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Kansan contracts disease related to mad cow ???

flounder

Well-known member
Kansan contracts disease related to mad cow

BY KAREN SHIDELER

The Wichita Eagle

Health officials think a Kansas man has died of Creutzfeldt-Jakob Disease, a rare disease that affects the central nervous system and turns brain tissue spongy.

One variation of the disease is the so-called mad cow disease but the human form of that has never been seen in the United States in someone who hadn't had exposure elsewhere.

Because the incubation period for the disease is years or even decades, health officials don't know how or when the Kansas man got the disease, nor what its source may have been.

They won't know for several weeks, until testing is complete, which form of the disease he had.

The man died Friday at Wesley Medical Center, where he had been a patient since December. His name was not released, but he was a 53-year-old from the Colby area.

The diagnosis at this time is Creutzfeldt-Jakob Disease, or CJD, said Wesley spokesman Paul Petitte. The only way to confirm CJD is through testing of brain tissue, which will be done through the National Prion Disease Pathology Surveillance Center.

Kansas has an average of three CJD cases a year, according to Joe Blubaugh, spokesman for the Kansas Department of Health and Environment.

Nationwide, according to the Centers for Disease Control and Prevention, one to two people per million have a spontaneous case of CJD each year. On average, 250 to 300 cases of CJD are reported annually.

In addition to the spontaneous cases, a certain form of CJD can come from consumption of beef that has been infected with mad cow disease, as happened in Great Britain in the mid-1990s. The United States and other countries implemented various measures in response, to prevent the disease and better track infected cattle.

CJD can also come from blood transfusions, and it can be hereditary in very rare cases.

Richard Liepins, who was the attending physician in the local case, said, "We have no idea of how he possibly contracted this."

The man worked in a meatpacking plant "quite a few years ago" and was also an elk hunter, Liepins said, though there's no way to say whether either of those contributed to his disease.

Chronic wasting disease, found in some deer and elk, is another form of spongiform encephalopathy. It can be spread from animal to animal, but so far there's no strong evidence of its transmission to humans.

The CDC said studies are under way to see whether people exposed to the meat of sick deer and elk are at increased risk for CJD but because of the long incubation period that won't be known for years. Hunters and others are advised to avoid meat from animals that seem sick or test positive for chronic wasting disease.

The disease is rare enough that Liepins and some of the other doctors who worked on the case had never seen it before. Tom Moore, an infectious disease specialist in Wichita, said he has seen about three cases over the past decade.

When the man first became ill doctors suspected a brain tumor, Liepins said, because of his neurological symptoms. Such symptoms include personality changes, other mental changes and dementia, which are also among the symptoms of CJD.

Liepins said he wouldn't speculate on the most likely cause of the man's disease, but he said there is no reason for concern among the general public.

"It's a rare disease that people can contract at any time, but it's rare -- it's very rare," he said.

Reach Karen Shideler at 316-268-6674 or [email protected]


http://www.kansas.com/news/updates/story/281275.html



> Liepins said he wouldn't speculate on the most likely cause of the man's disease,


> but he said there is no reason for concern among the general public.


???



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


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

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.

there you have it........TSS

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


Friday, January 11, 2008

CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html


Saturday, January 12, 2008

Prominent and Persistent Extraneural Infection in Human PrP Transgenic Mice Infected with Variant CJD

http://cjdmadcowbaseoct2007.blogspot.com/2008/01/prominent-and-persistent-extraneural.html


ANIMAL HEALTH REPORT 2006 (BSE h-BASE ALABAMA)

http://animalhealthreport2006.blogspot.com/


SEAC 99th meeting on Friday 14th December 2007

http://seac992007.blogspot.com/


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/


BSE OIE USDA

http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html


CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA

http://cjdmadcowbaseoct2007.blogspot.com/


SCRAPIE USA

http://scrapie-usa.blogspot.com/


NOR-98 ATYPICAL SCRAPIE CASES USA

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


Transmissible Mink Encephalopathy TME

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


CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/


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

http://cjdusa.blogspot.com/


CJD QUESTIONNAIRE

http://cjdquestionnaire.blogspot.com/


TSEAC MEETINGS

http://tseac.blogspot.com/


I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

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


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.

