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From: TSS ()
Subject: CJD SURVEILLANCE UK FIFTEENTH ANNUAL REPORT 2006
Date: November 30, 2007 at 8:49 am PST

CJD SURVEILLANCE UK FIFTEENTH ANNUAL REPORT 2006


SUMMARY

The national surveillance programme for Creutzfeldt-Jakob disease (CJD) in
the UK was
initiated in May 1990. In 1999, the National CJD Surveillance Unit (NCJDSU)
became a
WHO Collaborative Centre for Reference and Research on the surveillance and
epidemiology
of human transmissible spongiform encephalopathies (TSEs). In September 2001
the
National Care Team was formed, which currently comprises a care coordinator
and a secretary. It
is based within the NCJDSU and was formed in response to concerns regarding
the care of CJD
patients.

The information provided in this fifteenth report continues to provide
evidence of a good level of
case ascertainment. There has been a lower number of referrals since 2003
but analysis suggests
that much, if not all, of the decline is due to changes in the number of
referrals who turn out not
to be CJD cases. The number of sporadic cases remains relatively stable (the
data for 2006 may
still be incomplete). Detailed clinical and epidemiological information has
been obtained for the
great majority of patients. Although the post mortem rate for patients with
suspected CJD has
declined, in line with general autopsy rates in the UK, it remains high
(around 60%). The number
of brain specimens examined in the neuropathology laboratory for sporadic
CJD declined from 52
in 2003 to 32 in 2004 but has remained stable (at 32) in both 2005 and 2006.

In 1990-2006 mortality rates from sporadic CJD in England, Wales, Scotland
and Northern
Ireland were, respectively, 0.89, 0.95, 0.95 and 0.57/million/year. The
differences between these
rates are not statistically significant (p>0.6). The mortality rates from
sporadic CJD in the UK are
comparable to those observed in most other European countries and elsewhere
in the world,
including countries that are free of BSE. The highest and lowest mortality
rates from sporadic
CJD were observed in the South West (SMR=132) and Northern Ireland (SMR=77).

The
variation in the observed mortality rates between the different regions
within the UK is not
statistically significant (p>0.1).

Up to 31 December 2006, there were 158 deaths from definite or probable
variant CJD (vCJD) in
the UK. Of these, 112 were confirmed by neuropathology. A further 7 probable
cases were alive
on 31st December 2006. The clinical, neuropathological and epidemiological
features of these
cases of vCJD are remarkably uniform and consistent with our previous
descriptions. Risk factors
for the development of vCJD include age, residence in the UK and methionine
homozygosity at
codon 129 of the prion protein gene - all 145 clinically affected cases of
vCJD with available
genetic analysis have been methionine homozygotes. The incidence of vCJD is
higher in the
north of the UK than in the south. Analysis of the incidence of vCJD onsets
and deaths from
January 1994 to December 2006 indicates that a peak has been passed. While
this is an
encouraging finding, the incidence of vCJD may increase again, particularly
if different genetic
subgroups with longer incubation periods exist. The identification of
disease-related PrP in the
spleen of a clinically unaffected blood recipient of PRNP-129 MV genotype is
not inconsistent
Section 1

T
Fifteenth Annual Report 2006 4

with such an hypothesis. This case, along with the report of the prevalence
of abnormal PrP in
the large study of appendix and tonsil tissues, suggests the possibility of
a greater number of
preclinical or subclinical cases in the population than might be indicated
by the present numbers of
confirmed clinical cases.

The only statistically significant geographic cluster of vCJD cases in the
UK was in Leicestershire.
All geographically associated cases of vCJD are considered for investigation
according to a
protocol which involves the NCJDSU, colleagues at the HPA, HPS and local
public health
physicians.

The activities of the NCJDSU are strengthened by collaboration with other
surveillance projects,
including the Transfusion Medicine Epidemiology Review and the study of
Progressive
Intellectual and Neurological Deterioration in Children. The collaboration
of our colleagues in
these projects is greatly appreciated; the effectiveness of this
collaboration allowed the
identification in 2003 of a case of vCJD associated with blood transfusion
and the identification in
2004 of PrPres in the spleen of a recipient of blood donated by someone
incubating vCJD. In
2006 a further two cases of vCJD associated with blood transfusion were
identified.
The success of the National CJD Surveillance Project continues to depend on
the extraordinary
level of co-operation from the neuroscience community and other medical and
paramedical staff
throughout the UK. We are particularly grateful to the relatives of patients
for their help with this
study.

snip...

please see full text 42 pages at link below. ...tss


http://www.cjd.ed.ac.uk/report15.pdf

PRION DISEASE UPDATE 2007 (07)
******************************
A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases

[Note: With continuing decline of the number of cases of variant
Creutzfeldt-Jacob disease (abbreviated previously as vCJD or CJD (new
var.) in ProMED-mail) in the human population, it has been decided to
broaden the scope of the occasional ProMED-mail reports to include
other prion-related diseases. These updates supersede the previous
update thread.

