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From: TSS (216-119-143-128.ipset23.wt.net)
Subject: Regulators see more quarantines over mad cow
Date: January 4, 2005 at 9:44 am PST

-------- Original Message --------
Subject: Regulators see more quarantines over mad cow
Date: Tue, 4 Jan 2005 11:11:56 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE


##################### Bovine Spongiform Encephalopathy #####################

Monday, Jan 3, 2005

Regulators see more quarantines over mad cow


By OLIVER MOORE
Globe and Mail Update

More quarantines may become necessary as regulators investigate the
recent discovery of an Alberta cow with BSE, federal officials said Monday.

They stressed that the cow's infection poses no risk to the
health of Canadians and should not slow the full re-opening of U.S.
borders to live beef imports, which is expected in March.

A suspected case of bovine spongiform encephalopathy, the proper name
for mad-cow disease, was announced last week and confirmed on Sunday.

Offering more details about the case, federal officials said Monday that
the animal had been born a year before restrictions on feeding animal
parts to cows were put in place in the late 1990s.

(The 1997 Ruminant Ingredient Feed Ban prohibited the use of material
that originated from a mink or ruminant [cattle, sheep, goats, deer,
bison, llamas, etc.] to feed a ruminant animal. Milk, blood, gelatin,
rendered fats and their products were exempt from the ban.)

Canadian officials suspect that the cow was infected in its first year
of life. They say that rarity of the case – which comes nearly two years
after another such diagnosis sent in the beef industry into a serious
decline – shows that federal regulations to limit BSE are working.

Canadian Food Inspection Agency veterinarian Gary Little said Monday
that all of the cattle on the cow's farm has been quarantined and that
inspectors are poring over records of all the animals raised on the
premises.

“We are now tracing the whereabouts of the animal's most recently born
offspring and any animals born on the farm of origin within a year of
the infected animal,” he told an Ottawa press conference. “As the
investigation continues, additional quarantines may be necessary.”

Agriculture Secretary Andy Mitchell that he had spoken to his U.S.
counterpart, outgoing Agriculture Secretary Ann Venneman, and had been
assured that the borders would open on schedule.

“No part of the animal entered the human food or animal feed systems,”
he told the same press conference.

A spokesman for the U.S. Department of Agriculture confirmed Monday that
regulators on that side of the border remain content with Canadian
safety measures.

“USDA remains confident that the animal and public health measures that
Canada has in place ... provide the utmost protections to U.S. consumers
and livestock,” Ron DeHaven said.

“Considering Canada has roughly 5.5 million cattle over 24 months of
age, under [World Organization for Animal Health] guidelines, they could
detect up to 11 cases of BSE in this population and still be considered
a minimal-risk country.”

Dr. Little has been offering similar assurances since news of the
suspected case emerged late last week.

On Monday, he continued his positive tone, even as he acknowledged that
it may be impossible to pinpoint so many years after the fact the feed
source that caused the infection.


http://www.theglobeandmail.com/servlet/story/RTGAM.20050103.wmcow0103/BNStory/Front

Greetings,

> They stressed that the cow's infection poses no risk to the

> health of Canadians


HOW in the hell can _MORE_ documented cases of mad cow disease in
Canada _NOT_ raise the risk level of this agent to Canadians?

WOULD not the documentation of more cases add to the reallity of
more cases in the overall cattle population, thus giving more risk to the
human/animal population as a whole?

> Canadian officials suspect that the cow was infected in its first year
> of life. They say that rarity of the case – which comes nearly two
> years after another such diagnosis sent in the beef industry into a
> serious decline – shows that federal regulations to limit BSE are working.
>

THIS is total BSeee (or crap in laymans terms) and everybody knows it.
WHO is to say that the animal was not infected _after_ the first year
of it's life? ESPECIALLY after these recent reports;

Union: Meat plants violate mad cow rules
Banned brains, spinal cords may still enter food supply
By Jon Bonné
MSNBC
Updated: 6:21 p.m. ET Dec. 20, 2004

The National Joint Council of Food Inspection Locals, which represents
meat and poultry inspectors in federally regulated plants nationwide,
told the U.S. Department of Agriculture in a letter earlier this month
that body parts known as "specified risk materials" were being allowed
into the production chain...

snip...

In its letter, sent to the head of the USDA's Food Safety and Inspection
Service, the union also reported that some inspectors were "told not to
intervene" when they saw body parts of some older animals, sent for
packing with those of younger animals. This is despite export
requirements for certain parts that have been set by U.S. trading partners.

