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From: TSS (216-119-156-137.ipset36.wt.net)
Subject: 25 YEAR OLD DIES OF VCJD
Date: January 9, 2005 at 9:50 am PST

-------- Original Message --------
Subject: 25 YEAR OLD DIES OF VCJD
Date: Sun, 09 Jan 2005 11:51:29 -0600
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy


Brain disease death

A trainee childcarer died from a disease caused by eating infected meat.
Tracy Yates, 25, of Birchwood Avenue, Coppull, near Chorley, was
diagnosed with variant Creutzfeldt Jakob Disease, a debilitating brain
disease, on December 3 last year, Preston Coroner's Court was told.
She lost her battle against the disease seven months later.
The variant form of CJD is associated with eating meat from cattle
infected with BSE, or mad cow disease. Early symptoms include memory
problems, mood changes and lack of co-ordination. The disease progresses
to dementia.
Those who are affected are eventually unable to move or speak. This year
147 people have died from the variant form of CJD.
Tracy's symptoms started with dizzy spells and a change in her moods.
Doctors diagnosed her with depression and she saw a psychiatrist, the
inquest heard.
But as time went on she became unable to feed herself and eventually had
to be fed through a tube.
After her diagnosis, Tracy's condition deteriorated. She lost weight and
became susceptible to infections.
Her parents, Ronald and Mary, cared for her at the family home until she
died on July 21.
Ronald said: "We ended up seeing specialist doctors from Edinburgh, As
far as they know, they say her condition came from infected meat.
"They asked us where we used to shop and lots of other things.
"I wouldn't say she ever ate a lot of beef burgers, no more than any
other person her age."
Dr Tim Dawson, consultant pathologist at the Royal Preston Hospital,
conducted a post mortem examination.
He said: "The examination showed variant CJD, which was the cause of death.
"This form of CJD usually affects younger individuals and begins with a
psychiatric episode, often depression.
"It is thought to be connected to infected meat."
The Preston coroner, Howard McCann, recorded a verdict of death by
misadventure.
e-mail: stef.hall@lep.co.uk
23 December 2004

http://www.prestontoday.net/ViewArticle2.aspx?sectionid=73&articleid=909777

IN light of Asante/Collinge et al findings that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;

-------- Original Message -------- Subject: re-BSE prions propagate as

either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43

-0000 From: "Asante, Emmanuel A" To:
"'flounder@wt.net'"

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I am

a Senior Scientist in the MRC Prion Unit and the lead author on the

paper. I have attached a pdf copy of the paper for your attention. Thank

you for your interest in the paper.

In respect of your first question, the simple answer is, yes. As you

will find in the paper, we have managed to associate the alternate

phenotype to type 2 PrPSc, the commonest sporadic CJD.

It is too early to be able to claim any further sub-classification in

respect of Heidenhain variant CJD or Vicky Rimmer's version. It will

take further studies, which are on-going, to establish if there are

sub-types to our initial finding which we are now reporting. The main

point of the paper is that, as well as leading to the expected new

variant CJD phenotype, BSE transmission to the 129-methionine genotype

can lead to an alternate phenotype which is indistinguishable from type

2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I

can be of any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<> ____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial

College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG

Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:

e.asante@ic.ac.uk (until 9/12/02)

New e-mail: e.asante@prion.ucl.ac.uk (active from now)

____________________________________

snip...

full text ;

http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm

BSE prions propagate as either variant CJD-like or sporadic CJD-like
prion strains in transgenic mice expressing human prion protein

Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth and John Collinge1

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1 Corresponding author e-mail: j.collinge@prion.ucl.ac.uk

Received August 1, 2002; revised September 24, 2002; accepted October 17, 2002

Abstract


Variant CreutzfeldtJakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure...

http://embojournal.npgjournals.com/cgi/content/full/21/23/6358

THE new findings of BASE in cattle in Italy of Identification of a
second bovine amyloidotic spongiform encephalopathy: Molecular
similarities with sporadic Creutzfeldt-Jakob disease


http://www.pnas.org/cgi/content/abstract/0305777101v1


Adaptation of the bovine spongiform encephalopathy agent to primates
and comparison with Creutzfeldt- Jakob disease: Implications for
human health

THE findings from Corinne Ida Lasmézas*, [dagger] , Jean-Guy Fournier*,
Virginie Nouvel*,

Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp [Dagger

] , Jean-Jacques Hauw§, James Ironside¶, Moira Bruce [||] , Dominique

Dormont*, and Jean-Philippe Deslys* et al, that The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is
very different from vCJD but is similar to that found in one case of
sporadic CJD and one sheep scrapie isolate;

http://www.pnas.org/cgi/content/full/041490898v1

Characterization of two distinct prion strains
derived from bovine spongiform encephalopathy
transmissions to inbred mice

Sarah E. Lloyd, Jacqueline M. Linehan, Melanie Desbruslais,
Susan Joiner, Jennifer Buckell, Sebastian Brandner,
Jonathan D. F. Wadsworth and John Collinge

Correspondence
John Collinge
j.collinge@prion.ucl.ac.uk

MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology,
University College, London WC1N 3BG, UK
Received 9 December 2003
Accepted 27 April 2004

Distinct prion strains can be distinguished by differences in incubation period, neuropathology
and biochemical properties of disease-associated prion protein (PrPSc) in inoculated mice.
Reliable comparisons of mouse prion strain properties can only be achieved after passage in
genetically identical mice, as host prion protein sequence and genetic background are known
to modulate prion disease phenotypes. While multiple prion strains have been identified in
sheep scrapie and CreutzfeldtJakob disease, bovine spongiform encephalopathy (BSE) is
thought to be caused by a single prion strain. Primary passage of BSE prions to different lines
of inbred mice resulted in the propagation of two distinct PrPSc types, suggesting that two
prion strains may have been isolated. To investigate this further, these isolates were
subpassaged in a single line of inbred mice (SJL) and it was confirmed that two distinct prion
strains had been identified. MRC1 was characterized by a short incubation time (110±3 days),
a mono-glycosylated-dominant PrPSc type and a generalized diffuse pattern of PrP-immunoreactive
deposits, while MRC2 displayed a much longer incubation time (155±1 days),
a di-glycosylated-dominant PrPSc type and a distinct pattern of PrP-immunoreactive deposits
and neuronal loss. These data indicate a crucial involvement of the host genome in modulating
prion strain selection and propagation in mice. It is possible that multiple disease phenotypes
may also be possible in BSE prion infection in humans and other animals.

http://vir.sgmjournals.org/cgi/content/abstract/85/8/2471

TSS





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