- Not only is Mad Cow/CJD found in meat, it could be in
a glass of milk, slice of cheese, bowl of ice cream.
- Now there is 'official' confirmation CJD is in human
blood...and transmissible via that blood. Just like HIV, just like Hep
C, and so many other 'emerging diseases.' Ergo, Mad Cow prions are also
in the blood of infected cattle. There is little reason to think otherwise.
And remember, there is no way to tell if an animal or human is infected...and
infectious...until they practically drop dead. Blood is where dairy milk
comes from in the udder. Therefore, one must suspect that these incredibly
small proteins (prions) could easily find their way into dairy products
of all types. Infected batches of milk mixed with untold thousands of gallons
of uninfected milk at any dairy is all it would take...and that is exactly
what happens with milk. The dairy and beef industries are probably working
around the clock, planning new milk moustache and hamburger ads to assure
everyone their products are completely safe. Let's watch how the media
is played and manipulated to keep the public from connecting the dots.
Oh yes, remember there has never been a single case of Mad Cow/CJD reported
in a single cow in America...ahem. Also, keep in mind, the Mad Cow prion
and the CJD prion are exactly the same...see following story below. No,
pastuerization will not eradicate prions from dairy products...prions can
withstand temperatures of 1,000 degrees fahrenheit. How many prions does
it take to become infected? As Clint Eastwood once said: "Do you
feel lucky today?"
- Blood Donors Feared to Have Spread CJD
- By Jonathon Leake - Science Editor http://www.sunday-times.co.uk/news/pages/Sunday-Times/stinwenws02008.html
- Blood donated by seven people who subsequently developed
variant CJD, the human form of mad cow disease, may have infected transfusion
products given to many more patients, it was revealed this weekend.
- The National Blood Authority has confirmed that some
of the blood taken from the seven was pooled - mixed with the blood or
blood products of many other donors - before it was distributed to hospitals.
- The number of people who may have been affected is unknown.
The authority has objected to suggestions that thousands are at risk, but
has no estimates of its own.
- The revelations follow experiments which show that blood
from sheep that are incubating BSE but have no symptoms can transmit the
disease to other sheep. Humans are equally vulnerable: blood taken from
anybody incubating vCJD could theoretically spread the disease to people
given blood products.
- Such a case has not yet been seen with blood, although
dozens of people contracted a slightly different form of CJD after being
given a human growth hormone that had been extracted from corpses.
- Blood from donors is usually split into its components,
such as red cells, which carry oxygen; plasma, with white cells that help
fight infection; and platelets, which aid clotting.
- This weekend the authority confirmed that it is now considering
a complete ban on the use of plasma from British donors. Most plasma is
already imported, but about 100,000 units come from within Britain. The
possibility that recipients of transfusions have been infected may also
disqualify them from becoming blood donors.
- Carlene Dyas, a spokeswoman for the authority, confirmed
that the blood donated by the seven vCJD victims was taken before 1999,
when the authority introduced new safety procedures designed to remove
prions, the infectious proteins thought to transmit vCJD. She said: "It
is very worrying, but there is nothing to show that what happens in sheep
does apply to humans."
- Dyas said most of the blood recipients could not be traced
because records were not sufficiently detailed. More than a dozen patients
known to have received blood products from people who later developed vCJD
have been identified, but will not be told of the danger.
- The problem is reminiscent of the spread of HIV in the
1980s when blood products transmitted the Aids virus to more than 1,200
haemophiliacs. The mistake cost the government £80m in compensation
- Professor Peter Smith, acting chairman of the government's
spongiform encephalopathy advisory committee, confirmed there was a risk:
"The concern with pooled blood products is that, as with growth hormone,
an infection in one person could be spread."
- Smith also acknowledged that the measures taken so far
to prevent donated blood infecting others may be insufficient. Since last
year, all Britishdonated blood has been stripped of its white cells, which
are thought most likely to carry the infectious prion particles. Recent
research indicates, however, that prions may also be carried by red cells.
- CJD And Mad Cow/BSE Shown To Be The SAME Infectious Protein
- From The University California, San Francisco 1-5-2000
- "Researchers are reporting what they say is the
most compelling evidence, to date, that the infectious proteins called
prions that cause bovine spongiform encephalopathy (BSE), or "mad
cow" disease, have infected humans, causing fatal brain degeneration.
- Recent studies have suggested that the outbreak of mad
cow disease in the late 1980s in Great Britain was responsible for the
emergence of a new variant of Creutzfeldt-Jakob disease, a fatal brain-degenerative
disease in humans also caused by prions. However, the link has been inconclusive.
The current study establishes that the particular strain of prions, responsible
for mad cow disease, is, in fact, the same strain that causes new variant
- The finding, reported in the December 20 issue of Proceedings
of National Academy of Sciences, is particularly unsettling because it
undermines the comforting presumption that a "species barrier"
dramatically lessened the likelihood that people exposed to "mad cow"
disease through meats, cosmetics, and medicinal supplies would be infected.