Specifically, the union said, kidneys from older animals were sent down
the line to be packed for the Mexican market, which prohibits them from
cows over 30 months. When the inspectors complained, Painter said, "The
agency basically told the inspectors, 'Don't worry about it.'"

snip...

http://www.msnbc.msn.com/id/6738982/
http://msnbc.msn.com/id/6738982/


FURTHER NORTH

Vancouver Sun (December 16, 2004)
Secret tests reveal cattle feed contaminated by animal parts
Mad cow fears spark review of 'vegetable-only' livestock feeds
By Chad Skelton
A series of secret tests on cattle feed conducted by the federal
government earlier this year found that more
than half the feed tested contained animal parts not listed on the
ingredients, according to internal documents
obtained by The Vancouver Sun.
The test results raise troubling questions about whether rules banning
the feeding of cattle remains to other
cattle -- the primary way in which mad cow disease is spread -- are
being routinely violated.
According to internal Canadian Food Inspection Agency documents --
obtained by The Sun through the
Access to Information Act -- 70 feed samples labelled as vegetable-only
were tested by the agency between
January and March of this year. Of those, 41 (59 per cent) were found to
contain "undeclared animal
materials."
"The presence of animal protein materials [in vegetable feeds] may
indicate ... deliberate or accidental
inclusion of animal proteins in feeds where they are not supposed to
be," said an internal memo to the
president of the Canadian Food Inspection Agency last April that
described the test results as "worrisome."
The memo, from Sergio Tolusso, feed program coordinator for the CFIA,
said the contamination could also
have been caused inadvertently -- for example, through the transporting
of different feeds in the same trucks.
Controlled experiments have shown an animal needs to consume as little
as one milligram of infected material
-- about the size of a grain of sand -- from an animal with bovine
spongiform encephalopathy (BSE) to
develop the brain-wasting disease.
Michael Hansen, an expert on mad cow disease with the U.S.-based
Consumers Union, the independent
research institute that publishes Consumer Reports, said the CFIA tests
are troubling.
"The fact that stuff that is labelled as vegetable feed, that 59 per
cent of it has animal material, that's incredibly
high," said Hansen, who has a PhD in biology. "This should be a wake-up
call to CFIA. It doesn't look good."
Michael McBane, national co-ordinator for the Canadian Health Coalition,
a watchdog group, said the tests
suggest the feed ban is not being adequately enforced.
"It demonstrates the fact that the [feed] ban is basically meaningless,"
McBane said. "It's pretty well
recognized that we have mad cow disease in Canada because of
contaminated feed. It's the frontlines in the
battle to stop the spread."
Consumption of beef from cows infected with BSE has been linked to the
development in humans of variant
Creutzfeldt-Jakob disease (vCJD), a deadly brain-wasting illness.
In the 1990s, the United Kingdom suffered an outbreak of BSE that was
followed by more than 100 people
dying of vCJD.
In 1997, as a precaution, Canada implemented a ban on feeding ruminants
-- like sheep and cattle -- to other
ruminants. However, ruminant remains can still be fed to chicken and
pigs, and chicken and pig remains can
be fed to cattle.
With the discovery of a lone Alberta cow with BSE in May 2003, the feed
ban took on added importance.
"Compliance with the existing ban is a critical factor in preventing the
disease from spreading to other
animals," Tolusso wrote in January in an internal memo to CFIA president
Dick Fadden. "Major noncompliance
with the feed ban cannot be tolerated, and measures to address the risks
of domestic ruminants
being exposed to prohibited animal proteins must be initiated promptly."
According to the documents, concerns about the integrity of Canada's
feed were first raised in the summer of
2003, when U.S. authorities turned back seven separate shipments of
vegetable feed from Canada because
they were contaminated with animal parts.
"The animal proteins detected in these [shipments] were not supposed to
be in the feeds," Tolusso explained to
Fadden in an August 2003 memo. "While the results initially appear to be
very worrying, it is difficult to
interpret the real significance of these findings."
To determine if there was a wider problem with Canadian feed, the CFIA
initiated a nationwide testing
program of both domestic and imported feed in early 2004.
To make the job easier for its scientists, the agency collected only
samples that were labelled as vegetableonly,
such as soy meal or grain -- feed that shouldn't have any animal parts
in it at all.
The samples were tested by CFIA scientists in Ottawa, who looked at a
few grams of each sample under a
microscope.
The first batch of 70 samples found that a majority contained animal
protein.
And the worst results were for feed manufactured in Canada.
Of the 28 domestic feed samples tested by the agency, 20 had undeclared
animal protein in them -- 71 per cent
of all the samples.
In comparison, just under half of the imported samples -- 19 of 39 --
contained animal parts.
(Three of the 70 samples were of undetermined origin.)
In an interview with The Sun, Tolusso said he couldn't say how many of
the contaminated feed samples
contained cattle remains.
"In the absence of real identifiable material like feathers and hairs,
[scientists are] left looking at bone
fragments and pieces of muscle tissue, and those are virtually
impossible to determine what species they might
come from," Tolusso said.
As a result, he said, the agency doesn't have a clear idea of how much
cattle remains have been fed to other
cattle.
"We knew entering this testing survey that there was a possibility we
could generate more questions for
ourselves than we could answer," he said. "We hadn't done this before
and to some extent we weren't sure
what we were going to find. And it does make it worse that you can't
explain what they actually are."
In addition to concerns over testing, the CFIA documents obtained by The
Sun also reveal problems with the
feed mills that produce animal feed.
There are about 550 commercial feed mills in Canada.
According to a memo to Fadden last March, an initial inspection last
year of several hundred of those mills
found that 21 per cent were not complying with federal regulations.
Most of those violations were minor and quickly corrected.
However, the report notes that seven mills had "major non-compliance
issues" involving things like proper
labelling and record-keeping.
And three mills were failing "to prevent the contamination of ruminant
feeds with non-ruminant feeds
containing ruminant meat and bone meal" -- the exact type of
contamination that can spread BSE.
Two of those three mills successfully recalled their contaminated
product, but the report notes that in one case,
some of the feed was sent out and consumed by cattle.
Tolusso said the CFIA's feed tests led to some follow-up inspections in
feed mills, but no further recalls of
feed.
Earlier this month, the CFIA announced it would ban the parts of cattle
most susceptible to BSE infection --
such as the spine and brains -- from all feed, including that destined
for pigs and chickens.
Such animal parts are known as specified risk materials (SRMs).
Tolusso acknowledged the agency's tests were one reason for the stricter
regulations.
"If we recognize there are lots of opportunities for the wrong kind of
protein to get in the wrong kind of feed
... then perhaps the more prudent thing to do is to remove some of these
higher-risk tissues altogether," he
said.
Some experts have argued that Canada should go even further and keep
cattle remains out of feed altogether,
as is done in Europe.
"What they need to do is cut out the loopholes [and] stop feeding
mammalian protein to food animals,"
Hansen said.
McBane agreed.
"At the end of the day, the only way to stop the transmission of BSE is
a complete stop on recycling animal
protein," he said.
Tolusso said the CFIA believes a ban on just the riskiest materials --
like cow brains -- will eliminate most of
the risk of BSE spreading in Canada.
But he said the agency hasn't ruled out a total ban on cattle remains in
feed.
"At this point, we've put our best guess forward [on] the most
appropriate approach," he said. "But that doesn't
preclude that ... we might have to go to a more strict ban."

