To: ccooper@kgbt4.com
CC: crystal@theexaminer.com, bpatterson@dentonrc.com, lmclendon@dentonrc.com, jcrutchfield@thebeaconjournal.com
GREETINGS everyone,
re-Tests to see if death connected to mad cow disease BEAUMONT, Texas
http://www.team4news.com/Global/story.asp?S=2596396
why does everyone miss the bigger picture ???
it's been here, my mother died from it and sporadic/spontaneous is a
word used to confuse. why don't you print this;
-------- Original Message --------
Subject: GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN
HUMANS ARE INFECTED WITH BSE
Date: Wed, 10 Nov 2004 14:34:35 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Ref: MRC/62/04
Under strict embargo until 19.00 British Time Thursday 11 November 2004
GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE
INFECTED WITH BSE
New research published today (19.00 hours Thursday 11th November) by a
team from the Medical Research Council (MRC) Prion Unit offers an
explanation about why only people with a particular genetic make-up have
so far developed vCJD. It also provides evidence that other types of
BSE-derived prion infection with a different pattern of symptoms might
occur in humans. The findings are published in the journal Science.
Variant CJD (vCJD) is the human disease thought to be caused by eating
food contaminated with the infectious agent, known as a prion,
responsible for the epidemic of BSE or mad cow disease in cattle. So
far, everyone known to have developed vCJD has been of a particular
genetic type known as MM. Until now it has been a mystery why everyone
that has developed vCJD is of the MM type and one possibility is that
they are simply the first to develop the disease when infected with BSE,
and that people with the other genetic types1 (known as VV and MV)
infected with BSE prions will also develop vCJD, but some years later.
In a series of experiments spanning more than ten years, the MRC team
has been studying mice genetically modified so that they make human
prion proteins which are used to model human susceptibility to BSE.
The team has now shown that mice with the human VV genetic type do
become infected when given BSE or vCJD prions, but manifest a different
form of the disease which looks quite different to vCJD and has a novel
prion strain type.
Remarkably, when these novel prions were used to infect mice of the MM
genetic type, the mice either developed a disease very like vCJD, or
else a pattern of disease that looks like so-called sporadic CJD the
classical form of CJD. This form has been known about for many years,
is seen all over the world and has not hitherto been associated with
BSE. However, the new strain identified in the mice, being called type
5, has not been seen yet in people and we do not know what pattern of
disease it would cause. It could look like one of the forms of classical
or sporadic CJD or perhaps be yet another different variant form.
The work from the MRC team suggests that type 4 prions, the type
associated with vCJD, can only propagate themselves in people that make
the M form of the protein. It seems the V form of the protein just
cannot adopt the particular molecular shape that characterises type 4.
The studies in mice also suggest that if these prions were to pass from
person to person (for example by blood transfusion) then, depending on
the genetic type of the person becoming infected, at least three
different patterns of disease might result: type 2 (which is seen in
sporadic CJD); type 4 (which causes vCJD) or type 5 (which may cause a
new pattern of disease).
Professor John Collinge, Director of the MRC Prion Unit, which is based
at University College London, said: These mouse studies give us vital
clues about the behaviour of prions and how they appear to modify and
adapt depending on the genetic makeup of the individual they are infecting.
We always have to be cautious about making direct comparison to the
human condition, but our work strongly suggests that we can not assume
only those with one genetic profile are vulnerable to BSE infection.
At this stage it is not possible to say how this should alter estimates
of those likely to become ill, but our findings do suggest we should be
taking steps to draw up a more sophisticated system of categorizing the
disease so that we dont mistake BSE related infection for a version of
sporadic CJD.
ENDS
For more information call the MRC press office on 020 7 637 6011
Notes to Editors
1The human prion protein comes in two common forms, known as M and V.
Because everyone has two copies of this gene, there are three possible
genetic types: MM, MV and VV.
Paper - Human Prion protein v129 prevent expression of vCJD phenotype
Science On line 11.11.04
Prions are rogue forms of one of the bodys own proteins known as the
prion protein which are misshapen. There are several different rogue
or misshapen forms that can infect humans, and these different types of
prions are known as strains . This is analogous to different strains of
other germs such flu virus causing influenza or strains of salmonella
causing different forms of food poisoning for example.
The strain of prion causing vCJD is known as type 4, types 1-3 cause the
different forms of sporadic or classical CJD. Each strain causes a
different pattern or type of disease. It is known that prion strains can
change or mutate when they pass between different animals.