The definitions of the designations deaths, definite cases, probable
vCJD cases, can be found by accessing the Department of Health website
()
or by reference to a previous ProMED-mail post in the vCJD thread.

Data on vCJD cases from any part of the world are now included in
these updates where appropriate, and other forms of CJD (sporadic,
iatrogenic, familial, and GSS Gerstmann-Straussler-Scheinker disease)
are included also when they have some relevance to the incidence and
etiology of vCJD.

In addition, prion-related diseases of domesticated and free-living
animals may also be included if relevant. - Mod.CP]

In this update:

[1] UK: National CJD Surveillance Unit - Monthly statistics
[2] USA: National Prion Disease Pathology Surveillance Center

******
[1] UK National CJD Surveillance Unit - Monthly statistics
Date: Mon 5 Nov 2007
Source: UK National CJD Surveillance Unit, Monthly Statistics, 2007 [edited]


Monthly Creutzfeldt-Jakob disease statistics - as of 2 Nov 2007

[N.B. The Department of Health ceased issuing monthly CJD press
notices at the end of September 2007 because the same data are also
published by the National CJD Surveillance Unit in Edinburgh at
.]

These following figures show the number of suspect cases of CJD
referred to the CJD surveillance unit in Edinburgh and the number of
deaths of definite and probable variant Creutzfeldt-Jakob disease
[abbreviated in ProMED-mail as CJD (new var.) or vCJD], the form of
the disease thought to be linked to BSE (bovine spongiform encephalopathy).

Definite and probable vCJD cases in the UK as of 2 Nov 2007
----------------------

Summary of vCJD cases -- deaths
----------------------
Deaths from definite vCJD (confirmed): 114
Deaths from probable vCJD (without neuropathological confirmation): 47
Deaths from probable vCJD (neuropathological confirmation pending): 1
Number of deaths from definite or probable vCJD (as above): 162

Summary of vCJD cases -- alive
----------------------
Number of probable vCJD cases still alive: 4

Total
-----
Number of definite or probable vCJD (dead and alive): 166

These data indicate that there have been no new cases diagnosed
during the past month, but one patient has died, raising the vCJD
death toll to 162.

These data are still consistent with the view that the vCJD outbreak
in the UK is in decline. The peak number of deaths was 28 in the year
2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in 2004, 5 in
2005, 5 in 2006, and so far 4 in 2007.

Totals for all types of CJD cases in the year 2007 so far
-----------------------------
As of 2 Nov 2007 in the UK in the year 2007, so far there have been
93 referrals, 38 deaths from sporadic CJD, 2 deaths from iatrogenic
CJD, 2 deaths from familial CJD, one from GSS, and 4 deaths from vCJD.

--
Communicated by:
ProMED-mail

******
[2] USA: National Prion Disease Pathology Surveillance Center
Date: June 2007
Source: National Prion Disease Pathology Surveillance Center (USA) [edited]


CJD Cases examined
----------------------
Year / Referrals / Prion disease / Sporadic / Familial / Iatrogenic / vCJD

1996 / 42 / 32 / 26 / 4 / 0 / 0
1997 / 115 / 68 / 57 / 9 / 0 / 0
1998 / 93 / 53 / 45 / 7 / 1 / 0
1999 / 114 / 69 / 61 / 8 / 0 / 0
2000 / 151 / 103 / 89 / 14 / 0 / 0
2001 / 208 / 116 / 106 / 9 / 0 / 0
2002 / 255 / 143 / 118 / 23 / 2 / 0
2003 / 272 / 174 / 132 / 41 / 0 / 0
2004 / 334 / 183 / 157 / 21 / 0 / 1*
2005 / 352 / 195 / 152 / 37 / 1 / 0
2006 / 372 / 186 / 143 / 30 / 0 / 1**
2007 / 120 / 68 / 35 / 7 / 0 / 0
TOTAL / 2428*** / 1390**** / 1121 / 210 / 4 / 2

*Acquired in UK
** Acquired in Saudi Arabia
*** Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007.
**** Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36
type pending (2 from 2005, 8 from 2006, 26 from 2007).

Notes:

-- Cases are listed based on the year of death when available. If the
year of death is not available, the year of sample receipt is used.

-- Referrals: Cases with possible or probable prion disease from
which brain tissue or blood in the case of familial disease were submitted.

-- Inconclusive: Cases in which the samples were not sufficient to
make a diagnosis.

-- Non-vCJD type unknown are cases in which the tissue submitted was
adequate to establish the presence but not the type; in all cases,
vCJD could be excluded.