http://www.healthcoalition.ca/new-bse.pdf

> under [World Organization for Animal Health] guidelines, they could
> detect up to 11 cases of BSE in this population and still be
> considered a minimal-risk country.”


THIS is totally unacceptable. what about the ones that are not documented
due to the limited testing?

> On Monday, he continued his positive tone, even as he acknowledged
> that it may be impossible to pinpoint so many years after the fact the
> feed source that caused the infection.
>

THEY will continue there positive tone to there grave, or our grave.
IT's simply not about science anymore$ IT's about nothing more than
opening the borders regardless, cause GW said he would. AND by
Golly what GW says goes, regardless the outcome. HE has proven
this time and time again.

WHO is to say the feed did not come from the USA?

> Milk, blood, gelatin, rendered fats and their products were exempt
> from the ban.)


OH, and by all means BLOOD poses no risk...............RIGHT! ($$$)

STUDY DESIGN AND METHODS: BSE was passaged through macaque monkeys and

then adapted to the prosimian microcebe (Microcebus murinus ). Brain

homogenate and buffy coat from an affected microcebe were separately

inoculated intracerebrally into three healthy microcebes (two animals

received brain and one received buffy coat).

RESULTS: All three inoculated microcebes became ill after incubation

periods of 16 to 18 months. Clinical, histopathologic, and

immunocytologic features were similar in each of the recipients.

CONCLUSION: Buffy coat from a symptomatic microcebe infected 17 months

earlier with BSE contained the infectious agent. This observation

represents the first documented transmission of BSE from the blood of an

experimentally infected primate, which in view of rodent buffy coat

infectivity precedents and the known host range of BSE is neither

unexpected nor cause for alarm.

http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction=showAbstract&doi=10.1046/j.1537-2995.2002.00098.x

Transmission of prion diseases by blood transfusion

Nora Hunter,1 James Foster,1 Angela Chong,1 Sandra McCutcheon,2 David

Parnham,1 Samantha Eaton,1 Calum MacKenzie1 and Fiona Houston2

see full text;

http://www.socgenmicrobiol.org.uk/JGVDirect/18580/18580ft.pdf

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 Related Articles,

Help Links

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by

electrodes contaminated during neurosurgery.

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.

