaluating blood transmission risk in a non-human primate model.


Material and Methods, Cynomolgus macaques were inoculated with brain or blood specimens from vCJD infected humans or monkeys. Neuropathological and biochemical findings were obtained using current methods used for human patients.


Results, Thirteen out of 23 primates exposed to various human or macaque blood products exhibited a previously undescribed myelopathic syndrome, devoid of the classical features of prion disease, notably abnormal prion protein (PrPres) deposition, whereas the 14 corresponding brain-inoculated donor animals and 1 transfused animal exhibited the classical vCJD pattern. In passage experiments, plasma transfusion induced the same atypical phenotype after two years (again, with no detectable PrPres), whereas the intracerebral inoculation of spinal cord led to a typical prion disease with cerebral spongiosis and PrPres accumulation in the brain of the primate recipient. Interestingly, passage experiments in transgenic mice were largely unsuccessful.


In another experiment designed to test the efficacy of antiprion filters, three recipients of filtered red blood cells suspended in plasma are still healthy 4.5 y after transfusion whereas the recipients of unfiltered inocula died after 2.5 y with the atypical neurological profile.


Conclusion. We describe a new fatal neurological myelopathic syndrome in monkeys exposed to various vCJD/BSE-infected blood components.


Secondary transmission in primates confirms


(I) the transmissibility of this myelopathy, and


(2) its prion origin which could not be diagnosed as such in the first recipients.


This myelopathy might be compared in some respects to certain forms of human lower motor neuron disease, including neuromyelitis optica, the flail arm syndrome of amyotrophic lateral sclerosis (ALS), and the recently described FOSMN (facial onset sensory and motor neuronopathy) syndrome.


http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf


www.landesbioscience.com



AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice


Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama


National Institute of Animal Health; Tsukuba, Japan


H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE).

*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.



http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf


www.landesbioscience.com




see also ;



Thursday, August 15, 2013


The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice


http://bse-atypical.blogspot.com/2013/08/the-emergence-of-novel-bse-prions-by.html



Friday, November 09, 2012


*** Chronic Wasting Disease CWD in cervidae and transmission to other species


http://chronic-wasting-disease.blogspot.com/2012/11/chronic-wasting-disease-cwd-in-cervidae.html




Sunday, November 11, 2012


*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012


http://chronic-wasting-disease.blogspot.com/2012/11/susceptibilities-of-nonhuman-primates.html



Friday, December 14, 2012


Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012


http://chronic-wasting-disease.blogspot.com/2012/12/susceptibility-chronic-wasting-disease.html



Sunday, August 25, 2013


Prion2013

Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission


http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html




NOW, let’s take a look at what the science is saying on the risk factors of human TSE prion disease from CWD prion disease of cervids.



first, from the cdc/nih et al prion gods, and what they said on human cwd potential, and what that might look like ;


now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????



“Our conclusion stating that we found no strong evidence of CWD transmission to humans”



From: TSS (216-119-163-189.ipset45.wt.net)


Subject: CWD aka MAD DEER/ELK TO HUMANS ???


Date: September 30, 2002 at 7:06 am PST


From: "Belay, Ermias"


To:


Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM


Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.



Ermias Belay, M.D. Centers for Disease Control and Prevention


-----Original Message-----


From:


Sent: Sunday, September 29, 2002 10:15 AM


To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS



Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.


snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...

full text ;


http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


http://chronic-wasting-disease.blogspot.com/2006_12_01_archive.html




Monday, February 09, 2009


Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD


snip...



Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain


Date: August 25, 2007 at 12:42 pm PST


our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.


http://www.jbc.org/



Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II


http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html



CWD TO HUMAN RISK FACTORS PRION2013



PRION2013 CONGRESSIONAL ABSTRACTS


HD.13: CWD infection in the spleen of humanized transgenic mice


Liuting Qing and Qingzhong Kong


Case Western Reserve University; Cleveland, OH USA


Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.


=====


Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system


Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1


1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK


Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.


Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.


Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.


Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.


=====


Invited.16: Studies of chronic wasting disease transmission in cervid and non-cervid species


Edward A, Hoover,1 Candace K. Mathiason,1 Davin M. Henderson,1 Nicholas J. Haley,1 Davis M. Seelig,1 Nathaniel D. Denkers,1 Amy V. Nalls,1 Mark D. Zabe,1 Glenn C. Telling,1 Fernando Goni2 and Thomas Wisniewski,2


1Prion Research Center; Colorado State University; Fort Collins, CO USA; 2New York University School of Medicine; New York, NY USA


How and why some misfolded proteins become horizontally transmitted agents and occasionally cross species barriers are issues fundamental to understanding prion disease. Chronic wasting disease (CWD) of cervids is perhaps a prototype of horizontal prion transmission, encompassing efficient mucosal uptake, lymphoid amplification, neuroinvasion, peripheralization, and dissemination via mucosal excretion. Efficient mucosal transmission of CWD in deer has been demonstrated by oral, nasal, aerosol, and indirect contact exposure. In addition, other studies (Mathiason CK, et al.) reported at the symposium support a significant role for pre- and/or postnatal transmission of CWD from doe to offspring. Accumulating, yet still incomplete, evidence also suggests that the period of relatively covert CWD infection may be longer than originally thought. Given the above, minimally invasive sensitive assays based on body fluids from live animals would aid substantially in understanding the biology of CWD. We have been applying seeded realtirne quaking-induced amplification of recombinant PrP substrates (i.e., RT-QuIC methodology) to: (1) investigate antemortem CWD detection, and (2) model PrP-based species barriers and trans-species adaptation-topics we previously explored using sPMCA and in vivo bioassays. At this symposium, we report sensitive and specific detection CWD prions in saliva, urine, blood (Mathiason lab), and rectal and pharyngeal lymph node samples (Haley NJ, et al.) from pre-symptomatic and symptomatic experimentally and naturally exposed deer. Other ongoing studies are employing RT-QuIC methodology to model amplification barriers among CWD, FSE, BSE, and CJD prions using cervine, feline, bovine, human, and promiscuous rPrP substrates and the above species prion seeds, cellular co-factors, and transgenic mice. Finally, in collaboration with the Wisniewski laboratory, we are conducting of experimental CWD vaccination studies in deer employing oral administration of an attenuated Salmonella vector expressing cervid PrP epitopes.


