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From: TSS (216-119-144-16.ipset24.wt.net)
Subject: SECOND PROBABLE CASE OF CJD INFECTION FROM BLOOD TRANSFUSION (pp 477, 527) LANCET PRESS RELEASE
Date: August 7, 2004 at 9:19 am PST

-------- Original Message --------
Subject: SECOND PROBABLE CASE OF CJD INFECTION FROM BLOOD TRANSFUSION (pp 477, 527) LANCET PRESS RELEASE
Date: Sat, 07 Aug 2004 11:20:20 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
CC: cjdvoice@yahoogroups.com


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“Unless WHO’s African office is transformed from a political club to an
effective health agency, its right to existence is questionable.”
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ISSUE: 7–13 August 2004
EMBARGO: 0001 H (London time) Friday 6 August 2004. In North America
the embargo for Lancet press material is 6:30pm ET Thursday 5 August
2004.
SECOND PROBABLE CASE OF CJD INFECTION
FROM BLOOD TRANSFUSION (pp 477, 527)
A research letter in this week’s issue of THE LANCET details the second
case of
variant Creutzfeldt-Jakob disease (vCJD) infection that was probably
caused by
blood transfusion. The rogue prion responsible for vCJD was identified
at postmortem
five years after an elderly person received a blood transfusion from a
donor who later developed vCJD.
The first case of vCJD associated with blood transfusion was announced
at the
end of last year (see Lancet 2004; 363: 417–21). Also identified at that
time were
17 people who had received blood donated from donors who later went on to
develop vCJD. The case reported today—who did not have clinical symptoms of
vCJD and died of other causes—was one of those 17 individuals.
The current case is the first of its kind to identify a heterozygous
genotype for
the prion protein, suggesting that a larger population of people could
become
infected. James Ironside, one of the investigators from the CJD Surveillance
Unit, Edinburgh,UK, , comments: “This finding has major implications for
future
estimations of numbers of vCJD cases in the UK, since individuals with this
genotype constitute the largest genetic subgroup in the population. This
subgroup might have a different incubation period after exposure to either
primary infection by the bovine spongiform encephalopathy (BSE) agent or
secondary infection by blood transfusion. A very lengthy incubation
period might
explain why no clinical cases of vCJD have yet been observed in this
subgroup”.
Professor Ironside adds: “This case highlights the need for continuing
surveillance for CJD in the UK, and strongly reinforces the role of the
autopsy in
the investigation and diagnosis of both clinical and preclinical forms
of human
prion disease”.
An accompanying commentary (p 477) by Kumanan Wilson (Toronto General
Hospital) and Maura Rickets (Health Canada) is supportive of UK policies
introduced to limit the spread of vCJD. With regard to the blood-transfusion
case Dr Wilson comments: “The true clinical and public-health
significance, with
respect to the issue of whether the individual would have subsequently
developed clinically evident vCJD or whether this individual poses a
risk for
iatrogenic transmission of the disease, remains uncertain. Nevertheless,
combined with the animal studies by Houston and Hunter and their colleagues
showing transfusion transmission of the disease in preclinical models,
and the
previous case report of probable transfusion transmission, there now
appears to
be sufficient evidence that individuals without clinical signs of vCJD
harbour,
and therefore potentially transmit, the infection”.
A policy of leucoreduction (removal of white blood cells) for blood
transfusion to
reduce the risk of possible vCJD transmission was introduced in the UK
in 1999.
Authors of a second research letter (p 529) highlight how leucoreduction
only
reduced infectivity by around 40% in an animal model where hamsters were
infected with scrapie-infected tissue. Lead investigator Luisa Gregori (VA
Maryland Health Care System/University of Maryland, USA) comments:
“Although leucoreduction is a necessary step for removing
white-cell-associated
TSE infectivity from blood, this process is insufficient to remove the
risk from an
infected transfusion unit”.
Transmission of vCJD from surgical instruments is another public-health
concern, especially as the prion protein responsible for vCJD is
resistant to
conventional sterilising procedures. In an article in this week’s issue
(p 521),
Jean Philippe Deslys and colleagues (CEA/DSV/DRM/GIDTIP, France) identify a
new technique for disinfecting prion-contaminated medical devices. They
report
how specific alkaline agents or an original vaporized hydrogen peroxide
treatment can be effective decontaminants without damaging delicate medical
or surgical instruments; conventional autoclaving alone does not fully
reduce
transmission risk and can often damage surgical devices. Dr Deslys
comments :
“Decontamination of prions from surgical instruments has been a major
problem
since vCJD was first identified. The results of our study should provide
reassurance that practical solutions now exist which can be implemented
without delay to reduce risk of prion transmission from medical and surgical
instruments”.
Contact: Professor James W Ironside, CJD Surveillance Unit, c/oRonald Kerr,
University of Edinburgh Press Office, UK; T) +44 (0)131 650 9547/2250 ;
ronald.kerr@ed.ac.uk
(commentary) Dr Kumanan Wilson, Toronto General Hospital, University Health
Network, Toronto, ON M5G 2C4, Canada; T) +1 416 340 4800 ext 6559;
Kumanan.Wilson@uhn.on.ca
(leucoreduction research letter) Sharon Boston, Media Relations,
University of
Maryland School of Medicine, USA; T) +1 410 328 8919; SBOSTON@umm.edu or
Monica Smith, Public Relations/Community Outreach, VA Maryland Health Care
System, USA; T) +1 410 605 7098; monica.smith@med.va.gov
(medical and surgical instruments article) Dr Jean Philippe Deslys,
Groupe d'Innovation
Diagnostique et Thérapeutique sur les Infections à Prions, CEA/DSV/DRM,
18 Route du
Panorama, 92265 Fontenay-aux-Roses, France ; T) +33 1 46 54 82 79;
jpdeslys@cea.fr
ISSUE: 7–13 August 2004
EMBARGO: 0001 H (London time) Friday 6 August 2004. In North America
the embargo for Lancet press material is 6:30pm ET Thursday 5 August
2004.
TSS





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