Laboratory of Central Nervous System Studies, National Institute of

Neurological Disorders and Stroke, National Institutes of Health,

Bethesda, MD 20892.

Stereotactic multicontact electrodes used to probe the cerebral

cortex of a middle aged woman with progressive dementia were previously

implicated in the accidental transmission of Creutzfeldt-Jakob disease

(CJD) to two younger patients. The diagnoses of CJD have been confirmed

for all three cases. More than two years after their last use in humans,

after three cleanings and repeated sterilisation in ethanol and

formaldehyde vapour, the electrodes were implanted in the cortex of a

chimpanzee. Eighteen months later the animal became ill with CJD. This

finding serves to re-emphasise the potential danger posed by reuse of

instruments contaminated with the agents of spongiform encephalopathies,

even after scrupulous attempts to clean them.

PMID: 8006664

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract

It is possible to transmit BSE to a sheep
by transfusion with whole blood taken from
another sheep during the symptom-free phase
of an experimental BSE infection'

It is well known that variant Creutzfeldt-Jakob
disease (vCJD) is caused by the same strain of
agent that causes bovine spongiform encephalopathy
(BSE) in cattle. F Houston and colleagues
report the preliminary findings of transfusing
blood from 19 UK Cheviot sheep fed with 5 g
BSE-affected cattle brain into Cheviot sheep from
scrapie-free flock of New Zealand-derived
animals. The investigators found BSE clinical
signs and pathology in one recipient of blood taken
from a BSE infected animal. Immunocytochemistry on
tissues taken from the transfused sheep
showed widespread PrPSC deposition throughout the
brain and the periphery. This finding
suggests that blood donated by symptom-free
vCJD-infected human beings could transmit
infection to recipients of blood transfusions.
In a Commentary, Paul Brown states that these
observations are consistent with previous reports
in experimentally infected rodents.

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

Research letters
Volume 356, Number 9234 16 September 2000

Transmission of BSE by blood transfusion
in sheep


Lancet 2000; 356: 999 - 1000
Download PDF (1 Mb)


F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock

See Commentary

We have shown that it is possible to transmit
bovine spongiform encephalopathy (BSE)
to a sheep by transfusion with whole blood
taken from another sheep during the
symptom-free phase of an experimental BSE
infection. BSE and variant
Creutzfeldt-Jakob disease (vCJD) in human
beings are caused by the same infectious
agent, and the sheep-BSE experimental model
has a similar pathogenesis to that of
human vCJD. Although UK blood transfusions
are leucodepleted--a possible protective
measure against any risk from blood
transmission--this report suggests that blood
donated by symptom-free vCJD-infected human
beings may represent a risk of spread
of vCJD infection among the human population
of the UK.

The demonstration that the new variant of
Creutzfeldt-Jakob disease (vCJD) is caused by the
same agent that causes bovine spongiform
encephalopathy (BSE) in cattle1 has raised concerns
that blood from human beings in the symptom-free
stages of vCJD could transmit infection to
recipients of blood transfusions. There is no
evidence that iatrogenic CJD has ever occurred as a
result of the use of blood or blood products,
but vCJD has a different pathogenesis and could
present different risks. CJD is one of the
transmissible spongiform encephalopathies (TSEs)
characterised by the deposition of an abnormal
form of a host protein, PrPSc; the normal
isoform (PrPC) is expressed in many body tissues.
Available evidence, based on detection of
infectivity in blood in rodent models, and absence
of infectivity in naturally occurring TSEs, adds
to the uncertainty in risk assessments of the
safety of human blood. PrPSc has been reported in
blood taken from preclinical TSE-infected sheep,2
but it does not follow that blood is infectious.
Bioassays of human blood can only be carried out
in non-human species, limiting the sensitivity
of the test. One way of avoiding such a species
barrier is to transfer blood by transfusion in an
appropriate animal TSE model. BSE-infected sheep
harbour infection in peripheral tissues3 and
are thus similar to humans infected with vCJD.4
BSE infectivity in cattle does not have
widespread tissue distribution.

We report preliminary data from a study
involving blood taken from UK Cheviot sheep
challenged orally with 5 g BSE-affected cattle
brain and transfused into Cheviot sheep from a
scrapie-free flock of New Zealand-derived animals
(MAFF/SF flock). MAFF/SF sheep do not
develop spontaneous TSE and the transfused
animals are housed separately from other sheep.
All sheep in the study have the PrP genotype
AA136QQ171 which has the shortest incubation
period of experimental BSE in sheep.5 19 transfusions from
BSE-challenged sheep have been
done, mostly with whole blood. Sheep have
complex blood groups and only simple
cross-matching can be done by mixing recipient
serum and donor erythrocytes and vice versa.
Therefore single transfusions only were made
between sedated cross-matched animals to
minimise the risk of severe reactions. Negative
controls were MAFF/SF sheep transfused with
blood from uninfected UK Cheviot sheep. As a
positive control, MAFF/SF sheep were
intravenously injected with homogenised BSE-affected
cattle brain.

