VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS, and the infamous
UKBSEnvCJD only theory, i.e. God save the industry at all cost $$$
J Neurol Neurosurg Psychiatry 2013;84:e2 doi:10.1136/jnnp-2013-306573.17
Association of British Neurologists (ABN) joint meeting with the Royal College
of Physicians (RCP), London, 23–24 October 2013 017
VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS
Graham Mackay⇓, Richard Knight, Robert Will + Author Affiliations
Southern General Hospital, Glasgow; National CJD research and surveillance
unit, Edinburgh Abstract Introduction Variant Creutzfeldt–Jakob (vCJD) has an
established clinical phenotype and diagnostic criteria. However, this phenotype
has largely been described in a cohort of young vCJD cases, with a median age of
onset of 27.
Methods Having reviewed the 176 definite and probable vCJD cases referred
to UK CJD surveillance, six older cases, over 55 years were found. The clinical
records of these cases were reviewed.
Results The six older vCJD cases were all male. Two had received blood from
donors confirmed to have had vCJD. Only two of these cases met the diagnostic
criteria for vCJD in life. Three cases had atypical clinical histories without
either early psychiatric symptoms or involuntary movements. Only one of five
patients had the typical pulvinar sign on their MRI scan.
Conclusion No cases of vCJD were diagnosed in the UK in 2012. However,
clinicians should be aware of the occurrence of vCJD, with less typical
phenotypes, in older patients. vCJD should be considered in older patients dying
with dementia deteriorating in under three years, with ataxia and a rapid final
deterioration. Post mortem should be considered in such cases, given the public
health risks among a population more prone to undergoing medical procedures.
The age distribution has a political aspect. Scientists sought to sell
BSE-based CJD to politicians on the basis of its novelty: early onset, florid
plaques, strain type 4 and so on. Now that they have made the sale, and with the
Inquiry Report as received wisdom (?!?), it becomes timely to reveal an older
case and that they had blown off 5 years of elderly demented data (which has far
higher frequency than young and demented so potentially holds more nvCHD cases).
If nvCJD had been presented primarily a disease of the elderly demented
(scarcely a charismatic group, fundraisers use a poster-child), it would have
been met with near-total indifference and business as usual. Elderly are written
off as likely to die soon of one thing or another anyway, and daftness is
perceived as normal. Why spend money on diagnosing them?
Subject: The 'Chosen Ones' (nvCJD) will fall, young and old... but
sporadic, will stay just that, $$$$$ 'sporadic' $$$$$
Date: Fri, 27 Apr 2001 09:38:12 –0700
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Thursday April 26 8:26 PM ET
Human Mad Cow Disease Claims Oldest Victim
LONDON (Reuters) - More elderly people will fall victim to the human form
of mad cow disease, medical experts said on Friday after a 74-year-old man
became the oldest victim of the fatal brain affliction.
Variant Creutzfeldt-Jakob disease (news - web sites) (vCJD) was diagnosed
after an autopsy was requested for the 74-year-old man on the basis that some of
his symptoms were not associated with dementia and he died just seven months
after they began.
Professor James Ironside of the CJD Surveillance Unit at Western General
Hospital in Edinburgh said the death of the unidentified man is unlikely to be
an isolated event, saying more cases of the disease could occur in people in
their 50s, 60s and 70s.
Most of the 95 cases of the brain-wasting illness reported in Britain have
been in people decades younger than the oldest victim.
``This case has important implications for the surveillance of vCJD, and
raises the possibility that cases of vCJD in the elderly might be missed,'' they
said in a letter to The Lancet medical journal.
Symptoms of the illness, which include loss of co-ordination, confusion and
personality changes, can be mistaken for dementia in older people. Cases of vCJD
are usually confirmed by an autopsy, which is not commonly performed on the
elderly.
Doctors ``should be aware that vCJD can arise in elderly patients so that
appropriate investigations are done,'' the experts added.
Doctors should request scans and autopsies in suspected cases of vCJD in
the elderly.
The elderly man, a retired electrician, had no family history of brain
disease and was healthy until he complained of pains in his hands and then
became forgetful and started having hallucinations and paranoid delusions.
But the scientists said he ate meat pies and sausages at least once every
week and pate every month. Researchers suspect humans get vCJD, which was first
identified in 1996, by eating meat contaminated with mad cow disease or bovine
spongiform encephalopathy (BSE (news - web sites)).
Last month an inquiry into a cluster of vCJD deaths in central England said
local butchering practices were the most likely cause of the vCJD cases.
Because of its long incubation period, which can be up to 30 years,
scientists say it is impossible to predict how many people will be struck down
by the disease. Estimates range from thousands to tens of thousands over the
coming years.
Thursday, 26 April, 2001, 12:48 GMT 13:48 UK
Third French CJD victim dies
The Eboli family is suing governments over the disease A 19-year-old man
has become the third victim in France to die of the human form of mad cow
disease.
Arnaud Eboli died on Wednesday from variant Creutzfeldt-Jakob disease
(vCJD), the human type of BSE, his family have announced.
Last year, a lawyer acting for Mr Eboli and Laurence Duahamel - another
victim of the disease - sued the French, British and EU authorities alleging
they had failed to take all the necessary steps to contain the epidemic.
The law suits - filed in a Paris civil court - accuse Britain of knowingly
exporting possibly contaminated material, and France and the European Commission
of not taking the threat of disease seriously enough.
Britain, where the outbreak of BSE has been most severe, has so far
confirmed 97 deaths from vCJD and the Republic of Ireland one.
Feed investigation
The news of Mr Eboli's death comes a day after French magistrates placed
under official investigation a firm allegedly distributing contaminated feed.
Youssef Chataoui, head of the French company Euro Feed, is accused of
illegal involvement in trafficking meat-based animal feed.
Feed products were allegedly brought from France, Ireland and the
Netherlands to Belgium, where they were relabelled.
France banned bone meal from animal feed in 1990 and further tightened its
controls in 1996.
"This discovery, if confirmed, could explain the scientific mystery of how
certain cows born after the ban on animal derivatives in their feed could
develop mad cow disease," the Le Parisien newspaper commented.
someone inside the Gov. told me this recently, one who knows;
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 travelled 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.
======================================
> Feed investigation
> The news of Mr Eboli's death comes a day > after French magistrates
placed under > official investigation a firm allegedly > distributing
contaminated feed.
this is exactly why 'sporadic' will stay 'sporadic' $$$$$
disgusted again in Bacliff, Terry S. Singeltary Sr., Bacliff, Texas USA
LANCET
Volume 357, Number 9265 28 April 2001
Research letters
Variant Creutzfeldt-Jakob disease in an elderly patient
J W Lorains, C Henry, D A Agbamu, M Rossi, M Bishop, R G Will, J W Ironside
We report a case of variant Creutzfeldt-Jakob disease (vCJD) in a 74-year
old man in whom diagnosis was made at necropsy. The occurrence of vCJD in an
individual in this age group is unlikely to be an isolated event. Doctors need
to be aware that vCJD can arise in elderly patients so that appropriate
investigations (including magnetic resonance imaging) can be done, and
permission for neuropathological necropsy requested, in suspected cases.
This case could also have important implications for public health policy
decisions and surveillance programmes that target the younger age range of vCJD
cases.