http://www.thepathologicalprotein.com/


doi:10.1016/S1473-3099(03)00715-1Copyright © 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


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


Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284


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 wide spread 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. ...

http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html


DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen)USA: Loch in der MauerDie
BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in
Texasverbotenes Tiermehl ins Rinderfutter - die Kontrollen der
Aufsichtsbehördensind lax. Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755"

Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA
regulations. ...

http://service.spiegel.de/digas/servlet/find/DID=18578755


Thu Dec 6, 2007 11:38

FDA IN CRISIS MODE, AMERICAN LIVES AT RISK

http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html


FDA SCIENCE AND MISSION AT RISK

http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf


2 January 2000
British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


15 November 1999
British Medical Journal

vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;

http://cjdtexas.blogspot.com/


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

flounder

Well-known member
here's another potential work related exposure and death from sporadic CJD in another country. this UKBSEnvCJD only myth needs to be abolished, burried, or something......


Farewell Olga
By Nicola Fifield
Comment | Read Comments (2)

The horse-drawn carriage carrying the coffin of Olga Franklin arrives at St Stephen's Church, Acomb, York
A STRIKING funeral cortege brought traffic to a halt as mourners followed the coffin of a much-loved mother-of-five in a Victorian horse-drawn carriage.

Olga Franklin - the former wife of Len Franklin, one of the country's first victims of Creutzfeldt-Jakob Disease (CJD) - died last week at the age of 64.

Yesterday, a beautiful glass carriage, drawn by two white horses with plumes, carried the coffin from her home in Murray Street to nearby St Stephen's Church, in Acomb, York.

After the funeral service, her family released white doves and 200 white helium balloons into the skies above the city.

Her son, Colin Cain, a joint-partner of Otisdale Estate Agents with his brother Michael, said: "It is very rare to get a woman so special as my mum and we wanted to give her a good send off.

"We have filmed it all for her grandchildren and great grandchildren to remember her by in the future." Following the death of her former husband in February 1996, Mrs Franklin became well-known for the public support she gave other families of CJD victims.

advertisement
An inquest into Mr Franklin's death decided he died of a strain of CJD that was unconnected to Mad Cow Disease (BSE) in cattle.

But his family always maintained that the former abattoir worker was killed by the new variant of CJD, thought to be caused by contact with BSE-infected cattle or beef.

In 1998, they were supported by an expert on the diseases, Dr Harash Narang.

Following an examination of both his behaviour and samples of his brain tissue, Dr Harash said he was convinced Mr Franklin did die of new variant CJD.

He said he also believed that contact with cattle at the abattoir might have been to blame.

Mr Cain said: "To the day she died, my mum was totally convinced that it was Mad Cow Disease that killed him.

"She felt like the Government was trying to cover things up - that's why she went on national TV to speak about it."

Mrs Franklin was diagnosed with lung cancer in July, when she was given only six months to live by doctors.

Mr Cain said: "The respect that my mother had from everybody she knew was so strong. She was just a very genuine, honest and hard-working woman. Christmas was a very emotional time for us because we knew it would be her last one. We miss her already."

* The Press was invited to the funeral.

9:19am today

http://www.thisisyork.co.uk/display.var.1965489.0.coffin_taken_to_funeral_by_horsedrawn_carriage.php


another senseless death, another work related source for the TSE agent, another coincident $$$

i am sorry for your loss. but let us look at this non-sense of the UKBSEnvCJD ONLY theory, it's as bogus today, as it was
18 years ago or so. ...tss


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


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

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.

there you have it........TSS

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


Friday, January 11, 2008

CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html


Saturday, January 12, 2008

Prominent and Persistent Extraneural Infection in Human PrP Transgenic Mice
Infected with Variant CJD

http://cjdmadcowbaseoct2007.blogspot.com/2008/01/prominent-and-persistent-extraneural.html


