bse-tester said:
MRJ wrote:
Along with the lack of proof of verified connection between BSE and vCJD, does anyone have the dates of those 160+/- deaths? It seems to me that it was 'forever', more or less, as the time frame.
How many names and dates of their deaths do you want?
Further, it is painfully obvious that some here do not know the difference between the classic form of CJD or one the markedly different form -variant CJD (vCJD). Do not consider them to be identical as they are not - similar in many ways yes, but not exactly the same. There is a slight difference that provides for an identification protocol that catagorically shows the difference between the two. Also, please do not ask me to provide you the two protocols - you can do your own DD.
So before you guys start to hurl rocks, learn the difference between the diagnostic of typical CJD and the variant form. Then you might not be so hasty to form your own interpretations of what science has already proven to be fact. Basically, I see this ongoing argument as something that is borne out of being overprotective of an industry. An industry that either refuses to accept the truth or simply wishes to ignore it and hope it will go away.
So do not forget about the incubation period in humans - typically, it can be decades. So perhaps, in Europe and especially in the UK, we may well see a boom of cases in 20 or 30 years from now, if not sooner!
The attitude here is ofte truly sad that those who wish to share information are subjected to rhetoric and interoogation that smacks of the classic Inquisition. Conform to the main [uninformed] opinion of be gone more like!!!
hello BSE-tester,
i was not going to even post to this stupid thread. but since you decided to comment the way you did, i decided i had to post.
do you believe in the ukbsenvcjd only theory too???
this theory is beyond ignorance. makes no sense.
BSE-tester stated ;
>>>Further, it is painfully obvious that some here do not know the difference between the classic form of CJD or one the markedly different form -variant CJD (vCJD). <<<
do you ???
different strains, different routes, different titre of infectivity, does not make different disease. there are so many TSE with just the names of different people going for gold i.e. CJD or JCD depending whom was first Creutzfeldt or Jakob, then i don't know which one of these were first Gerstmann, Straussler, or Scheinker, and dont forget Mr. Heidenhain, then you had the FFI's, until that pathology did not match to any familial, so Gambetti et al i think, had to name that bad boy sporadic FFI, so, we jumped from a familial TSE, BACK to a sporadic TSE, but not CJD. confusious is confused again here, and i think they have been for some time ;
http://bmb.oxfordjournals.org/cgi/content/abstract/66/1/213
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10371520&dopt=Abstract
THE diagnostic criteria for differentiating between the different human TSE has been wrong from day one. we just got through discussing this on another list, and i just got back a letter from SEAC, i was deeply disturbed about there refusing to speak about the 'other' CJDs in there annual report. but they will speak of it soon i have been told. these 'other' CJDs have route and source too.
BSE-tester, are you of the 'spontaneous' of 85%+ of all human TSE clan ???
no route, no source, just spontaneous in most human cases i.e. sporadic 85%+ of all human TSE, with new unknown strains being documented, of which now are documented at 6 different phenotypes ???
i am confused about you stance here ???
snip...
ODD how we are seeing more and more CJD victims here with pain.
looks like they will have to go back to the drawing board on this myth as well.
this is normally associated with nvCJD, not sporadic CJD, from previous peer
review studies. this was the case with the kuru type plaques as well, we have seen those
in some sporadic CJD autopsies and this too was first only to be associated with the nvCJD. we also have
seen sCJD victims with psychiatric symptoms, * depression, anxiety, apathy, withdrawal, delusions,
and some that were young too, we have also seen some of this with sporadic CJD victims. so, as i have said
time and time again, the diagnostic criteria differentiating between the different human TSEs has been
wrong from day one. ... just my opinion.....tss
B) PERSISTENT PAINFUL SENSORY SYMPTOMS **
** this includes both frank pain and/ or unpleasant dysaesthesia
WITH the new BASE TSE in bovine, the one that does not look like nvCJD but like some of the sporadic CJD
pathologically in humans via tmice, i would seriously take a look at this again, then go back and look at the pathology of the BSE farmers and there wives that died from the sporadic CJD, I would seriously go back and re-evaluate all this again...................tss
a.. HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory - TSS 1/29/06 (0) (SEE last)
snip...
more on this topic of BASE and sporadic CJD later. SEAC told me they WILL address this issue later this year.
i was very upset they did not even mention spordic CJDs in there 2006 annual report, and i told them so. for whatever that was worth. ...TSS
----- Original Message -----
From: xxxxxxxxx (SEAC)
To: '
[email protected]'
Sent: Friday, February 23, 2007 8:13 AM
Subject: RE: SEAC ANNUAL REPORT 2006
Dear Mr Singeltary
Thank you for your email about a possible relationship between BASE and sCJD.
SEAC is continually informed about and considers the emerging science on both animal and human TSEs. The committee regularly receives updates from the UK's National CJD Surveillance Centre Unit on the epidemiology of vCJD and sCJD and is also aware of emerging research on BASE. It is envisaged that SEAC will conduct a detailed consideration of the available science and the possible animal and human health implications of BASE at its meeting on 10th May 2007.