Wirral Hospital, Clatterbridge (J W Lorains FRCP); National CJD
Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh,
EH4 2XU, UK (C Henry MRCPI, M Bishop BSC, R G Will FRCP, Prof J W Ironside
FRCPath); Wirral Hospital, Arrowe Park (D A Agbamu MRCPath); and Walton Centre,
Liverpool (M Rossi FRCPath)
Correspondence to: Prof J W Ironside (e-mail:j.w.ironside@ed.ac.uk)
TSS
===============================
From: TSS (216-119-138-130.ipset18.wt.net)
Subject: Death toll may rise to one a day from madcow disease
Date: October 28, 2000 at 7:39 pm PST
###### Bovine Spongiform Encephalopathy #########
Greetings List Members,
it seems old Prof. Will at the CJD surveillance unit may have to think
twice now about Mrs. Soukups from the U.S., and probably many more...
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
October 29 2000 BRITAIN
Death toll may rise to one a day
Youngest CJD victim dies at 14
Jonathon Carr-Brown
BRITAIN'S youngest victim of CJD, 14-year-old Zoe Jeffries, died yesterday
as scientists began to increase estimates of the possible death toll from the
illness.
Jeffries, from Wigan, Greater Manchester, contracted the disease two years
ago. She became the country's 81st person confirmed to have died from CJD, the
human equivalent of "mad cow" disease.
Her death coincided with a series of predictions and discoveries by
government advisers and scientists. These include:
A death rate of one person a week by next September, rising to one a day by
2003.
A rise in the minimum number of deaths in Britain to 1,000, 10 times higher
than previously forecast.
The emergence of two potential new clusters of the disease - in Glasgow,
where so far five people have died from new variant CJD (nvCJD), and in
Doncaster where there have been two CJD deaths. Regarded as statistically
significant, these follow the discovery of a cluster in Queniborough,
Leicestershire, where five have died.
The death of a 79-year-old American woman from CJD who spent part of the
1970s in the same area of Leicestershire, and the death of a 74-year-old from
nvCJD.
Deaths among older people from nvCJD raise the possibility that the disease
may have a longer incubation period than previously thought, which would
indicate a higher death toll than previously forecast.
Scientists had believed that most people were infected in the late 1980s
but there is now evidence from the Phillips inquiry into BSE, published last
week, that the disease may have entered the food chain in the 1970s.
The latest developments have led Professor John Collinge, a member of the
government's advisory body on BSE and CJD, to revise the minimum number of
expected deaths from 100 - which will be reached early next year - to 1,000.
"The longer the incubation period, the more potentially worrying it could be."
said Collinge.
However, he emphasised that accurate predictions are impossible because of
uncertainty over key causal factors including the dose of BSE-tainted meat that
is needed to infect a victim, the route of exposure, the incubation period,
genetic susceptibility and the extent of species barrier.
Research by Professor Roy Anderson, another advisory committee member,
initially put the range of deaths between 100 and 136,000. In August he said the
most likely number was about 6,000 and predicted that deaths of hundreds of
thousands of people were unlikely.
These figures have, however, been criticised by scientists including Dr
Stephen Deallar, a pathologist at Burnley hospital, Lancashire, who in the 1970s
was one of the first to guess how BSE entered the food chain. "I think
Collinge's revision is on the optimistic side," he said. "This is going to keep
doubling for a number of years to come."
The death of the 74-year-old, believed to be from North Yorkshire, could
have significant implications, he said. "If this man ate hamburgers in the 1970s
and has been incubating it for 30 years, the doubling process is going to go on
longer with a much bigger pool of people."
The death of Jeffries highlights the difficulties of diagnosing nvCJD four
years after the government acknowledged both its existence and the poor standard
of care that victims have received.
Her symptoms emerged in June 1998. Her mother, Helen Jeffries, said: "One
morning Zoe got up and just didn't do anything. She just cried.
"It was as though she went to bed one person and got up a different one."
It was not until June 1999 that doctors from the CJD Surveillance Unit
diagnosed her illness as nvCJD.
Although her mother said she was filled with remorse because she had fed
her daughter cheap beef burgers, she criticised the lack of information and
knowledge about BSE and CJD.
"It's just as if someone had stuck a knife into Zoe's body," she said. "I
really do think she has been murdered."
==========================
Sunday, August 09, 2009
***CJD...Straight talk with...James Ironside...and...Terry Singeltary...
2009 ***
Wed, 29 Nov 2000 14:14:18 -0500
a private email from the late Dr. Gibbs, a true pioneer in the research of
human/animal TSEs and one that never wavered on helping the families and victims
of this horrible disease, and one that helped me many times in trying to seek
out the truth;
Subject: Re: Hello Dr. Gibbs...........
Date: Wed, 29 Nov 2000 14:14:18 –0500
From: "Clarence J. Gibbs, Jr., Ph.D."
To: "Terry S. Singeltary Sr." References: 3a254430.9fb97284@wt.net
Hi Terry:
326 E Stret N.E., Washington, D. C. 20002.
Better shrimp and oysters than cards!!!!
Have a happy holiday and thanks for all the information you bring to the
screen.
Joe Gibbs
==========
MAD COW TESTING ONLY CATCHES SOME MAD COWS
SPREADING IT ALL AROUND
Saturday, October 19, 2013
***A comparative study of modified confirmatory techniques and additional
immuno-based methods for non-conclusive autolytic Bovine spongiform
encephalopathy cases
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
Wednesday, September 25, 2013
Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE
PRION 2013
SPORADIC CJD AND BSE IN FARMERS, FARMERS WIVES
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
Dr. 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.
(ONLY PROBLEM IS, VICKY RIMMER, 16, DID NOT DIE FROM nvCJD, SHE DIED FROM
SPORADIC CJD, the same damn thing. ...TSS)
IN light of Asante/Collinge et al findings that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;
-------- Original Message --------
Subject: re-BSE prions propagate as
either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43
-0000 From: "Asante, Emmanuel A" To: "[log in to unmask]"
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I
am
a Senior Scientist in the MRC Prion Unit and the lead author on the
paper. I have attached a pdf copy of the paper for your attention.
Thank
you for your interest in the paper.
In respect of your first question, the simple answer is, yes. As you
will find in the paper, we have managed to associate the alternate
phenotype to type 2 PrPSc, the commonest sporadic CJD.
It is too early to be able to claim any further sub-classification in
respect of Heidenhain variant CJD or Vicky Rimmer's version. It will
take further studies, which are on-going, to establish if there are
sub-types to our initial finding which we are now reporting. The main
point of the paper is that, as well as leading to the expected new
variant CJD phenotype, BSE transmission to the 129-methionine
genotype
can lead to an alternate phenotype which is indistinguishable from
type
2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I
can be of any further assistance please to not hesitate to ask. Best
wishes.
Emmanuel Asante
<> ____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept.
Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG
Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:
[log in to unmask] (until 9/12/02)
New e-mail: [log in to unmask] (active from now)
____________________________________
snip...
full text ;
WHAT ABOUT U.S.A. ???
CJD YOUNG PEOPLE
in the USA, a 16 year old in 1978;
ALSO IN USA;
(20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. see
second url below)
in France, a 19 year old in 1982;
in Canada, a 14 year old of UK origin in 1988;
in Poland, cases in people aged 19, 23, and 27 were identified in a
retrospective study (published 1991), having been originally misdiagnosed with a
viral encephalitis;
Creutzfeldt's first patient in 1923 was aged 23.