ANIMAL HEALTH REPORT 2006 (BSE h-BASE ALABAMA)

http://animalhealthreport2006.blogspot.com/


SEAC 99th meeting on Friday 14th December 2007

http://seac992007.blogspot.com/


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/


BSE OIE USDA

http://madcowtesting.blogspot.com/2008/01/bse-oie-usda.html


CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA

http://cjdmadcowbaseoct2007.blogspot.com/


SCRAPIE USA

http://scrapie-usa.blogspot.com/


NOR-98 ATYPICAL SCRAPIE CASES USA

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


Transmissible Mink Encephalopathy TME

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


CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/


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

http://cjdusa.blogspot.com/


CJD QUESTIONNAIRE

http://cjdquestionnaire.blogspot.com/


TSEAC MEETINGS

http://tseac.blogspot.com/


I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

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


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.

http://www.thepathologicalprotein.com/


doi:10.1016/S1473-3099(03)00715-1Copyright © 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


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


Like lambs to the slaughter
31 March 2001
Debora MacKenzie
Magazine issue 2284


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 wide spread 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. ...

http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html


DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen)USA: Loch in der MauerDie
BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in
Texasverbotenes Tiermehl ins Rinderfutter - die Kontrollen der
Aufsichtsbehördensind lax. Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755"

Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA
regulations. ...

http://service.spiegel.de/digas/servlet/find/DID=18578755


Thu Dec 6, 2007 11:38

FDA IN CRISIS MODE, AMERICAN LIVES AT RISK

http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html


FDA SCIENCE AND MISSION AT RISK

http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf


2 January 2000
British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/cgi/eletters/320/7226/8/b#6117


15 November 1999
British Medical Journal

vCJD in the USA * BSE in U.S.

http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;

http://cjdtexas.blogspot.com/


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

Bill

Well-known member
Kansas man's death not tied to mad cow: officials
Thu Jan 17, 2008 12:41am IST Preliminary tests indicate that a 53-year-old Kansas man, who died on Friday, had the rare brain disease Creutzfeldt-Jakob Disease, which is not related to mad cow disease, health officials said on Wednesday.

However, it will be several weeks before final tests are completed to positively identify the disease.

A physician who treated the man had said the brain disease was "not the mad cow version," said a spokesman for the Wesley Medical Center in Wichita, where the man was treated.

Talk had circulated in the Chicago Mercantile Exchange cattle market early on Wednesday that the man might have died from variant CJD, which scientists believe can be contracted by eating contaminated parts from cattle with mad cow disease.

Normal CJD is naturally occurring and the Kansas Department of Health said the state averages about three cases a year.

"We have no reason to believe it is not anything but CJD," said Joe Blubaugh, spokesman for the Kansas Department of Health.

The United States has had three cases of mad cow disease in cattle.

(Reporting by Bob Burgdorfer; Editing by Christian Wiessner)
 

Mrs.Greg

Well-known member
Flounder....you should have held off on that until a positive diagnosis was made.CJD is NOT linked to beef.My sis's MIL died from CJD and gossip thats not true hurts alot of people involved and not involved and spreads havok :?
 

flounder

Well-known member
Mrs.Greg said:
Flounder....you should have held off on that until a positive diagnosis was made.CJD is NOT linked to beef.My sis's MIL died from CJD and gossip thats not true hurts alot of people involved and not involved and spreads havok :?


i just disagree with you Mrs. Greg, the science to dispute that is mounting by the day.



we must stress that the U.K. B.S.E. hamburger eating adolescent ONLY theory, is and always has been bogus, and the ramifications from the medical, surgical, dental, tissue donor, blood, etc., the ramifications from this is far more critical than again what i call the ukbsenvcjd only
theory. this is what has caused this to become so confusing to most, and also caused the continued spreading of the TSE agent. when your dead, your dead, period. it was the industry that drove this bogus theory. there are many strains, and many proven routes, but it is the strain typing from those routes and sources that is paramount to finding the cause of these sporadic CJD. for Pete's sake, the now have classified a ''sporadic'' FATAL FAMILIAL INSOMNIA. when does it end. but while gambetti et al here in the USA continue to dispute what others are saying i.e. Collinge et al of the U.K. and others, on the diagnostic criteria, and just how terribly flawed it has been from the beginning, and the ramifications from that
i.e. 'spreading', in my opinion, nothing will change until this happens.