Yours sincerely
xxxxxxxxxxxxxxxx
--------------------------------------------------------------------------------
From: Terry S. Singeltary Sr. [mailto:
[email protected]]
Sent: 02 February 2007 16:44
To: Bovine Spongiform Encephalopathy
Cc: SEACsecretariat (AHEG);
[email protected];
[email protected];
[email protected]; Sustainable Agriculture Network Discussion Group
Subject: SEAC ANNUAL REPORT 2006
Date: February 2, 2007 at 8:25 am PST
SEAC ANNUAL REPORT 2006 (ignoring the obvious)
http://www.seac.gov.uk/publicats/annualreport2006.pdf
i guess the sporadic CJD cases have all be resolved, and the route and cause classified.
to this day, i cannot figure this out. if BSE farmers died from sporadic CJD, and now another study seems to point
that BSE and BASE may be the same thing, and that BASE does not produce vCJD like pathology, but pathology resembling that of sporadic CJD, then why does SEAC still seem to put sporadic CJD on the back burners ??? IN fact, SEAC could not even speak about it in there 2006 report. would it not seem prudent to mention these findings in this 2006 SEAC report ;
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
***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
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.
http://www.seac.gov.uk/minutes/95.pdf
Asante/Collinge et al, 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;
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
I STILL think to ignore these findings below is not only rediculous, but indeed very suspicious ;
CJD FARMERS WIFE 1989
http://www.bseinquiry.gov.uk/files/yb/1989/10/13007001.pdf
http://www.bseinquiry.gov.uk/files/yb/1989/10/13003001.pdf
cover-up of 4th farm worker ???
http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
http://www.bseinquiry.gov.uk/files/yb/1995/10/20006001.pdf
CONFIRMATION OF CJD IN FOURTH FARMER
http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.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/yb/1995/11/13010001.pdf
4th farmer, and 1st teenager
http://www.bseinquiry.gov.uk/files/yb/1996/02/27003001.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/yb/1995/01/31004001.pdf
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/yb/1995/10/27013001.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/yb/1995/10/04004001.pdf
FOR SEAC TO continue to flounder with this ukbsenvcjd only theory, when we know that sporadic CJD's were proven long ago to transmit via the medical and surgical arena, will only continue to spread this agent around the globe via a multitude of proven routes and sources.
IN my opinion, for SEAC to continue to go down this same road, year after year, and continue to ignore sporadic CJD's, and continue to say that "BSE in the UK sheep population is most likely to be zero, or very low if present at all." "Consequently, any impact of the schemes on human health from removing BSE from sheep is likely to be negligible." when in fact they do not know. and in fact science is 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." IN my opinion this continued neglect of other TSEs in human and animals, the continued belief in this ukbsenvcjd only theory, and the risk thereof, is reckless, dangerous, and in my mind, criminal. SEAC has failed the public terribly in this regard. ...TSS
====================================
NAME: Terry S. Singeltary Sr.
E-MAIL:
[email protected]
------------------------------------------------------------
COMMENTS:
I wish to submit the following ;
HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory
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.
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
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
SOURCES
Full Text
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al.
JAMA.2001; 285: 733-734
http://jama.ama-assn.org/
Coexistence of multiple PrPSc types in individuals with
Creutzfeldt-Jakob disease
Magdalini Polymenidou, Katharina Stoeck, Markus
Glatzel, Martin Vey, Anne Bellon, and Adriano Aguzzi
Summary
Background The molecular typing of sporadic
Creutzfeldt-Jakob disease (CJD) is based on the size
and glycoform
ratio of protease-resistant prion protein (PrPSc), and
on PRNP haplotype. On digestion with proteinase K, type
1 and
type 2 PrPSc display unglycosylated core fragments of
21 kDa and 19 kDa, resulting from cleavage around amino
acids 82 and 97, respectively.
Methods We generated anti-PrP monoclonal antibodies to
epitopes immediately preceding the differential proteinase
K cleavage sites. These antibodies, which were
designated POM2 and POM12, recognise type 1, but not
type 2, PrPSc.
Findings We studied 114 brain samples from 70 patients
with sporadic CJD and three patients with variant CJD.
Every patient classified as CJD type 2, and all variant
CJD patients, showed POM2/POM12 reactivity in the
cerebellum and other PrPSc-rich brain areas, with a
typical PrPSc type 1 migration pattern.
Interpretation The regular coexistence of multiple
PrPSc types in patients with CJD casts doubts on the
validity of
electrophoretic PrPSc mobilities as surrogates for
prion strains, and questions the rational basis of
current CJD
classifications.
snip...
The above results set the existing CJD classifications
into debate and introduce interesting questions about
human CJD types. For example, do human prion types
exist in a dynamic equilibrium in the brains of affected
individuals? Do they coexist in most or even all CJD
cases? Is the biochemically identified PrPSc type simply
the dominant type, and not the only PrPSc species?
Published online October 31, 2005
http://neurology.thelancet.com
snip...end...TSS