The species barrier refers to the relative lack of susceptibility of one
species to prions derived from another species.
- While Great Britain took the necessary measures in the
late 1980s to limit spread of the disease, the disease is believed to incubate
for at least 10 years, making it impossible to predict, the researchers
said, how many people have been infected.
- More than 175,000 cattle, primarily dairy cows have died
of BSE during the past decade. More than 50 teenagers and young adults
have died of new-variant Creutzfeldt-Jakob disease (nvCJD) since 1995.
Nine new deaths from CJD were reported in the last quarter of 1998.
- While the origins of BSE remain obscure, one possibility
is that the cattle developed the disease by being fed meat and bone meal
contaminated with prions from the sheep with the disease, scrapie. ...
- The researchers conducted their study by first creating
a line of transgenic mice genetically engineered to contain genes for the
bovine prion protein. (Prion proteins are not, in themselves, lethal. They
exist in all mammals and birds that have been examined, including humans,
and become destructive only when their shape is altered, a change that
occurs either through infection by an already infectious protein or through
a genetic mutation.) The line of mice was known as Tg(BOPrP).
- The researchers then inoculated the mice with prions
from diseased cows. And approximately 250 days after being inoculated,
all of the transgenic mice developed the neurologic disease.
- Next, another group of mice was inoculated with prions
from the diseased mice, and this group became sick after a virtually identical
period of time, confirming that the transgenic mice transmit mad cow disease
prions with no detectable change of strain or species-specific properties
attributable to the mice, themselves.
- Finally, and most important, transgenic mice inoculated
with prions from human cases of new variant Creutzfeldt-Jakob disease produced
the same incubation period and pattern of brain damage as had inoculation
with prions from diseased cows.
- To test their findings, the researchers inoculated transgenic
mice with prions from sheep with scrapie, another prion disease causing
neurological damage, and determined that these prions have dramatically
different biological properties.
- "BSE and new variant CJD produce the identical disease
pattern of disease in Tg(BOPrP) mice, and those characteristics were those
different than that found with inocula from other CJD cases or scrapie
from sheep. These findings argue unequivocally that BSE and new variant
CJD are the same strain of prion," said senior author DeArmond.
- "The fact that the human new-variant CJD prions
so precisely duplicate the properties of native bovine BSE prions in their
behavior on transmission to the transgenic mice creates a compelling argument
for a persuasive link between BSE and nvCJD," said Michael R. Scott,
PhD, UCSF associate adjunct professor in the Institute for Neurodegenerative
Diseases and the lead author of the study.
- Given the enormity of the affected cattle population
in Great Britain, a means of assessing risk to the human population is
paramount, and more sensitive methods for detection of prions are urgently
needed, the researchers said. The newly developed mouse model, Tg (BoPrP),
should provide a sensitive test for detecting BSE prions, they said."
- Comment (webmaster): This work was presented at the International
Virology Congress in Sydney, Australia in August 1999. The full text of
the PNAS article became available mid-morning on Tuesday 21 Dec 99.
- This is a solid paper and another nail in England's coffin.
It is fairly well described by the UCSF press release. In conjunction with
earlier work, this paper shows beyond any reasonable doubt that the nvCJD
is the same strain of TSE as BSE. A signficant species barrier between
cattle and humans is wishful thinking given this paper and earlier data.
- The paper is a watershed in that influential scientists
at both the Neuropathology Unit and UCSF, while not throwing caution to
the winds, are now convinced that BSE is the causal agent of nvCJD and
that little by way of species barrier can be expected. It is no coincidence
of timing that ten new nvCJD cases were announced yesterday, the first
time ante-mortem cases have been added into the total (62 in 3 countries).
- The paper is already being criticized in a whisper campaign
as 'alarmist and fear-mongering' -- the idea being floated (by those responsible
for the epidemic) is that nothing should be revealed because the public
might panic. The top scientists are saying with this paper that they no
longer can support a cover-up. The hour is late: it is high time to get
out of denial and instead really light a burner under the current half-baked
research effort. There will not be money for research when the government
can say 'Oh, it is only 62 victims so we mustn't alarm beef importing nations
- The bovine prion gene was inserted in knockout mice that
were then challenged by US Suffolk scrapie, BSE, and nvCJD. The final genomic
sequence is not described in the paper despite all the problems with doppel
in different knockout backgrounds -- the reader is sent off on a wild goose
chase in mouse strain nomenclature in older papers. The scrapie genotypes
are not provided either, other than Q at 171. Was either really determined?
- While it is all well and good to test nvCJD and scrapie
in these mice, this is testing the species barrier from human to cow, not
really the issue except possibly for animals grazing in cemetaries. Species
barriers are not necessarily symmetric, as the UCSF lab well knows from
studies of mouse-to-hamster compared to hamster-to-mouse.
- To test cow-to-human, a met 129 human prion in transgenic
mice is needed. No one will do this, though we have val 129 (these became
ill from cow, suggesting valine will prove no protection at codon 129)
and chimeric met 129 mouse-human data.
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