=====


AD.06: Detecting prions in the brain and blood of TSE-infected deer and hamsters


Alan Elder,1 Davin Henderson,1 Anca Selariu,1 Amy Nalls,1 Byron Caughey,2 Richard Bessen,1 Jason Bartz3 and Candace Mathiason1


1Colorado State University; Fort Collins, CO USA; 2NIH Rocky Mountain Laboratories; Hamilton, MT USA; 3Creighton University; Omaha, NE USA


While large quantities of protease resistant prion protein (PrPres) can be demonstrated by western blot or IHC in lymphoid biopsies or post-mortem brain tissues harvested from prion-infected animals, these conventional assays are less reliable as means to detect the small quantities of prions thought to be present in bodily fluids or associated with early and asymptomatic phases of TSE disease. The Real Time-Quaking Induced Conversion (RT-QuIC) assay is capable of detecting prions at concentrations below the level of sensitivity of conventional assays and provides a real-time fluorescent readout negating the use of proteases. We have made modifications to the RT-QuIC assay to utilize it for the detection of PrPres in brain and blood harvested from various species infected with prions. In this study, we analyzed CWD-infected deer and CWD/TME-infected hamster whole blood to determine the effect of:


(1) various anticoagulants,


(2) freezing and


(3) NaPTA precipitation.


Brain tissue and blood collected from naive deer and hamsters served as negative controls.


We were able to demonstrate amplifiable prions in


 (1) brain and blood samples harvested from CWD/TME-infected animals,


 (2) heparinized blood,


(3) frozen vs. fresh blood and


(4) NaPTA treated samples.


The RT-QuIC assay is able to detect PrPres in various species of animals and shows promise as an antemortem diagnostic tool for blood-borne TSEs.

=====

http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf

www.landesbioscience.com


Sunday, July 21, 2013

*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

http://chronic-wasting-disease.blogspot.com/2013/07/as-chronic-wasting-disease-cwd-rises-in.html


sCJDMM1-2 should be considered as a separate entity at this time.

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

http://creutzfeldt-jakob-disease.blogspot.com/2009/08/characteristics-of-established-and.html

http://cjdusa.blogspot.com/2009/09/co-existence-of-scrapie-prion-protein.html


 *** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf


Saturday, September 21, 2013

CJD CONFIRMED in patient at New Hampshire Department of Health and Human Services (DHHS), Catholic Medical Center (CMC), and the Manchester Health Department (MHD)

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/cjd-confirmed-in-patient-at-new.html


Thursday, September 26, 2013

Minimise transmission risk of CJD and vCJD in healthcare settings Guidance

http://creutzfeldt-jakob-disease.blogspot.com/2013/09/minimise-transmission-risk-of-cjd-and.html


Sunday, March 31, 2013

Creutzfeldt Jakob Disease CJD worlds youngest documented victim, 11 years old, shall we pray

http://creutzfeldt-jakob-disease.blogspot.com/2013/03/creutzfeldt-jakob-disease-cjd-worlds.html


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

http://transmissiblespongiformencephalopathy.blogspot.com/2013/01/gambetti-et-al-usa-prion-unit-change.html


Monday, December 31, 2012

Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012

http://creutzfeldt-jakob-disease.blogspot.com/2012/12/creutzfeldt-jakob-disease-and-human-tse.html


Saturday, December 29, 2012

MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT

http://creutzfeldt-jakob-disease.blogspot.com/2012/12/mad-cow-usa-human-tse-prion-disease.html


 MAD COW USDA ATYPICAL L-TYPE BASE BSE, the rest of the story...

http://bse-atypical.blogspot.com/2012/06/clinical-and-pathologic-features-of-h.html


Tuesday, November 6, 2012

Transmission of New Bovine Prion to Mice, Atypical Scrapie, BSE, and Sporadic CJD, November-December 2012 update

http://transmissiblespongiformencephalopathy.blogspot.com/2012/11/transmission-of-new-bovine-prion-to.html


 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

http://creutzfeldt-jakob-disease.blogspot.com/2012/06/creutzfeldt-jakob-disease-human-tse.html


Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html


Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/national-prion-disease-pathology.html


Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?

http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html


Wednesday, March 28, 2012

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS TRANSMISSIBLE IN BANK VOLES Nonno

http://prionopathy.blogspot.com/2012/03/variably-protease-sensitve-prionopathy.html


Sunday, August 09, 2009

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html


Tuesday, August 18, 2009

BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009

http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html



Saturday, September 21, 2013


Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT


FOR 4 YEARS, THE USDA NSLP fed our children all across the USA, from school to school, county to county, state to state, the most high rish cattle for mad cow type disease i.e. the TSE prion disease, they fed our children dead stock downer cows. did your children consume this, and will you have to wait 5 decades to see if they become exposed and go clinical with CJD TSE prion disease ???


http://downercattle.blogspot.com/2013/09/westlandhallmark-2008-beef-recall-case.html

 



 TSS

 

posted by Terry S. Singeltary Sr. at 10:55 AM