--
Communicated by:
Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to
the steady increase in the "type unknown" category, which, according
to their definition, comprises cases in which vCJD could be excluded.
The total of 26 cases for the current year (2007) is disturbing,
possibly symptomatic of the circulation of novel agents.
Characterization of these agents should be given a high priority. - Mod.CP]

[see also:

snip...


************************************************************
Become a ProMED-mail Premium Subscriber at

************************************************************
Visit ProMED-mail's web site at .


http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html

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/resources-casereport.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/06/transcripts/1006-4240t1.htm


http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase
in ''TYPE UNKNOWN''. ...TSS


1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17
inconclusive and 9 pending (1 from 2006, 8
from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1
from 2001, 1 from 2003, 4 from 2004, 3
from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,

*** 26 from 2007)

http://www.cjdsurveillance.com/pdf/case-table.pdf

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535


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


doi:10.1016/S1473-3099(03)00715-1
Copyright © 2003 Published by Elsevier Ltd.
Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.


Volume 3, Issue 8, August 2003, Page 463


“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.”
............................


http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext

http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf


see history of cjd questionnaire

http://brain.hastypastry.net/forums/showthread.php?t=2408


Sent: Monday May 28, 2007

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


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=25276


Subject: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the
UKBSEnvCJD only theory
Date: January 29, 2006 at 9:03 am PST

Comments sent via JAMA Feedback Page
------------------------------------------------------------
NAME: Terry S. Singeltary Sr.
E-MAIL: flounder9@verizon.net
IP ADDRESS: xxxxxxxx
HOSTNAME: xxxxxxxx
PREVIOUS PAGE: http://jama.ama-assn.org/misc/authors.dtl
BROWSER: Mozilla/5.0 (Windows; U; Win98; en-US; rv:1.0.2) Gecko/20030208
Netscape/7.02
PROMOTIONAL USE: (not answered)


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.
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 2007. 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 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.


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 sub-clinical to clinical disease,
and key to all this, is to stop the amplification and transmission of this
agent, the spreading of, no matter what strain. In my opinion, to continue
with this myth that the U.K. strain of BSE (one strain TSE in cows), and the
nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just
one single strain i.e. sporadic CJD (when to date there are 6 different
phenotypes of sCJD, and growing per Gambetti et al), 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 i.e. Heidenhain
Variant CJD, 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. ...


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in
the United States


http://cjdusa.blogspot.com/


i am reminded of a few things deep throat (high ranking official at usda)
told me years ago;


==========================================


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,


https://www.blogger.com/comment.g?blogID=7842737484277562285&postID=5759550357128128100

BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS


http://madcowtesting.blogspot.com/


MADCOW USDA the untold story

http://madcowusda.blogspot.com/

MADCOW USDA the untold story continued

https://www.blogger.com/comment.g?blogID=6472149427883113751&postID=4829467681293855400

USA NOR-98 SCRAPIE UPDATE AUGUST 31, 2007 RISES TO 5 DOCUMENTED CASES


http://nor-98.blogspot.com/


Government Accountability Project


https://www.blogger.com/comment.g?blogID=3995372399492420922&postID=295754279213239559

Transmissible Mink Encephalopathy TME

http://transmissible-mink-encephalopathy.blogspot.com/

TME hyper/drowsy, INTER-SPECIES TRANSMISSION CWD and strain
properties


https://www.blogger.com/comment.g?blogID=37955408&postID=116577315153980667


USA NVCJD BLOOD RECALLS ONLY ;


http://www.google.com/search?hl=en&q=CJD+BLOOD+RECALLS+TSS&btnG=Search


vCJD case study highlights blood transfusion risk


http://vcjdblood.blogspot.com/


CREUTZFELDT JAKOB DISEASE MAD COW BASE, CWD, SCRAPIE UPDATE OCT 2007


http://cjdmadcowbaseoct2007.blogspot.com/


TSEAC MEETINGS


http://tseac.blogspot.com/

ABSTRACTS SPORADIC CJD AND H BASE MAD COW ALABAMA AND TEXAS SEPTEMBER 2007

Date: Mon, 24 Sep 2007 21:31:55 -0500

I suggest that you all read the data out about h-BASE and sporadic CJD, GSS,
blood, and some of the other abstracts from the PRION2007. ...

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&F=&S=&P=19744

*** PLEASE READ AND UNDERSTAND THE RAMIFICATIONS OF THIS !!! THE PRICE OF
POKER INDEED GOES UP. ...TSS

USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it
today), please note that both the ALABAMA COW, AND THE TEXAS COW, both were
''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007
11:52 PM. ...TSS

http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0708&L=sanet-mg&T=0&P=19779

From: "Terry S. Singeltary Sr."
Subject: CWD UPDATE 88 AUGUST 31, 2007


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0709&L=sanet-mg&T=0&P=450

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






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