SPORADIC CREUTZFELDT JAKOB DISEASE


there are 26790 hits on 'sporadic' at pub-med.

there are 12830 hits on 'sporadic disease' at pub-med.

with the first few being ;


Comparison Analysis of Gene Expression Patterns between Sporadic Alzheimer's
and Parkinson's Disease.

http://www.ncbi.nlm.nih.gov/pubmed/18198416?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Sporadic ALS with early onset respiratory failure is not associated with
IGHMBP2 gene mutations.

http://www.ncbi.nlm.nih.gov/pubmed/18187479?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Sporadic Multiple Cerebral Cavernomatosis: Report of a Case and Review of
Literature

http://www.ncbi.nlm.nih.gov/pubmed/18195658?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


A sporadic disease is one that occurs only occasionally in a population
(i.e., prevalence is zero).

http://mansfield.osu.edu/~sabedon/biol2045.htm


sporadic CJD is NOT a single strain, phenotype.

sporadic CJD is simply a human TSE, which routes, sources, strains, are
unknown.

there are 6 different documented phenotypes of the sporadic CJD, with
'UNKNOWN' sub-types growing.

spontaneous TSE in the field ??? never has been proven, and highly unlikely
that 85%+ of all human TSE i.e. sporadic CJD, just happen without route and
source.


please see full text ;


http://nor-98.blogspot.com/2008/01/atypicalnor98-scrapie-properties-of.html



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. ...


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


SOURCES


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



Detection of Type 1 Prion Protein in Variant Creutzfeldt-Jakob Disease


Helen M. Yull,* Diane L. Ritchie,*

Jan P.M. Langeveld,? Fred G. van Zijderveld,?

Moira E. Bruce,? James W. Ironside,* and

Mark W. Head*

From the National CJD Surveillance Unit,* School of
Molecular

and Clinical Medicine, University of Edinburgh, Edinburgh,

United Kingdom; Central Institute for Animal Disease
Control

(CIDC)-Lelystad, ? Lelystad, The Netherlands; Institute
for Animal

Health, Neuropathogenesis Unit, ? Edinburgh, United Kingdom

Molecular typing of the abnormal form of the prion

protein (PrPSc) has come to be regarded as a powerful

tool in the investigation of the prion diseases. All
evidence

thus far presented indicates a single PrPSc molecular

type in variant Creutzfeldt-Jakob disease (termed

type 2B), presumably resulting from infection with a

single strain of the agent (bovine spongiform
encephalopathy).

Here we show for the first time that the PrPSc

that accumulates in the brain in variant Creutzfeldt-

Jakob disease also contains a minority type 1 component.

This minority type 1 PrPSc was found in all 21

cases of variant Creutzfeldt-Jakob disease tested,
irrespective

of brain region examined, and was also

present in the variant Creutzfeldt-Jakob disease tonsil.

The quantitative balance between PrPSc types was maintained

when variant Creutzfeldt-Jakob disease was

transmitted to wild-type mice and was also found in

bovine spongiform encephalopathy cattle brain, indicating

that the agent rather than the host specifies their

relative representation. These results indicate that PrPSc

molecular typing is based on quantitative rather than

qualitative phenomena and point to a complex relationship

between prion protein biochemistry, disease phenotype

and agent strain.


(Am J Pathol 2006, 168:151-157;

DOI: 10.2353/ajpath.2006.050766)


snip...