20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19
year old died from sCJD in France in 1985. There is no evidence of an iatrogenic
cause for those cases....
NOW BACK TO THOSE FARMERS WITH BSE HERDS THAT DIED FROM SPORADIC CJD
CJD FARMERS WIFE 1989
Dear Bob,
An otherwise enjoyable dinner last night as guest of the Association of
Clinical Pathology was marred by a conversation with a neuropathologist who was
just about to write CMO with details of a case of CJD he had just seen. When
first mentioning the case, he claimed she was only 36, but after a few more
glasses of wine he became less certain of that and thought she could have been
older. Locally, they made quite an assoctiation with BSE, since she ws a farmers
wife on that farm that, atypically for that area of S Yorkshire, had several BSE
cases. I was told the clinical and pahtological pictures were typical of CJD.
...
cover-up of 4th farm worker ???
CONFIRMATION OF CJD IN FOURTH FARMER
now story changes from;
SEAC concluded that, if the fourth case were confirmed, it would be
worrying, especially as all four farmers with CJD would have had BSE cases on
their farms.
to;
This is not unexpected...
was another farmer expected?
4th farmer, and 1st teenager
2.
snip...
Over a 5 year period, which is the time period on which the advice from
Professor Smith and Dr. Gore was based, and assuming a population of 120,000
dairy farm workers, and an annual incidence of 1 per million cases of CJD in the
general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an
individual in the general population to develop CJD. Using the actual current
annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5
TIMES.
3. You will recall that the advice provided by Professor Smith in 1993 and
by Dr. Gore this month used the sub-population of dairy farm workers who had had
a case of BSE on their farms - 63,000, which is approximately half the number of
dairy farm workers - as a denominator.
If the above sums are repeated using this denominator population, taking an
annual incidence in the general population of 1 per million the observed rate in
this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per
million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general
population...
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.
USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN
18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7
December 2006 are now available.
snip...
64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be more
virulent and infectious to a wider range of species than bovine derived
BSE.
Other work presented suggested that BSE and bovine amyloidotic spongiform
encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the
prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A
MUTATION FOUND IN CASES OF SPORADIC CJD.
snip...
3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized
Mouse
Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western
Reserve University
Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases were
also reported in other countries. The infectivity and phenotypes of these
atypical BSE strains in humans are unknown. In collaboration with Pierluigi
Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated
transgenic mice expressing human prion protein with brain homogenates from BASE
or BSE infected cattle. Our data shows that about half of the BASE-inoculated
mice became infected with an average incubation time of about 19 months; in
contrast, none of the BSE-inoculated mice appear to be infected after more than
2 years.
***These results indicate that BASE is transmissible to humans and suggest
that BASE is more virulent than classical BSE in humans.***
6:30 Close of Day One
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC
CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.
He estimates that it may be up to 14 or 15 persons which display
selectively SPRPSC and practically no detected RPRPSC proteins.
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or
Italian L-BASE (the last two cases of mad cow disease in the USA were in
Alabama, and Texas, both of which were atypical BSE).
Please remember, the last two mad cows documented in the USA i.e. Alabama
and Texas, both were of the 'atypical' BSE strain, and immediately after that,
the USDA shut down the testing from 470,000 to 40,000 in the U.S. in 2007 out of
about 35 million cattle slaughtered. also, science is showing that some of these
atypical cases are more virulent to humans than the typical UK BSE strain
;
***Atypical forms of BSE have emerged which, although rare, appear to be
more virulent than the classical BSE that causes vCJD.***
Progress Report from the National Prion Disease Pathology Surveillance
Center
An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti,
MD
April 3, 2008
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."
snip...
Mr Hughes returned a verdict of death by natural causes and concluded that
Miss Rimmer died of bronchial pneumonia caused by CJD. ...
SEE ;
SNIP...
***SEE FULL TEXT ;
Wednesday, October 09, 2013
*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'S FALLACY,
£41,078,281 in compensation REVISED
Thursday, October 10, 2013
*** CJD REPORT 1994 increased risk for consumption of veal and venison and
lamb ***
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
SNIP...
***However, they also show that there is no absolute barrier ro conversion
of human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
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 ;
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.
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
SEE MORE HERE ;
Saturday, October 19, 2013
ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE
PRION DISEASE)
Monday, October 14, 2013
Researchers estimate one in 2,000 people in the UK carry variant CJD
proteins
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
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
Sunday, October 13, 2013
CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
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 ***
Saturday, July 6, 2013
*** Small Ruminant Nor98 Prions Share Biochemical Features with Human
Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive
Prionopathy
Research Article
How reassuring is this absence of detectable PrPSc from a public health
perspective? The bioassays performed in this study are not titrations, so the
infectious load of the positive gut tissues cannot be quantifi ed, although
infectivity has been shown unequivocally. No experimental data are currently
available on the zoonotic potential of atypical scrapie, either through
experimental challenge of humanized mice or any meaningful epidemiologic
correlation with human forms of TSE. However, the detection of infectivity in
the distal ileum of animals as young as 12 months, in which all the tissues
tested were negative for PrPSc by the currently available screening and confi
rmatory diagnostic tests, indicates that the diagnostic sensitivity of current
surveillance methods is suboptimal for detecting atypical scrapie and that
potentially infectious material may be able to pass into the human food chain
undetected.
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 17, No. 5, May 2011
why do we not want to do TSE transmission studies on chimpanzees $
snip...
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
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
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. Subscribe and get 4 free issues. 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.
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2
December 2010
UPDATE PLEASE NOTE ;
AS of June 30, 2011,
snip...
INCLUDING 10 POSITIVE GOATS FROM THE SAME HERD (FIGURE 7).
snip...
see updated APHIS scrapie report ;
Tuesday, February 01, 2011
Sparse PrP-Sc accumulation in the placentas of goats with naturally
acquired scrapie
Research article
snip...
Date: Tuesday, February 01, 2011 5:03 PM
To: Mr Terry Singeltary
Subject: Your comment on BMC Veterinary Research 2011, 7:7
Dear Mr Singeltary
Thank you for contributing to the discussion of BMC Veterinary Research
2011, 7:7 .
Your comment will be posted within 2 working days, as long as it
contributes to the topic under discussion and does not breach patients'
confidentiality or libel anyone. You will receive a further notification by
email when the posting appears on the site or if it is rejected by the
moderator.
Your posting will read:
Mr Terry Singeltary,
retired
Scrapie cases Goats from same herd USA Michigan
Comment: " In spite of the poorly defined effects of PRNP genetics, scrapie
strain, dose, route and source of infection, the caprine placenta may represent
a source of infection to progeny and herd mates as well as a source of
persistent environmental contamination. "
Could this route of infection be the cause of the many cases of Goat
scrapie from the same herd in Michigan USA ?
Has this been investigated ?
(Figure 6) including five goat cases in FY 2008 that originated from the
same herd in Michigan. This is highly unusual for goats, and I strenuously urge
that there should be an independent investigation into finding the common
denominator for these 5 goats in the same herd in Michigan with Scrapie. ...
Kind Regards, Terry
Thursday, January 07, 2010
Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010
and FISCAL YEAR 2008
In FY 2010, 72 cases of classical Scrapie and 5 cases of Nor-98 like
Scrapie were confirmed...
Scrapie Nor-98 like case in California FY 2011 AS of December 31,
2010.
Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat
cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS
cases)
Last herd with infected goats disignated in FY 2008 Michigan 8 cases
Tuesday, February 01, 2011
Sparse PrP-Sc accumulation in the placentas of goats with naturally
acquired scrapie
Research article
"In spite of the poorly defined effects of PRNP genetics, scrapie strain,
dose, route and source of infection, the caprine placenta may represent a source
of infection to progeny and herd mates as well as a source of persistent
environmental contamination."
Could this route of infection be the cause of the many cases of Goat
scrapie from the same herd in Michigan USA ?
Has this been investigated ?
(Figure 6) including five goat cases in FY 2008 that originated from the
same herd in Michigan. This is highly unusual for goats, and I strenuously urge
that there should be an independent investigation into finding the common
denominator for these 5 goats in the same herd in Michigan with Scrapie.
...
Kind Regards, Terry
SNIP...
Scrapie Nor-98 like case in California FY 2011 AS of December 31,
2010.
Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat
cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS
cases)
Last herd with infected goats disignated in FY 2008 Michigan 8 cases
UPDATED RESPONSE ON MY CONCERNS OF GOAT SCRAPIE IN MICHIGAN ;
----- Original Message -----
From: "BioMed Central Comments"
To:
Sent: Wednesday, February 16, 2011 4:13 AM
Subject: Your comment on BMC Veterinary Research 2011, 7:7
Your discussion posting "Scrapie cases Goats from same herd USA Michigan"
has been rejected by the moderator as not being appropriate for inclusion on the
site.
Dear Mr Singeltary,
Thank you for submitting your comment on BMC Veterinary Research article
(2011, 7:7). We have read your comment with interest but we feel that only the
authors of the article can answer your question about further investigation of
the route of infection of the five goats in Michigan. We advise that you contact
the authors directly rather than post a comment on the article.
With best wishes,
Maria
Maria Kowalczuk, PhD Deputy Biology Editor BMC-series Journals
BioMed Central 236 Gray's Inn Road London, WC1X 8HB
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Regards
BMC Veterinary Research
SNIP...PLEASE SEE FULL TEXT ;
Tuesday, February 01, 2011
Sparse PrP-Sc accumulation in the placentas of goats with naturally
acquired scrapie
Research article
Tuesday, April 30, 2013
Transmission of classical scrapie via goat milk
Veterinary Record2013;172:455 doi:10.1136/vr.f2613
Friday, May 10, 2013
Evidence of effective scrapie transmission via colostrum and milk in
sheep
Thursday, March 29, 2012
atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012
NIAA Annual Conference April 11-14, 2011San Antonio, Texas
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH
CODE
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe
WITH BOVINE MAD COW DISEASE
*** The discovery of previously unrecognized prion diseases in both humans
and animals (i.e., Nor98 in small ruminants) demonstrates that the range of
prion diseases might be wider than expected and raises crucial questions about
the epidemiology and strain properties of these new forms. We are investigating
this latter issue by molecular and biological comparison of VPSPr, GSS and
Nor98.
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States'
risk classification for mad cow disease to "negligible" from "controlled", and
risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further
exposing the globe to the TSE prion mad cow type disease
I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform
Encephalopathies (BSE): Public Health Risk Assessment ''IS the h-BSE more
virulent than typical BSE as well, or the same as cBSE, or less virulent than
cBSE? just curious.....'' Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or
another, but we have found that H-BSE can infect humans. I hope we could publish
these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of
Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice. The possibility of
more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
please see below from PRION2013 ;
*** This study imply the possibility that the novel BSE prions with high
virulence in cattle will be emerged during intraspecies transmission.
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.
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in
bovinized mice
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.
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...
see follow-up here about North America BSE Mad Cow TSE prion risk factors,
and the ever emerging strains of Transmissible Spongiform Encephalopathy in many
species here in the USA, including humans ;
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...
PRIONOPATHY OR PRIONOBALONEY $$$
Tuesday, July 2, 2013
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals
Eliminating ALL remaining BSE barriers to export market
Sunday, August 21, 2011
The British disease, or a disease gone global, The TSE Prion Disease
(see video here)
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ?
(see video at bottom)
Sunday, September 6, 2009
MAD COW USA 1997
(SEE SECRET VIDEO)
Creutzfeldt-Jakob Disease Public Health Crisis
Letters
JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr Bacliff, Tex
Since this article does not have an abstract, we have provided the first
150 words of the full text.
KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their
Research Letter, Dr Gibbons and colleagues1 reported that the annual US death
rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These
estimates, however, are based only on reported cases, and do not include
misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would
drastically change these figures. An unknown number of persons with a diagnosis
of Alzheimer disease in fact may have CJD, although only a small number of these
patients receive the postmortem examination necessary to make this diagnosis.
Furthermore, only a few states have made CJD reportable. Human and animal
transmissible spongiform encephalopathies should be reportable nationwide and
internationally.
References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB.
Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA.
2000;284:2322-2323.
Published March 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States
Terry S. Singeltary, retired (medically)
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Published March 26, 2003
THE PATHOLOGICAL PROTEIN
BY Philip Yam
Yam Philip Yam News Editor Scientific American www.sciam.com
Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system has errors
but stated that most of the errors will be confined to the older population.
CHAPTER 14
Laying Odds
Are prion diseases more prevalent than we thought?
Researchers and government officials badly underestimated the threat that
mad cow disease posed when it first appeared in Britain. They didn't think
bovine spongiform encephalopathy was a zoonosis-an animal disease that can
sicken people. The 1996 news that BSE could infect humans with a new form of
Creutzfeldt-Jakob disease stunned the world. It also got some biomedical
researchers wondering whether sporadic CJD may really be a manifestation of a
zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD
is?
Revisiting Sporadic CJD
It's not hard to get Terry Singeltary going. "I have my conspiracy
theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's
most relentless consumer advocate when it comes to issues in prion diseases. He
has helped families learn about the sickness and coordinated efforts with
support groups such as CJD Voice and the CJD Foundation. He has also connected
with others who are critical of the American way of handling the threat of prion
diseases. Such critics include Consumers Union's Michael Hansen, journalist John
Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web
site. These three lend their expertise to newspaper and magazine stories about
prion diseases, and they usually argue that prions represent more of a threat
than people realize, and that the government has responded poorly to the dangers
because it is more concerned about protecting the beef industry than people's
health.
Singeltary has similar inclinations. ...
snip...
THE PATHOLOGICAL PROTEIN
Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9
June 2003
BY Philip Yam
CHAPTER 14 LAYING ODDS
Answering critics like Terry Singeltary, who feels that the U.S. under-
counts CJD, Schonberger conceded that the current surveillance system has errors
but stated that most of the errors will be confined to the older population.
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember,
the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been
documented in North America, along with the typical scrapie's, and atypical
Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these
TSE in different species have been rendered and fed to food producing animals
for humans and animals in North America (TSE in cats and dogs ?), and that the
trading of these TSEs via animals and products via the USA and Canada has been
immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances
and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD
only theory in 2009. With all the science to date refuting it, to continue to
validate this old myth, will only spread this TSE agent through a multitude of
potential routes and sources i.e. consumption, medical i.e., surgical, blood,
dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and
the urgent need to make all human TSE in the USA a reportable disease, in every
state, of every age group, and to make this mandatory immediately without
further delay. The ramifications of not doing so will only allow this agent to
spread further in the medical, dental, surgical arena's. Restricting the
reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO
age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al
and many more, that the world of TSE Transmissible Spongiform Encephalopathy is
far from an exact science, but there is enough proven science to date that this
myth should be put to rest once and for all, and that we move forward with a new
classification for human and animal TSE that would properly identify the
infected species, the source species, and then the route.
