sporadic CJD in two adolescents (sCJD, the big lie)

[flatfish]

Subject: Sporadic creutzfeldt-jakob disease in two adolescents (see sCJD,
the big lie)
Date: May 28, 2007 at 7:58 am PST

J Neurol Neurosurg Psychiatry. Published Online First: 23 May 2007.
doi:10.1136/jnnp.2006.104570
© 2007 by BMJ Publishing Group Ltd

Original articles

Sporadic creutzfeldt-jakob disease in two adolescents

K Murray 1, D L Ritchie 1, M Bruce 2, C A Young 3, M Doran 3, J W Ironside 4
and R G Will 4*
1 NationalCJD Surveillance Unit, United Kingdom
2 Neuropathogenesis Unit, United Kingdom
3 Walton Centre for Neurology and Neurosurgery, United Kingdom
4 National CJD Surveillance Unit, United Kingdom

* To whom correspondence should be addressed. E-mail: r.g.will@ed.ac.uk.

Accepted 15 April 2007


Abstract


Background: Sporadic Creutzfeldt-Jakob disease (CJD) is a condition
predominantly affecting older age groups, with cases aged less than 45 years
rare and an age at onset or death of less than 20 years exceptional.

Methods: Data from the systematic study of sporadic CJD in the UK are
available from 1970 onwards. Clinical and pathological data are reviewed in
order to identify atypical cases, including those at the extremes of the age
range of sporadic CJD. Detailed analysis of atypical cases is undertaken and
in selected cases laboratory transmission studies are carried out in order
to provide information on the characteristics of the infectious agent.

Results: In the UK two cases of sporadic CJD in adolescents have been
identified, dying aged 16 and 20 years. The first case predated the epidemic
of bovine spongiform encephalopathy and the characteristics of the second
case, including laboratory transmission studies, are consistent with a
diagnosis of sporadic rather than variant CJD.

Conclusion: The cases in this report indicate that sporadic CJD can develop
at a very young age, that variant CJD is not the only form of CJD occurring
in this age group and that neuropathological examination is essential to
accurate diagnosis of human prion disease.


http://jnnp.bmj.com/cgi/content/abst....2006.104570v1


Sent: Monday May 28, 2007

Subject: THE BIG LIE SPORADIC CJD AND MAD COW DISEASEs i.e. TSE

Terry S. Singeltary Sr.


POLICY IN CONFIDENCE; CONFIDENTIAL; CJD IN FARMER WITH BSE COW ie
OCCUPATIONAL EXPOSURE


Subject: POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW


POLICY IN CONFIDENCE: CJD IN FARMER WITH BSE COW

LIKELY TO ATRACT MEDIA ATTENTION

http://www.bseinquiry.gov.uk/files/y...8/13002001.pdf

http://www.bseinquiry.gov.uk/files/y...8/21002001.pdf

http://www.bseinquiry.gov.uk/files/y...8/21005001.pdf

CONFIRMED CJD IN FARMER WITH BSE COW

line to take, sporadic CJD

http://www.bseinquiry.gov.uk/files/y...0/22004001.pdf

http://www.bseinquiry.gov.uk/files/y...0/22005001.pdf

http://www.bseinquiry.gov.uk/files/y...0/22001001.pdf

http://www.bseinquiry.gov.uk/files/y...1/05002001.pdf

http://www.bseinquiry.gov.uk/files/y...1/05003001.pdf


SECOND CASE CJD IN DAIRY FARMER

http://www.bseinquiry.gov.uk/files/y...0/00001001.pdf


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.

http://www.bseinquiry.gov.uk/files/y...2/15003001.pdf


''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.
.........


http://www.bseinquiry.gov.uk/files/y...7/12001001.pdf


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....

http://www.bseinquiry.gov.uk/files/y...7/12002001.pdf


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. ...

http://www.bseinquiry.gov.uk/files/y...7/12003001.pdf



CONFIDENTIAL

CONFIRMED CASE OF CJD IN DAIRY FARMER

http://www.bseinquiry.gov.uk/files/y...7/14003001.pdf


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 ;

http://www.bseinquiry.gov.uk/files/y...7/19001001.pdf



Rocky Mountain oysters, mountain oysters, prairie oysters, Montana
tendergroin or swinging sirloin


POLICY IN CONFIDENCE


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)


http://www.bseinquiry.gov.uk/files/y...8/12002001.pdf


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)

http://www.bseinquiry.gov.uk/files/y...8/18004001.pdf


'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.

http://www.bseinquiry.gov.uk/files/y...8/26001001.pdf


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.



http://www.bseinquiry.gov.uk/files/y...0/11001001.pdf



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.....


http://www.bseinquiry.gov.uk/files/y...0/12001001.pdf



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.