Discussion

In the apparent absence of a foreign nucleic acid genome

associated with the agents responsible for transmissible

spongiform encephalopathies or prion diseases,

efforts to provide a molecular definition of agent strain

have focused on biochemical differences in the abnormal,

disease-associated form of the prion protein, termed

PrPSc. Differences in PrPSc conformation and glycosylation

have been proposed to underlie disease phenotype

and form the biochemical basis of agent strain. This

proposal has found support in the observation that the

major phenotypic subtypes of sCJD appear to correlate

with the presence of either type 1 or type 2 PrPSc in

combination with the presence of either methionine or

valine at codon 129 of the prion protein gene.2 Similarly,

the PrPSc type associated with vCJD correlates with the

presence of type 2 PrPSc and is distinct from that found in

sCJD because of a characteristically high occupancy of

both N-linked glycosylation sites (type 2B).6,11 The

means by which such conformational difference is detected

is somewhat indirect; relying on the action of proteases,

primarily proteinase K, to degrade the normal

Figure 6. Type 1 PrPSc is a stable minority component
of PrPSc from the vCJD

brain. Western blot analysis of PrP in a sample of
cerebral cortex from a
case

of vCJD during digestion with proteinase K is shown.
Time points assayed

are indicated in minutes (T0, 5, 10, 30, 60, 120, 180).
Duplicate blots were

probed with 3F4, which detects both type 1 and type 2
PrPSc, and with 12B2,

which detects type 1. The insert shows a shorter
exposure of the same time

course study from a separate experiment also probed
with 3F4. Both blots

included samples of cerebral cortex from a case of
sporadic CJD MM1 (Type

1) and molecular weight markers (Markers) indicate
weights in kd.

Figure 7. A minority type 1-like PrPSc is found in vCJD
tonsil, vCJD
transmitted

to mice and in BSE. Western blot analysis of PrPSc in a
concentrated

sample of tonsil from a case of vCJD (Tonsil), in a
concentrated brain
sample

of a wild-type mouse (C57BL) infected with vCJD and in
a sample of cattle

BSE brain (BSE) is shown. Tissue extracts were digested
with proteinase K.

Duplicate blots were probed with either 3F4 or 6H4,
both of which detect

type 1 and type 2 PrPSc, and with 12B2, which detects
type 1. The blots

included samples of cerebral cortex from a case of
sporadic CJD MM1 (Type

1) and molecular weight markers (Markers) indicate
weights in kd.

Type 1 PrPSc in Variant Creutzfeldt-Jakob Disease 155

AJP January 2006, Vol. 168, No. 1

cellular form of PrP and produce a protease-resistant

core fragment of PrPSc that differs in the extent of its

N-terminal truncation according to the original

conformation.

A complication has recently arisen with the finding that

both type 1 and type 2 can co-exist in the brains of

patients with sCJD.2,5-8 More recently this same phenomenon

has been demonstrated in patients with iatrogenically

acquired and familial forms of human prion disease.

9,10 The existence of this phenomenon is now

beyond doubt but its prevalence and its biological
significance

remain a matter of debate.

Conventional Western blot analysis using antibodies

that detect type 1 and type 2 PrPSc has severe quantitative

limitations for the co-detection of type 1 and type 2

PrPSc in individual samples, suggesting that the prevalence

of co-occurrence of the two types might be underestimated.

We have sought to circumvent this problem by

using an antibody that is type 1-specific and applied this

to the sole remaining human prion disease where the

phenomenon of mixed PrPSc types has not yet been

shown, namely vCJD.

These results show that even in vCJD where susceptible

individuals have been infected supposedly by a

single strain of agent, both PrPSc types co-exist: a
situation

reminiscent of that seen when similarly discriminant

antibodies were used to analyze experimental BSE in

sheep.14,17 In sporadic and familial CJD, individual

brains can show a wide range of relative amounts of the

two types in samples from different regions, but where

brains have been thoroughly investigated a predominant

type is usually evident.2,6,10 This differs from this
report

on vCJD, where type 1 is present in all samples
investigated

but always as a minor component that never

reaches a level at which it is detectable without a type

1-specific antibody. It would appear that the relative
balance

between type 1 and type 2 is controlled within

certain limits in the vCJD brain. A minority type-1-like

band is also detected by 12B2 in vCJD tonsil, in BSE

brain and in the brains of mice experimentally infected

with vCJD, suggesting that this balance of types is agent,

rather than host or tissue, specific. Interestingly the
"glycoform

signature" of the type 2 PrPSc found in vCJD (type

2B) is also seen in the type 1 PrPSc components, suggesting

that it could legitimately be termed type 1B.

PrPSc isotype analysis has proven to be extremely

useful in the differential diagnosis of CJD and is
likely to

continue to have a major role in the investigation of human

prion diseases. However, it is clear, on the basis of

these findings, that molecular typing has quantitative
limitations

and that any mechanistic explanation of prion

replication and the molecular basis of agent strain
variation

must accommodate the co-existence of multiple

prion protein conformers. Whether or not the different

conformers we describe here correlate in a simple and

direct way with agent strain remains to be determined. In

principle two interpretations present themselves: either

the two conformers can be produced by a single strain of

agent or vCJD (and, therefore, presumably BSE) results

from a mixture of strains, one of which generally
predominates.