We have seen BSE clinical signs and pathological
changes in one recipient of blood from a
BSE-infected animal, and we regard this finding
as sufficiently important to report now rather
than after the study is completed, several years
hence. The blood donation resulting in
transmission of BSE to the recipient was 400 mL
of whole blood taken from a healthy sheep
318 days after oral challenge with BSE. BSE subsequently
developed in this donor animal 629
days after challenge, indicating that blood was taken
roughly half way through the incubation
period. 610 days after transfusion, the transfused
sheep (D505) itself developed typical TSE
signs: weight loss, moderate pruritus, trembling
and licking of the lips, hind-limb ataxia, and
proprioceptive abnormalities. This is the first
experimental transmission of BSE from sheep to
sheep and so we have nothing with which to compare
this incubation period directly. In
cross-species transmissions, bovine BSE injected
intracerebrally gives incubation periods of
about 450 days in these sheep,5 and the donor animal
had an oral BSE incubation period of 629
days (see above). There are no similar data
available on other infection routes.
Immunocytochemistry with the antibody BG4 on tissues
taken from sheep D505 showed
widespread PrPSc deposition throughout the brain and
periphery. Western blot analysis of brain
tissue with the antibody 6H4 showed that the PrPSc
protein had a glycoform pattern similar to
that of experimental BSE in sheep and unlike that
of UK natural scrapie (figure), indicating that
the TSE signs resulted from transmission
of the BSE agent. All other recipients of transfusions
and positive and negative controls are
alive and healthy. The positive controls, which involve a
species barrier, are expected to have
lengthy incubation periods. With one exception, all
transfused animals are at earlier stages
post-transfusion than was D505. The exception is a
sheep which is healthy 635 days after transfusion
with BSE-blood donated at less than 30% of
the BSE incubation period of the donor sheep.

PrPSc (proteinase K treated) analysed by SDS-PAGE,
immunoblotted with 6H4, and
visualised with a chemiluminescent substrate

All lanes are from the same gel with different
exposure times. Size markers are to the left of
lane 1. Lane1: natural scrapie sheep brain,
3 min exposure. Lane 2: as lane 1, 10 min exposure.
Lane 3: sheep D505, blood-transfusion
recipient, 10 min exposure. Lane 4: experimental
BSE-affected sheep brain, 30 s exposure.
Lane 5: as lane 4, 10 min exposure. Each lane
loaded with amount of protein extracted from
0·1 g wet weight of brain, except lane 3 which
was extracted from 0·2 g brain.


Although this result was in only one animal, it
indicates that BSE can be transmitted between
individuals of the same species by whole-blood
transfusion. We have no data on blood fractions
or on levels of infectivity in blood of preclinical
vCJD cases, but whole blood is not now used in
UK transfusions. The presence of BSE infectivity
in sheep blood at an early stage in the
incubation period suggests that it should be
possible to identify which cells are infected, to test
the effectiveness of leucodepletion, and to
develop a diagnostic test based on a blood sample.

We thank Karen Brown, Moira Bruce, Calum
McKenzie, David Parnham, Diane Ritchie, and
the Scottish Blood Transfusion Service. The
project is funded by the Department of Health.

1 Bruce ME, Will RG, Ironside JW, et al.
Transmissions to mice indicate that 'new variant' CJD
is caused by the BSE agent. Nature 1997;
389: 488-501 [PubMed].

2 Schmerr MJ, Jenny A, Cutlip RC. Use of
capillary sodium dodecyl sulfate gel electrophoresis
to detect the prion protein extracted from
scrapie-infected sheep. J Chromatogr B Biomed
Appl 1997; 697: 223-29 [PubMed].

3 Foster JD, Bruce M, McConnell I, Chree A,
Fraser H. Detection of BSE infectivity in brain
and spleen of experimentally infected sheep.
Vet Rec 1996; 138: 546-48 [PubMed].

4 Hill AF, Zeidler M, Ironside J, Collinge J.
Diagnosis of new variant Creutzfeldt-Jakob disease
by tonsil biopsy. Lancet 1997; 349: 99-100.

5 Goldmann W, Hunter N, Smith G, Foster J,
Hope J. PrP genotype and agent effects in
scrapie: change in allelic interaction with
different isolates of agent in sheep, a natural host of
scrapie. J Gen Virol 1994; 75: 989-95 [PubMed].