The Medical Research Council (MRC) is a national organisation funded by
the UK tax-payer. Its business is medical research aimed at improving
human health; everyone stands to benefit from the outputs. The research
it supports and the scientists it trains meet the needs of the health
services, the pharmaceutical and other health-related industries and the
academic world. MRC has funded work which has led to some of the most
significant discoveries and achievements in medicine in the UK. About
half of the MRCs expenditure of £430 million is invested in its 40
Institutes, Units and Centres. The remaining half goes in the form of
grant support and training awards to individuals and teams in
universities and medical schools. Web site at: http://www.mrc.ac.uk
.
http://www.mrc.ac.uk/index/public-interest/public-press_office/public-press_releases_2004/public-11_november_2004.htm
Failure To Test Staggering Cow May Reflect Wider Problems
Rep. Waxman raises concerns that the recent failure of USDA to test an
impaired cow for BSE may not be an isolated incident, citing the failure
of USDA to monitor whether cows condemned for central nervous system
symptoms are actually tested for mad cow disease.
- Letter to USDA
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
FOR IMMEDIATE RELEASE
Statement
May 4, 2004
Media Inquiries: 301-827-6242
Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
Send Post-Publication Peer Review to journal:
Re: 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
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov;
BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION
TO DOCKET 2003N-0312]
Greetings FDA,
snip...
PLUS, if the USA continues to flagrantly ignore the _documented_ science
to date about the known TSEs in the USA (let alone the undocumented TSEs
in cattle), it is my opinion, every other Country that is dealing with BSE/TSE
should boycott the USA and demand that the SSC reclassify the USA BSE GBR
II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_
any longer on this issue, should also be regarded with great suspicion as
well. NOT to leave out the OIE and it's terribly flawed system of disease
surveillance. the OIE should make a move on CWD in the USA, and make a risk
assessment on this as a threat to human health. the OIE should also change
the mathematical formula for testing of disease. this (in my opinion and
others) is terribly flawed as well. to think that a sample survey of 400
or so cattle in a population of 100 million, to think this will find anything,
especially after seeing how many TSE tests it took Italy and other Countries
to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to
find 102 BSE cases), should be proof enough to make drastic changes of this
system. the OIE criteria for BSE Country classification and it's interpretation
is very problematic. a text that is suppose to give guidelines, but is not
understandable, cannot be considered satisfactory. the OIE told me 2 years
ago that they were concerned with CWD, but said any changes might take years.
well, two years have come and gone, and no change in relations with CWD
as a human health risk. if we wait for politics and science to finally make
this connection, we very well may die before any decisions
or changes are made. this is not acceptable. we must take the politics and
the industry out of any final decisions of the Scientific community. this
has been the problem from day one with this environmental man made death
sentence. some of you may think i am exaggerating, but you only have to
see it once, you only have to watch a loved one die from this one time,
and you will never forget, OR forgive...yes, i am still very angry... but
the transmission studies DO NOT lie, only the politicians and the industry
do... and they are still lying to this day...TSS
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
ONE YEAR LATER ;
EFSA Scientific
Report on the Assessment of the Geographical BSE-Risk (GBR) of the United
States of America (USA)
Publication date: 20 August 2004
Adopted July 2004 (Question N° EFSA-Q-2003-083)
* 167 kB Report
* 105 kB Summary
Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working
Group on the Assessment of the Geographical Bovine Spongiform
Encephalopathy (BSE) Risk (GBR) were asked by the European Commission
(EC) to provide an up-to-date scientific report on the GBR in the United
States of America, i.e. the likelihood of the presence of one or more
cattle being infected with BSE, pre-clinically as well as clinically, in
USA. This scientific report addresses the GBR of USA as assessed in 2004
based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached
domestic cattle in the middle of the eighties. These cattle imported in
the mid eighties could have been rendered in the late eighties and
therefore led to an internal challenge in the early nineties. It is
possible that imported meat and bone meal (MBM) into the USA reached
domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle
imports from BSE risk countries were slaughtered or died and were
processed (partly) into feed, together with some imports of MBM. This
risk continued to exist, and grew significantly in the mid 90s when
domestic cattle, infected by imported MBM, reached processing. Given the
low stability of the system, the risk increased over the years with
continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is
likely but not confirmed that domestic cattle are (clinically or
pre-clinically) infected with the BSE-agent. As long as there are no
significant changes in rendering or feeding, the stability remains
extremely/very unstable. Thus, the probability of cattle to be
(pre-clinically or clinically) infected with the BSE-agent persistently
increases.
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/573_en.html
Eye procedure raises CJD concerns
By Steve Mitchell
Medical Correspondent
Washington, DC, Nov. 18 (UPI) --
http://www.washtimes.com/upi-breaking/20041118-030642-2974r.htm
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, TEXAS USA 77518