Evidence for the isolation in mice of more than one

strain from individual isolates of BSE has been presented

previously.18,19

One practical consequence of our findings is that the

correct interpretation of transmission studies will depend

on a full examination of the balance of molecular types

present in the inoculum used to transmit disease, in
addition

to a thorough analysis of the molecular types that

arise in the recipients. Another consequence relates to

the diagnostic certainty of relying on PrPSc molecular

type alone when considering the possibility of BSE
infection

or secondary transmission in humans who have a

genotype other than methionine at codon 129 of the

PRNP gene. In this context it is interesting to note
that this

minority type 1B component resembles the type 5 PrPSc

described previously to characterize vCJD transmission

into certain humanized PRNP129VV transgenic mouse

models.12,20 This apparently abrupt change in molecular

phenotype might represent a selection process imposed

by this particular transgenic mouse model. Irrespective of

whether this proves to be the case, the results shown

here point to further complexities in the relationship
between

the physico-chemical properties of the prion protein,

human disease phenotype, and prion agent strain.

Acknowledgments


snip...


Type 1 PrPSc in Variant Creutzfeldt-Jakob Disease 157

AJP January 2006, Vol. 168, No. 1 ...TSS

http://ajp.amjpathol.org/cgi/content/abstract/168/1/151maxtoshow=&HITS=10&hits=10&
RESULTFORMAT=&fulltext=prion&searchid=1136646133963_237&FIRSTINDEX=0&volume=168&issue=1&journalcode=amjpathol


snip...end



Archive Number 20071105.3602
Published Date 05-NOV-2007
Subject PRO/AH/EDR> Prion disease update 2007 (07)

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



snip...

[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]


http://www.promedmail.org/pls/askus/f?p=2400:1001:6833194127530602005::NO::F2400_P1001_BACK_PAGE,F2400_P1001_PUB_MAIL_ID:1010,39963


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



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:

[email protected]

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


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.

http://www.thepathologicalprotein.com/


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


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


Like lambs to the slaughter

31 March 2001
Debora MacKenzie
Magazine issue 2284

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. ...


http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html


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 Aufsichtsbehörden
sind lax.
Link auf diesen Artikel im Archiv:
http://service.spiegel.de/digas/find?DID=18578755


"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA
regulations. ...


http://service.spiegel.de/digas/servlet/find/DID=18578755


Thu Dec 6, 2007 11:38

FDA IN CRISIS MODE, AMERICAN LIVES AT RISK


http://www.cidrap.umn.edu/cidrap/content/fs/food-disease/news/dec0407fda.html


FDA SCIENCE AND MISSION AT RISK

http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4329b_02_01_FDA%20Report%20on%20Science%20and%20Technology.pdf


2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well


http://www.bmj.com/cgi/eletters/320/7226/8/b#6117



15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406


vCJD case study highlights blood transfusion risk

http://vcjdblood.blogspot.com/


vCJD transfusion-associated Fourth Case UK

http://vcjdtransfusion.blogspot.com/


risk factors for sporadic CJD

http://creutzfeldt-jakob-disease.blogspot.com/2008/01/risk-factors-for-sporadic-creutzfeldt.html


Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPScType in a Young British Woman

http://creutzfeldt-jakob-disease.blogspot.com/2008/01/creutzfeldt-jakob-disease-prion-protein.html


BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;

http://cjdtexas.blogspot.com/


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

http://cjdusa.blogspot.com/


Creutzfeldt Jakob Disease

http://creutzfeldt-jakob-disease.blogspot.com/


CJD QUESTIONNAIRE

http://cjdquestionnaire.blogspot.com/


ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)

http://animalhealthreport2006.blogspot.com/


in the USA with the sporadic CJDs and BASE in USA cattle, and the 5 cases of the NOR-98 atypical scrapie cases that were documented in the USA, which by the way pathologically, both are more similar to some subtypes of the sporadic CJDs than the UK BSE nvCJD strain in humans. just another coincidence i suppose, but the ramifications to the medical and surgical arena, from these TSE already documented to be here, from friendly fire, second, third, fourth passage, is real, and the risk thereof should be treated as such, however, are going ignored.