Institute for Animal Health, Compton, Newbury,
UK (F Houston PhD, CJ Bostock
PhD); and Institute for Animal Health, Neuropathogenesis Unit,
Edinburgh, EH9
3JF, UK (N Hunter PhD, JD Foster BSc, Angela Chong BSc)


Correspondence to: Dr N Hunter

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

Commentary
Volume 356, Number 9234 16 September 2000

BSE and transmission through blood


Lancet 2000; 356: 955 - 956
Download PDF (55 Kb)
Wether the outbreak of variant Creutzfeldt-Jakob disease
(vCJD) in the UK will ultimately
affect hundreds, or tens of thousands of people,
cannot yet be predicted.1 If large numbers of
apparently healthy people are now silently incubating
infections with bovine spongiform
encephalopathy (BSE), the implications for public
health include the possiblity that blood from
such individuals may be infectious. Established facts
about infectivity in the blood of human
beings and animals with transmissible spongiform
encephalopathies (TSEs) are as follows:2-4

Blood, especially the buffy-coat component,
from animals experimentally infected with
scrapie or CJD and from either a clinical or
preclinical incubation phase, is consistently infectious
when bioassayed by intracerebral or intraperitoneal
inoculation into the same species;

In naturally infected animals (sheep and goats
with scrapie, mink with transmissible mink
encephalopathy, and cows with BSE), all attempts
to transmit disease through the inoculation of
blood have failed;

Blood from four of 37 human beings with
clinically evident sporadic CJD has been reported
to transmit the disease after intracerebral inoculation into guineapigs,
mice, or hamsters. But each
success has been questioned on technical grounds
and has not been reproducible; and

Epidemiological data have not revealed a
single case of CJD that could be attributed to the
administration of blood or blood products among
patients with CJD, or among patients with
haemophilia and other congenital clotting or
immune deficiencies who receive repeated doses of
plasma concentrates.

No comparable information about vCJD is available.
However, since lymphoreticular organs,
such as tonsils have been shown to contain the
prion protein (which is an excellent index of
infectivity), whereas it is not detectable in
patients with sporadic CJD, there is some reason to
worry that blood from individuals incubating
vCJD might be infectious.5 Data from studies into
the ability of blood from experimentally infected
rodents and primates with vCJD to transmit the
disease will not be available for months or years.

In this issue of The Lancet, F Houston and co-workers
report convincing evidence that blood
from a seemingly healthy sheep incubating BSE
(infected by the oral route with brain from a
diseased cow) was able to cause the disease when
transfused into another sheep. This
observation is entirely consistent with past
experience in experimentally infected rodents. It
extends current knowledge about blood infectivity
in experimental models to a host/TSE strain
pair that is closer to the human vCJD situation
than the earlier rodent studies. It is also the first
successful transfusion of BSE from blood taken
during the all-important incubation period of
infection. This result is part of a larger study
(n=19) that includes both positive and negative
control animals, all still healthy and in various
early stages of the incubation period.

Is it appropriate to publish an experimental
result from a single animal in a study that is not far
enough along even to have validated its positive
controls? Especially a result that does not in any
fundamental way change our current thinking about
BSE and vCJD and which would not seem
to have any practical consequences for public
health? The UK National Blood Transfusion
Service has already implemented leucodepletion
of donated blood, and imports all plasma and
plasma derivatives from BSE-free countries. No
further measures would seem possible--short
of a draconian decision to shut down the whole
UK blood-donor system. What, therefore, is the
rationale for this publishing urgency? The
answer, evidently, is a perceived need to "defuse", by
an immediate and accurate scientific report,
public reaction to possibly inaccurate media
accounts. The full study, when it appears, will
be an important addition to our knowledge of
TSEs, but science should not be driven to what
in certain medical quarters might be termed a
premature emission through fear of media misrepresentation.

Paul Brown


Laboratory of Central Nervous System Studies,
National Institutes of Health, Bethesda,
MD 20892, USA

1 Ghani AC, Ferguson NM, Donnelly CA, Anderson RM.
Predicted vCJD mortality in Great
Britain. Nature 2000; 406: 583-84 [PubMed].

2 Brown P. Can Creutzfeldt-Jakob disease be
transmitted by transfusion? Curr Opin Hematol
1995; 2: 472-77 [PubMed].

3 Brown P, Cervenáková L, McShane LM, Barber P,
Rubenstein R, Drohan WN. Further
studies of blood infectivity in an experimental
model of transmissible spongiform encephalopathy,
with an explanation of why blood components do not transmit
Creutzfeldt-Jakob disease in
humans. Transfusion 1999; 39: 1169-78 [PubMed].

4 Rohwer RG. Titer, distribution, and transmissibility
of blood-borne TSE infectivity. Presented
at Cambridge Healthtech Institute 6th Annual Meeting
"Blood Product Safety: TSE, Perception
versus Reality", MacLean, VA, USA, Feb 13-15, 2000.