CJD Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
SEE FULL TEXT ;
-------- Original Message --------
Subject: Tracking spongiform encephalopathies in North America LANCET
INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003
Date: Tue, 29 Jul 2003 17:35:30 –0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained
largely unsatisfied after being told that a close relative died from a rapidly
progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is
only reported in those areas known to be endemic foci of CWD. Moreover, US
authorities have been criticised for not having performed enough prionic tests
in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a
directive to state public-health and agriculture officials prohibiting material
from CWD-positive animals from being used as an ingredient in feed for any
animal species, epidemiological control and research in the USA has been quite
different from the situation in the UK and Europe regarding BSE.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
Norman Foster, director of the Cognitive Disorders Clinic at the University
of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion
disease in people in the USA is inadequate to detect whether CWD is occurring in
human beings; adding that, the cases that we know about are reassuring, because
they do not suggest the appearance of a new variant of CJD in the USA or
atypical features in patients that might be exposed to CWD. However, until we
establish a system that identifies and analyses a high proportion of suspected
prion disease cases we will not know for sure. The USA should develop a system
modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported
the cases of three hunterstwo of whom were friendswho died from pathologically
confirmed CJD, says that at present there are insufficient data to claim
transmission of CWD into humans; adding that [only] by asking [the questions of
venison consumption and deer/elk hunting] in every case can we collect suspect
cases and look into the plausibility of transmission further. Samii argues that
by making both doctors and hunters more aware of the possibility of prions
spreading through eating venison, doctors treating hunters with dementia can
consider a possible prion disease, and doctors treating CJD patients will know
to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC will not be investigating the
[Samii] cases because there is no evidence that the men ate CWD-infected meat.
He notes that although the likelihood of CWD jumping the species barrier to
infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that
CWD does not exist in humans& the data seeking evidence of CWD transmission
to humans have been very limited.
Greetings,
> > > he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source. < < <
actually, that quote was from a more recent article in the Journal of
Neurology (see below), not the JAMA article.
Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al.
JAMA.2001; 285: 733-734.
snip...end...tss
Re: vCJD in the USA * BSE in U.S.
15 November 1999 Terry S Singeltary, NA
In reading the recent article in the BMJ about the potential BSE tests
being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize
me, that the U.S. has been concealing vCJD. There have been people dying from
CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for
some time. It just seems that when there is one found, they seem to change the
clarical classification of the disease, to fit their agenda. I have several
autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of
age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt
Jakob disease.
Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so
bad at times, it would take 3 of us to hold her down, while she screamed "God,
what's wrong with me, why can't I stop this." 1st of symptoms to death, 10
weeks, she went blind in the first few weeks. But, then they told me that this
was just another strain of sporadic CJD. They can call it what ever they want,
but I know what I saw, and what she went through. Sporadic, simply means, they
do not know.
My neighbors Mom also died from CJD. She had been taking a nutritional
supplement which contained the following;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver
powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine
stomach. As I said, this woman taking these nutritional supplements, died from
CJD.
The particular batch of pills that was located, in which she was taking,
was tested. From what I have heard, they came up negative, for the prion
protein. But, in the same breath, they said their testing, may not have been
strong enough to pick up the infectivity. Plus, she had been taking these type
pills for years, so, could it have come from another batch?
CWD is just a small piece of a very big puzzle. I have seen while deer
hunting, deer, squirrels and birds, eating from cattle feed troughs where they
feed cattle, the high protein cattle by products, at least up until Aug. 4,
1997.
So why would it be so hard to believe that this is how they might become
infected with a TSE. Or, even by potentially infected land. It's been well
documented that it could be possible, from scrapie. Cats becoming infected with
a TSE. Have you ever read the ingredients on the labels of cat and dog food?
But, they do not put these tissues from these animals in pharmaceuticals,
cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and
the many more products that come from bovine, ovine, or porcine tissues and
organs. So, as I said, this CWD would be a small piece of a very big puzzle.
But, it is here, and it most likely has killed. You see, greed is what caused
this catastrophe, rendering and feeding practices. But, once Pandora's box was
opened, the potential routes of infection became endless.
No BSE in the U.S.A.? I would not be so sure of that considering that since
1990;
Since 1990 the U.S. has raised 1,250,880,700 cattle;
Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of
Oct. 4, 1999;
There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until
Aug. 4, 1997 went to the renders for feed;
Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of
Aug. 1999;
Our feeding and rendering practices have mirrored that of the U.K. for
years, some say it was worse. Everything from the downer cattle, to those
scrapie infected sheep, to any roadkill, including the city police horse and the
circus elephant went to the renders for feed and other products for consumption.
Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs,
chickens, dogs, and cats, and humans were exempt from that ban. So they can
still feed pigs and chickens those potentially TSE tainted by-products, and then
they can still feed those by-products back to the cows. I believe it was Dr. Joe
Gibbs, that said, the prion protein, can survive the digestinal track. So you
have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle
feeders, sent neurologically ill cattle, some with encephalopathy stamped on the
dead slips, were picked up and sent to the renders, along with sheep carcasses.
Speaking of autopsies, I have a stack of them, from CJD victims. You would be
surprised of the number of them, who ate cow brains, elk brains, deer brains, or
hog brains.
I believe all these TSE's are going to be related, and originally caused by
the same greedy Industries, and they will be many. Not just the Renders, but you
now see, that they are re-using medical devices that were meant for disposal.
Some medical institutions do not follow proper auto- claving procedures (even
Olympus has put out a medical warning on their endescopes about CJD, and the
fact you cannot properly clean these instruments from TSE's), and this is just
one product. Another route of infection.
Regardless what the Federal Government in the U.S. says. It's here, I have
seen it, and the longer they keep sweeping it under the rug and denying the fact
that we have a serious problem, one that could surpass aids (not now, but in the
years to come, due to the incubation period), they will be responsible for the
continued spreading of this deadly disease.
It's their move, it's CHECK, but once CHECKMATE has been called, how many
thousands or millions, will be at risk or infected or even dead. You can't play
around with these TSE's. I cannot stress that enough. They are only looking at
body bags, and the fact the count is so low. But, then you have to look at the
fact it is not a reportable disease in most states, mis-diagnosis, no autopsies
performed. The fact that their one-in-a- million theory is a crude survey done
about 5 years ago, that's a joke, under the above circumstances. A bad joke
indeed........
The truth will come, but how many more have to die such a hideous death.
It's the Government's call, and they need to make a serious move, soon. This
problem, potential epidemic, is not going away, by itself.
Terry S. Singeltary Sr.
P.O. Box 42, Bacliff, Texas 77518 USA
flounder@wt.net
Competing interests:None declared
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well...
2 January 2000
Terry S Singeltary
In reading your short article about 'Scientist warn of CJD epidemic' news
in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous
again. Why is the U.S. still sitting on their butts, ignoring the facts? We have
the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing
everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years.