what would CWD induced TSE in a human look like, lets' say from someone that consumed CWD infected venison, that was silently carrying the TSE agent, then went on to have surgery and or donate blood, or
had there cornea's removed (without concent, which is perfectly legal here in TEXAS, but that's another story), what would that look like pathologically. same with BASE in USA cattle in TEXAS and Alabama, i.e. friendly fire. you see this goes much further than 'CONSUMPTION' i.e. the UKBSEnvCJD hamurger eating adolecents only theory. same with Scrapie consumption, i.e. typical scrapie, not the atypicals. typical scrapie transmits to PRIMATES, and transmission studies have never been done on man. so some of the sporadic CJDs could just be related to scrapie in sheep and goats. remember, friendly fire, there are parts of sheep that are used in the medical and surgical arena. how far back does this go? hell, when all this first went down, it was the farmers and
there wives that were dieing from ''sporadic CJD''.



CONFIRMATION OF CJD IN FOURTH FARMER

http://www.bseinquiry.gov.uk/files/yb/1995/11/03008001.pdf


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


all coincidence $$$


i think not. ...


Friday, January 11, 2008

CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008


http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html



risk factors for sporadic CJD

http://creutzfeldt-jakob-disease.blogspot.com/2008/01/risk-factors-for-sporadic-creutzfeldt.html

Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc
Type in a Young British Woman

http://creutzfeldt-jakob-disease.blogspot.com/2008/01/creutzfeldt-jakob-disease-prion-protein.html

BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;

http://cjdtexas.blogspot.com/



P.S.


J. Biol. Chem., Vol. 282, Issue 49, 35878-35886, December 7, 2007


High Titers of Transmissible Spongiform Encephalopathy Infectivity
Associated with Extremely Low Levels of PrPSc in Vivo*

Rona M. Barron12, Susan L. Campbell13, Declan King, Anne Bellon, Karen E.
Chapman¶, R. Anthony Williamson, and Jean C. Manson
From the Neuropathogenesis Unit, Roslin Institute, Ogston Building, West
Mains Road, Edinburgh EH9 3JF, Scotland, United Kingdom, the Department of
Immunology, Scripps Research Institute, La Jolla, California 92037, and the
¶Centre for Cardiovascular Sciences, Queen's Medical Research Institute,
University of Edinburgh, 47 Little France Crescent, Edinburgh EH16 4TJ,
Scotland, United Kingdom

Diagnosis of transmissible spongiform encephalopathy (TSE) disease in humans
and ruminants relies on the detection in post-mortem brain tissue of the
protease-resistant form of the host glycoprotein PrP. The presence of this
abnormal isoform (PrPSc) in tissues is taken as indicative of the presence
of TSE infectivity. Here we demonstrate conclusively that high titers of TSE
infectivity can be present in brain tissue of animals that show clinical and
vacuolar signs of TSE disease but contain low or undetectable levels of
PrPSc. This work questions the correlation between PrPSc level and the titer
of infectivity and shows that tissues containing little or no proteinase
K-resistant PrP can be infectious and harbor high titers of TSE infectivity.
Reliance on protease-resistant PrPSc as a sole measure of infectivity may
therefore in some instances significantly underestimate biological
properties of diagnostic samples, thereby undermining efforts to contain and
eradicate TSEs.



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Received for publication, May 25, 2007 , and in revised form, September 24,
2007.

* This work was supported by United Kingdom Department for Environment,
Food, and Rural Affairs Grant SE1437. The costs of publication of this
article were defrayed in part by the payment of page charges. This article
must therefore be hereby marked "advertisement" in accordance with 18 U.S.C.
Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org)
contains supplemental Figs. S1–S3 and Table S1.

1 Both authors contributed equally to this work.

3 Current address: Medical Research Council Clinical Sciences Centre,
Imperial College, Hammersmith Campus, Du Cane Road, London W12 0NN, United
Kingdom.

2 To whom correspondence should be addressed. Tel.: 44-131-667-5204; Fax:
44-131-668-3872; E-mail: [email protected]


http://www.jbc.org/



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