5 Hill AF, Butterworth RJ, Joiner S, et al. Investigation
of variant Creutzfeldt-Jakob disease and
other human prion diseases with tonsil biopsy samples. Lancet 1999; 353:
183-89.
===========

Transmission of Creutzfeldt-Jakob Disease from Blood and Urine Into Mice

The Lancet, November 9, 1985

Sir,--Professor Manuelidis and his colleagues (Oct 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the
buffy coat from two patients. We also transmitted the disease from
whole blood samples of a patient (and of mice) infected with CJD.1
Brain, Cornea, and urine from this patient were also infectious, and
the clinicopathological findings2 are summarised as follows.

A 70-year-old man was noted to have a slowing of speech and writing
and some disorientation, all of which progressed rapidly. Decorticate
rigidity, forced grasping, positive snout reflex, and myoclonus
appeared within 2 months. Electroencephalogram revealed typical
periodic synchronous discharge, and he died of pneumonia and upper
gastrointestinal haemorrhage, about 3 months after onset of the
symptoms. The Brain weighed 1290g and showed severe histological
changes diagnostic of CJD, including spongiform change, loss of
nerve cells, and diffuse proliferation of astrocytes. There were no
inflammatory cells, microglia, neurofibrillary tangles, and
amyloid plaques, although virus-like particles were detected by
electron microscopy.

Results of innoculation in Mice

Inocula NO* Incubation period (days)+
Brain 7/10 (4) 789 (+ or - 112)
Cornea 1/6 (0) 1037
Blood 2/13 (0) 1080 (+ or - 69)
Urine 5/10 (1) 880 (+ or - 55)
CSF 0/10

* Number of mice with CJD change/number examined histologically.
Number with amyloid plaques shown in parentheses.

+ means + or - SD

Samples were taken aseptically at necropsy. 10% crude homogenates
of brain and cornea in saline, whole blood (after crushing a clot),
and untreated CSF and urine were innoculated intracerebrally into
CF1 strain mice (20 ul per animal). Some mice showed emaciation,
bradykinesia, rigidity of the body and tail, and sometimes tremor
after long incubation periods. Tissues obtained after the animal
died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes,
consisting of severe spongiform changes, glial proliferation, and
a moderate loss of nerve cells. A few mice inoculated with brain
tissue or urine had the same amyloid plaques found in patients and
animals with CJD.3

In our long-term experiments, inoculating materials taken from
twenty patients with CJD or Gerstmann-Straussler-Scheinker's
disease (GSS) into rodents, positive results were obtained in
seventeen cases, including this patient. Brain tissue transmitted
the disease most frequently within the shortes incubation period,
except for one case where the lymph node was the most infectious.
Transmission through the cornea has been noted in man4 and in
guineapigs.5 Whole blood samples taken from three patients were
inoculated and a positive transmission occured only in the case
recorded here. Mouse-to-mouse transmission through blood
inoculation was successful after a mean incubation period of 365
days.1 Transmission through urine was positive in this patient
only, and negative in one other patient and in many infected animals.
Transmission through the CSF from eight patients was negative, yet
transmission via the CSF of infected rats was positive.1

As viraemia has been proved in guineapigs,6 mice,1,7 and lately
in patients with CJD, blood for transfusion or blood products for
medical use must be tested for unconventional pathogens. For this
purpose, we inoculated blood products inot rodents.8 The CJD
pathogen was not found in the products examined. However, this
approach takes too long to be of practical value. More efficient
methods must be developed to detect pathogens and to eliminate
them from blood. One proposal9 is to apply membrane filtration to
the pruification protocol of human growth hormone suspected of
being contaminated with CJD. Similar methods are needed for blood
contamination.

Department of Neuropathology,
Neurological Institute,
Faculty of Medicine,
Kyushu University,
Fukuoka812, Japan

JUN TATEISHI

1. Tateishi J, Sato Y, Kaga M. Doi H, Ohta M. Experimental transmission
of human subacute spongiform encephalopathy to small
rodents 1: Clinical and histological observations.
Acta Neuropathol (Berl) 1980; 51: 127.

2. Shibayama Y, Sakaguchi Y, Nakata K, et al, Creutzfeldt-Jakob
disease with demonstration of virus-like particles.
Acta pathol Jpn 1982;32: 695.

3. Tateishi J, Nagara H, Hikita K, Sato Y. Amyloid plaques in the
brains of mice with Creutzfeldt-Jakob disease.
Ann Neurol 1984; 15: 278.

4. Duffy P, Wolf J, Colings G, DeVoe AG, Streeten B, Cowen D.
Possible person-to-person transmission of Creutzfeldt-Jakob disease.
N Engl J Med 1974; 290: 692.