In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25
page report by the USDA:APHIS:VS. It could have been done in one page. The first
page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering
technology and the lack of usage of solvents, however, large differences still
remain with other risk factors which greatly reduce the potential risk at the
national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the
U.S., with nothing more than the cattle to sheep ratio count, and the
geographical locations of herds and flocks. That's all the evidence they can
come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous
rendering technology which uses lower temperatures and accounts for 25 percent
of total output. This technology was _originally_ designed and imported from the
United States. However, the specific application in the production process is
_believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The
calculations are based on slaughter numbers, fallen stock estimates, and product
yield coefficients. This approach is used due to variation of up to 80 percent
from different reported sources. At 3.6 million tons, the United States produces
8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is
more acute in both relative and absolute terms in the United Kingdom (Figures 27
and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61
thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in
the United States. For sheep greater than 1 year, this is less than one-tenth of
one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat
and bone meal is much greater in the United States where it accounts for 59
percent of total product or almost 5 times more than the total amount of
rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate
the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug.
1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful
of scrapie infected material is lethal to a cow.
Considering all this, the sheep to cow ration is meaningless. As I said,
it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
Competing interests:None declared
DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die
BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes
Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link
auf diesen Artikel im Archiv:
"Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im
Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem
Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der
Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der
Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und
arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter
durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in
denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.
Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter
belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese
verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem
oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die
Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus
Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten
und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch
Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten
auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise
gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht
Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in
denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich
verpflichteten sich fünf Unternehmen, darunter Branchenführer wie
GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus
unverdächtigem Material herzustellen.
"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA
regulations. ...
STILL IS FULL OF HOLES 2013 ;
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
Greetings,
since our fine federal friends have decided not to give out any more
reports on the USA breaches of the feed ban and surveillance etc. for the BSE
TSE prion mad cow type disease in the USDA livestock, I thought I might attempt
it. I swear, I just don’t understand the logic of the SSS policy, and that
includes all of it. I assure you, it would be much easier, and probably better
for the FDA and the USDA INC., if they would simply put some kind of report out
for Pete’s sake, instead of me doing it after I get mad, because I am going to
put it all out there. the truth.
PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI,
RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to
the eventual suspect tainted feed reaching livestock. please, if any USDA
official out there disputes this, please explain then how they could not.
paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow
feed ban reaching livestock, or contamination and exposure there from, as well.
I would sure like to see the full reports of just these ;
4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL
61044-9605 OPR FR, OF HP 11/26/2012 OAI Y
9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO
81067 OPR RE, TH HP 2/27/2013 OAI N
9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley
CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods
13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N
see full list of the fda mad cow bse feed follies, toward the bottom, after
a short brief update on the mad cow bse follies, and our good friend Lester
Crawford that was at the FDA.
ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed
Inspections Firms Inventory (excel format)4 format, for reporting these breaches
of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters
the fda use to put out for each violations. simply put, this excel format sucks,
and the FDA et al intentionally made it this difficult to follow the usda fda
mad cow follies. this is an intentional format to make it as difficult as
possible to follow these breaches of the mad cow TSE prion safety feed
protocols. to have absolutely no chronological or numerical order, and to format
such violations in a way that they are almost impossible to find, says a lot
about just how far the FDA and our fine federal friends will go through to hide
these continued violations of the BSE TSE prion mad cow feed ban, and any
breaches of protocols there from. once again, the wolf guarding the henhouse $$$
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
Inspections conducted by State and FDA investigators are classified to
reflect the compliance status at the time of the inspection, based upon whether
objectionable conditions were documented. Based on the conditions found,
inspection results are recorded in one of three classifications:
OAI (Official Action Indicated) when inspectors find significant
objectionable conditions or practices and believe that regulatory sanctions are
warranted to address the establishment’s lack of compliance with the regulation.
An example of an OAI classification would be findings of manufacturing
procedures insufficient to ensure that ruminant feed is not contaminated with
prohibited material. Inspectors will promptly re-inspect facilities classified
OAI after regulatory sanctions have been applied to determine whether the
corrective actions are adequate to address the objectionable conditions.
VAI (Voluntary Action Indicated) when inspectors find objectionable
conditions or practices that do not meet the threshold of regulatory
significance, but warrant an advisory to inform the establishment that
inspectors found conditions or practices that should be voluntarily corrected.
VAI violations are typically technical violations of the 1997 BSE Feed Rule.
These violations include minor recordkeeping lapses or conditions involving
non-ruminant feeds.
NAI (No Action Indicated) when inspectors find no objectionable conditions
or practices or, if they find objectionable conditions, those conditions are of
a minor nature and do not justify further actions.
when sound science was bought off by junk science, in regards to the BSE
TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$
when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was
taken away that infamous day in December of 2003, all cards were off the table,
it was time to change the science, and change they did. ...tss
snip. ...please see full text ;
Thursday, June 6, 2013
BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI
ratings as at June 5, 2013
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES
[Docket No. APHIS-2006-0041] RIN 0579-AC01
January 28, 2007
Greetings APHIS,
I would kindly like to submit the following to ;
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES
[Docket No. APHIS-2006-0041] RIN 0579-AC01
January 28, 2007 - Regulations.gov
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS Regulations Comments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)
Page 1 of 98 8/3/2006
Greetings FSIS, I would kindly like to comment on the following ;
Response to Public Comments on the Harvard Risk Assessment of Bovine
Spongiform Encephalopathy Update, October 31, 2005
INTRODUCTION The United States Department of Agriculture’s Food Safety and
Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington,
D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform
Encephalopathy Update, October 31, 2005 (report and model located on the FSIS
website:
http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).
Comments on technical aspects of the risk assessment were then submitted to
FSIS. Comments were received from Food and Water Watch, Food Animal Concerns
Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S.
Singeltary. This document provides itemized replies to the public comments
received on the 2005 updated Harvard BSE risk assessment.
Please bear the following points in mind:
-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder@wt.net]
Sent: Tuesday, February 18, 2003 12:45 PM
To: Freas, William
Cc: Langford, Sheila
Subject: Re: re-vCJD/blood and meeting of Feb. 20, 2003
Greetings FDA,
Variant Creutzfeldt-Jakob Disease Guidance Topic of Feb. 20 TSE Cmte.