http://www.bseinquiry.gov.uk/files/y...0/18001001.pdf


INCREASE IN SPORADIC CJD

http://www.bseinquiry.gov.uk/files/y...1/11001001.pdf


occupational

http://www.bseinquiry.gov.uk/files/y...2/16001001.pdf


Dealler gets ''dixie chicked' again ;

http://www.bseinquiry.gov.uk/files/y...1/22001001.pdf

http://www.bseinquiry.gov.uk/files/y...2/08003001.pdf

http://www.bseinquiry.gov.uk/files/y...2/10006001.pdf

http://www.bseinquiry.gov.uk/files/y...2/14003001.pdf

http://www.bseinquiry.gov.uk/files/y...2/16006001.pdf

http://www.bseinquiry.gov.uk/files/y...2/17003001.pdf




continued

[flatfish]

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.
.....


http://www.bseinquiry.gov.uk/files/y...2/01003001.pdf


http://www.bseinquiry.gov.uk/files/y...1/00005001.pdf



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)


http://www.bseinquiry.gov.uk/files/y...7/00001001.pdf



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

http://www.bseinquiry.gov.uk/files/y...7/00001001.pdf


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.

http://www.bseinquiry.gov.uk/files/y...0/00003001.pdf

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

http://www.bseinquiry.gov.uk/files/y...0/00004001.pdf


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

http://www.bseinquiry.gov.uk/files/y...8/00004001.pdf


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.''

http://www.bseinquiry.gov.uk/files/y...2/11001001.pdf


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

http://www.bseinquiry.gov.uk/files/db/do01/tab03.pdf


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. ...

http://www.bseinquiry.gov.uk/files/y...1/14005001.pdf

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.

http://www.bseinquiry.gov.uk/files/y...1/20001001.pdf

STATEMENT FROM HOSPITAL

http://www.bseinquiry.gov.uk/files/y...1/20005001.pdf

http://www.bseinquiry.gov.uk/files/y...1/25001001.pdf

PREPARING FOR THE STORM 'LINE TO TAKE'

http://www.bseinquiry.gov.uk/files/y...1/25003001.pdf

BARONESS CUMBERLEGE TRYING TO MANIPULATE THE MEDIA

http://www.bseinquiry.gov.uk/files/y...1/25006001.pdf

http://www.bseinquiry.gov.uk/files/y...1/25006001.pdf

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).

http://www.bseinquiry.gov.uk/files/y...1/25007001.pdf

GIVE ME BACK MY LIFE

http://www.bseinquiry.gov.uk/files/y...1/25008001.pdf

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

http://www.bseinquiry.gov.uk/files/y...1/25009001.pdf

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

http://www.bseinquiry.gov.uk/files/y...1/25010001.pdf

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

http://www.bseinquiry.gov.uk/files/y...2/22009001.pdf

Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.

(now story changes that biopsy shows she does not have CJD...tss)

http://www.bseinquiry.gov.uk/files/y...6/06004001.pdf

now story changes to ;

continued

[flatfish]

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.

http://www.bseinquiry.gov.uk/files/y...6/08004001.pdf

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.

http://www.bseinquiry.gov.uk/files/y...6/08006001.pdf


(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:
"'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)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/...3923s1_OPH.htm


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.

http://www.bseinquiry.gov.uk/files/y...0/27013001.pdf

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....

http://www.bseinquiry.gov.uk/files/y...0/04004001.pdf


NOW BACK TO THOSE FARMERS WITH BSE HERDS THAT DIED FROM SPORADIC CJD


CJD FARMERS WIFE 1989

http://www.bseinquiry.gov.uk/files/y...0/13007001.pdf

http://www.bseinquiry.gov.uk/files/y...0/13003001.pdf

cover-up of 4th farm worker ???

http://www.bseinquiry.gov.uk/files/y...0/23006001.pdf

http://www.bseinquiry.gov.uk/files/y...0/20006001.pdf

CONFIRMATION OF CJD IN FOURTH FARMER

http://www.bseinquiry.gov.uk/files/y...1/03008001.pdf

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?

http://www.bseinquiry.gov.uk/files/y...1/13010001.pdf

4th farmer, and 1st teenager

http://www.bseinquiry.gov.uk/files/y...2/27003001.pdf

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...

http://www.bseinquiry.gov.uk/files/y...1/31004001.pdf


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...

http://www.seac.gov.uk/minutes/95.pdf


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


http://www.healthtech.com/2007/tse/day1.asp


SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resou...asereport.html

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.


http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/...006-4240t1.pdf


continued

[flatfish]

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

http://jama.ama-assn.org/http://www....s/60/2/176#535


BRITISH MEDICAL JOURNAL

BMJ

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

BMJ

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1


JOURNAL OF NEUROLOGY

MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

flounder@wt.net

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?