5. Manuelidis EE, Angelo JN, Gorgacz EJ, Kim JH, Manuelidis L.
Experimental Creutzfeldt-Jakob disease transmitted via the eye
with infected cornea. N Engl J Med 1977; 296: 1334.

6. Manuelidis EE, Gorgacz EJ, Manuelidis L. Viremia in experimental
Creutzfeldt-Jakob disease. Science 1978: 200: 1069.

7. Kuroda Y, Gibbs CJ Jr, Amyx HL, Gajdusek DC.
Creutzfeldt-Jakob disease in mice. Persistent viremiam and
preferential replication of virus in low-density lymphocytes.
Infect Immun 1983; 41: 154.

8. Tateishi J, Tsuji S. Unconventional pathogens causing spongiform
encephalopathis absent in blood products. J Med Virol 1985; 15: 11.

9. Tateishi J, Kitamoto T, Hiratani H. Creutzfeldt-Jakob disease
pathogen in growth hormone preparations is eliminatable.
Lancet (in press).


http://www.thelancet.com/

FAST FORWARD 2004

Date: September 09, 2004 Time: 10:45

PATIENT NOTIFICATION EXERCISE BEGINS

Health Secretary John Reid today announced further developments
concerning variant Creutzfeldt-Jakob disease and blood. He told MPs in a
written ministerial statement that an exercise has begun to notify some
recipients of blood products about the results of a risk assessment
exercise carried out by the Health Protection Agency. The exercise
follows the identification last December of the first suspected case of
vCJD transmission through blood transfusion.

The results of the risk assessment will be made public at the end of the
patient notification exercise.

John Reid said:

'It is important that Parliament is kept informed of developments on
this important subject, which is why I have made this statement today.

'However, it is equally important that the patients who need to know the
results of this risk assessment are given this information by the
clinicians who care for them, so that appropriate support can be provided.

'My Department will make a further announcement at the end of this
notification exercise.'

The written ministerial statement to Parliament is attached below.

WRITTEN MINISTERIAL STATEMENT

DEPARTMENT OF HEALTH

9 September 2004

The Secretary of State for Health: Written Ministerial Statement on
blood donation and vCJD.

The Secretary for State Health (Dr Reid):

Following my statements to the House on 17 December 2003 and 16 March
2004 concerning variant Creutzfeldt-Jakob disease (vCJD) and blood, I
wish to provide an update on some further developments in this area.

My statement on 17 December 2003 informed the House of the first case of
possible transmission of vCJD via blood transfusion and the
precautionary actions taken. Those actions included measures to protect
future blood supplies and contacting recipients of blood from donors who
subsequently went on to develop vCJD. A further written statement on 22
July 2004 indicated a second case of possible vCJD prion transmission
via blood transfusion had been confirmed.

I also made reference in December to the fact that other patients,
including people with haemophilia and other bleeding disorders, would
have received plasma products before they were sourced from the United
States of America. Although there are now two reports of possible
transmission of vCJD via blood, the risk of transmission via plasma
products, which will have been derived from large pools of plasma
donated from many thousands of people - and therefore heavily diluted -
is uncertain. But it cannot be excluded. The CJD Incident Panel (CJDIP)
were asked to advise on a case-by-case basis (having adopted a highly
precautionary approach) which recipients of plasma products will need to
be contacted. This advice has been received and a programme of action
has been agreed.

In June 2004 the Health Protection Agency (HPA), on behalf of the CJD
Incidents Panel, reported on an assessment of the risk associated with
each batch of product and advised my Department on: a) which patients
needed to be assessed and possibly subsequently contacted, and b)
managing the possible risk to public health of those patients.

In the light of these assessments, the HPA is today initiating a process
to notify relevant patients of these developments. The HPA are sending
information to clinicians to enable them to trace particular plasma
products. The clinicians will then notify any patients identified as 'at
risk' as a precaution. Any patients affected should expect to be
contacted by clinicians later this month.

Aside from patients with haemophilia or other bleeding disorders, the
other main group of patients who may have received significant amounts
of affected blood products are patients with primary immuno-deficiency
(PID).

Throughout this exercise we have been concerned to ensure that the
results of the risk assessment are communicated to patients by the
clinicians responsible for their day to day care, so that appropriate
supporting information can be provided.

Further details about the risk assessment exercise will not be disclosed
until after patients are informed of the outcome. I will make a further
statement at a later date, if necessary.

http://www.wired-gov.net/WGLaunch.aspx?ARTCL=26689


SO, IF we are now deferring blood donations due to documented proof of
transmission of CJD via blood for humans,
why in the world are we not doing it for animals, especially if humans
are going to be eating them...daaaaaaa


THE Three Stooges themselves could not have planned out such a scenerio
as this...

still disgusted in 2005 from Bacliff, Texas

TSS

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