[Committee Meeting on February 20, 2003]
FDA’s Transmissible Spongiform Encephalopathies Advisory Committee will
meet Feb. 20 to hear updates on the implementation of the agency’s variant
Creutzfeldt-Jakob Disease guidance and its effect on blood supply. FULL
STORY>>
my name is Terry S. Singeltary Sr., and i lost my mother to hvCJD, one of
six known phenotypes of sporadic CJD. i would like to observe this meeting or
participate, but have no financial means to do so with. i am disabled from neck
injury. anyway, i am not sure if a waiver of fees is possible? i belong to
several groups trying to track the true extent of CJDs and trying to find the
truth. with CJDs not being reportable but only in a handful of states, and the
fact there is no CJD Questionnaire being issued to victims and their families
that asks any questions pertaining to route and source, i think to track tainted
blood will be futile. i had a major neck surgery in 2001 (3rd), and not _one_
question pertaining to CJD/TSE on any paperwork (and damn near died from MRSA
after refusing blood and cadaver bone for fear of risk of CJD/TSEs, go figure, 7
weeks vancomycin via PIC long-line straight to heart). luckily i had informed my
neurosurgeon and he did use some disposable instruments and a bone grinder that
would not be used again. i would like to submit my concerns on the vCJD _only_
theory as being a total mistake, and that no one knows just how many strains are
actually linked to tainted meat and the oral route (one of many potential
routes). Asante/Collinge et al have major findings on sporadic CJD, why in the
hell is this not making big news in the USA? ($$$) the fact that with the new
findings from Collinge et al, that BSE transmission to the 129-methionine
genotype can lead to an alternate phenotype which is indistinguishable from type
2 PrPSc, the commonest sporadic CJD, i only ponder how many of the sporadic CJDs
in the USA are tied to this alternate phenotype? these new findings are very
serious, and should have a major impact on the way sporadic CJDs are now treated
as opposed to the vCJD that was thought to be the only TSE tied to ingesting
beef, in the medical/surgical arena. these new findings should have a major
impact on the way sporadic CJD is ignored, and should now be moved to the
forefront of research as with vCJD/nvCJD. the USA has many TSEs, the USA lacks
sufficient testing for TSEs in cattle, and the USA still refuses to rapid TSE
test USA cattle in sufficient numbers to find, when the late Dr. Richard Marsh
had proven that mink had gone down with a TSE (TME), from being fed on 95%+
downer cattle. the GAO has also warned the industry and the FDA that the
ruminant-to-ruminant feed ban has to significantly improved if they expect to
keep BSE/TSEs out of USA cattle. Scrapie has increased significantly, and CWD is
spreading. with the titre of infectivity for lethal dose getting smaller (.1
gram lethal), seems the risk of transmission through various potential routes
and sources are rising. all this should warrant CJD/TSEs in humans in the USA to
be made reportable on a National bases immediately, and a CJD questionnaire to
all CJD/TSE victims and their families. to flounder on these two very important
issues, will only allow the agent to spread further...
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a
Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have
attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, yes. As you will
find in the paper, we have managed to associate the alternate phenotype to type
2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any
further sub-classification in respect of Heidenhain variant CJD or Vicky
Rimmer's version. It will take further studies, which are on-going, to establish
if there are sub-types to our initial finding which we are now reporting. The
main point of the paper is that, as well as leading to the expected new variant
CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an
alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can
be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial
College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44
(0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until
9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________
Freas, William
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Monday, January 08,2001 3:03 PM
To: freas@CBS5055530.CBER.FDA.GOV
Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To
Scientific Advisors and Consultants Staff January 2001 Meeting (short
version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and
Consultants Staff 2001 Advisory Committee (short version).
I understand the reason of having to shorten my submission, but only hope
that you add it to a copy of the long version, for members to take and read at
their pleasure, (if cost is problem, bill me, address below).
So when they realize some time in the near future of the 'real' risks i
speak of from human/animal TSEs and blood/surgical products. I cannot explain
the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages,
but will attempt here:
remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?
no need to go into that, you know of this blunder:
DO NOT make these same stupid mistakes again with human/animal TSE's aka
MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD
as well (both cases confirmed). I have seen many deaths, from many diseases. I
have never seen anything as CJD, I still see my Mom laying helpless, jerking
tremendously, and screaming "God, what's wrong with me, why can't I stop this".
I still see this, and will never forget. Approximately 10 weeks from 1st of
symptoms to death. This is what drives me. I have learned more in 3 years about
not only human/animal TSE's but the cattle/rendering/feeding industry/government
than i ever wished to.
I think you are all aware of CJD vs vCJD, but i don't think you all know
the facts of human/animal TSE's as a whole, they are all very very similar, and
are all tied to the same thing, GREED and MAN.
I am beginning to think that the endless attempt to track down and ban,
potential victims from known BSE Countries from giving blood will be futile. You
would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT
SWIFTLY to find blood test for TSE's, whether it be blood test, urine test,
eyelid test, anything at whatever cost, we need a test FAST.
DO NOT let the incubation time period of these TSEs fool you.
To think of Scrapie as the prime agent to compare CJD, but yet overlook the
Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by
scrapie from a vaccine made of scrapie infected sheep brains, would be foolish.
I acquired this full text version of the event which was recorded in the Annual
Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the
BVA and the URL is posted in my (long version).
U.S.A. should make all human/animal TSE's notifiable at all ages, with
requirements for a thorough surveillance and post-mortem examinations free of
charge, if you are serious about eradicating this horrible disease in man and
animal.
There is histopathology reports describing “_florid_ plaques" in CJD
victims in the USA and some of these victims are getting younger. I have copies
of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will
most definitely be a problem.
THEN think of vaccineCJD in children and the bovine tissues used in the
manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS
-- Brown et al. 97 (7): 3418 scrapie agent live at 600*C
Then think of the CONFIDENTIAL documents of what was known of human/animal
TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to
hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's
from the polio vaccine, (one taken orally i think?), but yet neglect to act on
the other potential TSE vaccines (inoculations, the most effective mode to
transmit TSEs) of which thousands of doses were kept and used, to deplete
stockpile, again would be foolish.
--Oral polio; up to 1988, foetal calf serum was used from UK and New
Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large
stocks are held.
--Rubella; bulk was made before 1979 from foetal calf serum from UK and New
Zealand. None has been made as there are some 15 years stock.
--Diphtheria; UK bovine beef muscle and ox heart is used but since the end
of 1988 this has been sourced from Eire. There are 1,250 litres of stock.
--Tetanus; this involves bovine material from the UK mainly Scottish. There
are 21,000 litres of stock.
--Pertussis; uses bovine material from the UK. There are 63,000 litres of
stock.
--They consider that to switch to a non-UK source will take a minimum of
6-18 months and to switch to a non-bovine source will take a minimum of five
years.
3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are
sourced from the USA and the company believes that US material only is
used.
89/2.14/2.1
============
BSE3/1 0251
4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there
are 440,000 units of stock. They have also got MMR using bovine serum from the
UK.
5. XXXXXXXXXXX have influenza, rubella, measles, MMR vaccines likely to be
used in children. Of those they think that only MMR contains bovine material
which is probably a French origin.
6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial.
These use veal material, some of which has come from the UK and has been made by
XXXXXXXXXXX (see above).
I have documents of imports from known BSE Countries, of ferments, whole
blood, antiallergenic preparations,
2
human blood plasma, normal human blood sera, human immune blood sera, fetal
bovine serum, and other blood fractions not elsewhere specified or included,
imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us
not forget about 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.
ANNEX 6
MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO
BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL
How much of this was used in the U.S.?
Please do not keep making the same mistakes;
'Absence of evidence is not evidence of absence'. What are the U.S. rules
for importing and manufacturing vaccines, medicines and medical devices?
Does the U.S.A. allow sourcing of raw material of ruminants from the
U.S.A.?
U.S. cattle, what kind of guarantee can you give for serum or tissue donor
herds.?
The U.S. rendering system would easily amplify T.S.E.'s: Have we increased
the stability of the system (improved heat treatments) since the EU SSC report
on the U.S.A. was published in july 2000?
What is done to avoid cross-contaminations in the U.S.A.?
How can the U.S. control absence of cross-contaminations of animal TSE's
when pig and horse MBM and even deer and elk are allowed in ruminant feed, as
well as bovine blood?
I sadly think of the rendering and feeding policy before the Aug. 4, 1997
'partial' feed ban, where anything went, from the city police horse, to the
circus elephant, i will not mention all the scrapie infected sheep. I am
surprised that we have not included man 'aka soyent green'. It is a disgusting
industry and nothing more than greed fuels it.