http://www.neurology.org/cgi/eletters/60/2/176#535



HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory

<P> TSEs have been rampant in the USA for decades in many
species, and they all have been rendered and fed back
to animals for human/animal consumption. 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 2005.
With all the science to date refuting it, to continue
to validate this myth, will only spread this TSE agent
through a multitude of potential routes and sources
i.e. consumption, surgical, blood, medical, cosmetics
etc. I propose as with Aguzzi, Asante, Collinge,
Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE
Tranmissible 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. This would further have to be broken down to
strain of species and then the route of transmission
would further have to be broken down. Accumulation and
Transmission are key to the threshold from subclinical
to clinical disease, and of that, I even believe that
physical and or blunt trauma may play a role of onset
of clinical symptoms in some cases, but key to all
this, is to stop the amplification and transmission of
this agent, the spreading of, no matter what strain.
BUT, to continue with this myth that the U.K. strain of
BSE one strain in cows, and the nv/v CJD, one strain in
humans, and that all the rest of human TSE is one
single strain i.e. sporadic CJD (when to date there are
6 different phenotypes of sCJD), and that no other
animal TSE transmits to humans, to continue with this
masquerade will only continue to spread, expose, and
kill, who knows how many more in the years and decades
to come. ONE was enough for me, My Mom, hvCJD, DOD
12/14/97 confirmed, which is nothing more than another
mans name added to CJD, like CJD itself, Jakob and
Creutzfeldt, or Gerstmann-Straussler-Scheinker
syndrome, just another CJD or human TSE, named after
another human. WE are only kidding ourselves with the
current diagnostic criteria for human and animal TSE,
especially differentiating between the nvCJD vs the
sporadic CJD strains and then the GSS strains and also
the FFI fatal familial insomnia strains or the ones
that mimics one or the other of those TSE? Tissue
infectivity and strain typing of the many variants of
the human and animal TSEs are paramount in all variants
of all TSE. There must be a proper classification that
will differentiate between all these human TSE in order
to do this. With the CDI and other more sensitive
testing coming about, I only hope that my proposal will
some day be taken seriously.

<P> My name is Terry S. Singeltary Sr. and I am no
scientist, no doctor and have no PhDs, but have been
independently researching human and animal TSEs since
the death of my Mother to the Heidenhain Variant of
Creutzfeldt Jakob Disease on December 14, 1997
'confirmed'. ...TSS

<P> Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

<P> SOURCES

<P> Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al.
JAMA.2001; 285: 733-734

<P> http://jama.ama-
assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=
&fulltext=dignosing+and+reporting+creutzfeldt+jako b+disease&searchid=1048865
596978_1528&stored_search=&FIRSTINDEX=0&journalcod e=jama


<P> Coexistence of multiple PrPSc types in individuals with

<P> Creutzfeldt-Jakob disease

<P> Magdalini Polymenidou, Katharina Stoeck, Markus
Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi

<P> Summary

<P> Background The molecular typing of sporadic
Creutzfeldt-Jakob disease (CJD) is based on the size
and glycoform

<P> ratio of protease-resistant prion protein (PrPSc), and
on PRNP haplotype. On digestion with proteinase K, type
1 and

<P> type 2 PrPSc display ung*****ylated core fragments of
21 kDa and 19 kDa, resulting from cleavage around amino

<P> acids 82 and 97, respectively.

<P> Methods We generated anti-PrP monoclonal antibodies to
epitopes immediately preceding the differential proteinase

<P> K cleavage sites. These antibodies, which were
designated POM2 and POM12, recognise type 1, but not
type 2, PrPSc.

<P> Findings We studied 114 brain samples from 70 patients
with sporadic CJD and three patients with variant CJD.

<P> Every patient classified as CJD type 2, and all variant
CJD patients, showed POM2/POM12 reactivity in the

<P> cerebellum and other PrPSc-rich brain areas, with a
typical PrPSc type 1 migration pattern.

<P> Interpretation The regular coexistence of multiple
PrPSc types in patients with CJD casts doubts on the
validity of

<P> electrophoretic PrPSc mobilities as surrogates for
prion strains, and questions the rational basis of
current CJD

<P> classifications.

<P> snip...

<P> The above results set the existing CJD classifications

<P> into debate and introduce interesting questions about

<P> human CJD types. For example, do human prion types

<P> exist in a dynamic equilibrium in the brains of affected

<P> individuals? Do they coexist in most or even all CJD

<P> cases? Is the biochemically identified PrPSc type simply

<P> the dominant type, and not the only PrPSc species?

<P> Published online October 31, 2005

<P> http://neurology.thelancet.com

<P> Detection of Type 1 Prion Protein in Variant

<P> Creutzfeldt-Jakob Disease


snip...end


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texsas USA 77518