When will the U.S.. start real surveillance of the U.S. bovine population
(not passive, this will not work)?
When will U.S. start removing SRMs?
Have they stopped the use of pneumatic stunners in the U.S.?
If so, will we stop it in all U.S. abattoirs or only in those abattoirs
exporting to Europe?
If not, WHY NOT?
same questions for removal of SRM in the U.S.A., or just for export?
If not, WHY NOT?
How do we now sterilize surgical/dental instruments in the U.S.A.?
Where have we been sourcing surgical catgut?
(i have copies of imports to U.S., and it would floor you) hen will
re-usable surgical instruments be banned?
Unregulated "foods" such as 'nutritional supplements' containing various
extracts from ruminants, whether imported or derived from
3
US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or
at least very seriously regulated. (neighbors Mom, whom also died from CJD, had
been taking bovine based supplement, which contained brain, eye, and many other
bovine/ovine tissues for years, 'IPLEX').
What is the use of banning blood or tissue donors from Germany, France,
etc... when the U.S.A. continues exposing cattle, sheep and people to SRM,
refuses to have a serious feed ban, refuses to do systematic
BSE-surveillance?
The FDA should feel responsible for the safety of what people eat, prohibit
the most dangerous foods, not only prohibit a few more donors - the FDA should
be responsible for the safe sourcing of medical devices, not only rely on
banning donors "from Europe" The 'real' risks are here in the U.S. as well, and
nave been for some time.
We must not forget the studies that have proven infectivity in blood from
TSE's.
The Lancet, November 9, 1985
Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report "
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat
from two patients. We also transmitted the disease from whole blood samples of a
patient (and of mice) infected with CJD.1 Brain, Cornea, and urine from this
patient were also infectious, and the clinicopathological findings2 are
summarised as follows.
snip...
Samples,were taken aseptically at necropsy. 10% crude homogenates of brain
and cornea in saline, whole blood (after crushing a clot), and untreated CSF and
urine were innoculated intracerebrally into CF1 strain mice (20 ul per animal).
Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and
sometimes tremor after long incubation periods. Tissues obtained after the
animal died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes, consisting of
severe spongiform changes, glial proliferation, and a moderate loss of nerve
cells. A few mice inoculated with brain tissue or urine had the same amyloid
plaque found in patients and animals with CJD.3
snip...
Department of Neuropathology, Neurological Institute, Faculty of Medicine,
Kyushu University, Fukuoka812, Japan
JUN TATEISHI (full text-long version)
and
CWD and transmission to man will be no different than other TSE's.
"Clearly, it is premature to draw firm conclusions about CWD assing
naturally into humans, cattle and sheep, but the present esults suggest that CWD
transmissions to humans would be as limited by PrP incompatibility as
transmissions of BSE or sheep scrapie to humans. Although there is no evidence
that sheep scrapie has affected humans, it is likely that BSE has
4
caused variant CJD in 74 people (definite and probable variant CJD cases to
date according to the UK CJD Surveillance Unit). Given the presumably large
number of people exposed to BSE infectivity, the susceptibility of humans may
still be very low compared with cattle, which would be consistent with the
relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since
humans have apparently been infected by BSE, it would seem prudent to take
reasonable measures to limit exposure of humans (as well as sheep and cattle) to
CWD infectivity as has been recommended for other animal TSEs,"
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4,
P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B.
Caughey1,7
or more recently transmission of BSE to sheep via whole blood Research
letters Volume 356, Number 9234 16 September 2000
Transmission of BSE by blood transfusion in sheep Lancet 2000; 356: 999 –
1000
F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock
See Commentary
"We have shown that it is possible to transmit bovine spongiform
encephalopathy (BSE) to a sheep by transfusion with whole blood taken from
another sheep during the symptom-free phase of an experimental BSE infection.
BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by
the same infectious agent, and the sheep-BSE experimental model has a similar
pathogenesis to that of human vCJD. Although UK blood transfusions are
leucodepleted--a possible protective measure against any risk from blood
transmission-- this report suggests that blood donated by symptom-free
vCJD-infected human beings may represent a risk of spread of vCJD infection
among the human population of the UK."
"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD)
is caused by the same agent that causes bovine spongiform encephalopathy (BSE)
in cattle1 has raised concerns that blood from human beings in the symptom-free
stages of vCJD could transmit infection to recipients of blood transfusions
(full text long version)" and...
"The large number of cases (1040), temporal clustering of the outbreaks (15
in the first 6 months of 1997), the high in-flock incidence, and the exceptional
involvement of goats (390 cases), suggested an accidental infection. The source
of the epidemic might have been TSE-contaminated meat and bonemeal, but eight
flocks had never been fed any commercial feedstuff. Infection might have risen
from the use of a formol-inactivated vaccine against contagious agalactia
prepared by a single laboratory with brain and mammary gland homogenates of
sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the
donor sheep have not been found, it is possible that one or more of them were
harbouring the infectious agent. Between 1995 and 1996, this vaccine was given
subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these
animals the disease appeared between 23 and 35 months after vaccination. No
information is available for herd 13 because it was made up of stolen animals.
Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine,
thus suggesting a naturally occurring disease.” (again, full text long
version).
IN SHORT, please do under estimate this data and or human/animal TSE's
including CWD in the U.S.A.
A few last words, please.
The cattle industry would love to have us turn our focus to CWD and forget
about our own home grown TSE in Bovines. This would be easy to do. Marsh's work
was from downer cattle feed, NOT downer deer/elk feed. This has been proven.
DO NOT MAKE THAT MISTAKE.
There should be NO LESS THAN 1,000,000 tests for BSE/TSE in 2001 for U.S.A.
French are testing 20,000 a week. The tests are available. Why wait until we
stumble across a case from passive surveillance, by then it is to late. IF we
want the truth, this is a must???
United States Total ,Bovine Brain Submissions by State,
May 10, 1990 thru October 31, 2000
Total 11,700
FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???
with same feeding and rendering practices as that of U.K. for years and
years, same scrapie infected sheep used in feed, for years and years, 950
scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known
to date. (hmmm, i am thinking why there is not a variant scrapid, that is
totally different than all the rest)? just being sarcastic.
with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need
to reconsider that blood meal etc. 'TOTAL BAN')
AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied
to this environmental death sentence. "PROVE IT". It's just not true. The
'CHOSEN ONES' are not the only ones dying because of this man-made death
sentence. When making regulations for human health from human/animal TSEs, you
had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic
CJD with the 'prehistoric' testing available to date. This could be a deadly
mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death,
and hvCJD is the fastest. Could it just be a higher titre of infectivity, or
route or source, or all three?
Last, but not least. The illegal/legal harvesting of body parts and tissues
will come back to haunt you. Maybe not morally, but due to NO background checks
and human TSEs, again it i will continue to spread.
Stupidity, Ignorance and Greed is what fuels this disease. You must stop
all of this, and ACT AT ONCE...
"different strains (of same disease), different routes of infection (of
same disease), different infectivity levels (dose rate) of the (same disease) =
different symptoms, different lengths of illness from 1st onset of illness to
death, (of the same disease) + different cultures = different geographical
locations = different strains (of same disease)...TSS"
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
aggressively 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.)
CJD QUESTIONNAIRE USA
CJD VOICE
TSS
