su-texas
Wed, Dec-04-02, 23:55
Today, I read an article in a magazine about CWD, & it sounds
like very scary stuff.
-------------
From: The Rock Garden (hensler@povn.com), Subject: CWD
article, Newsgroups: misc.rural, Date: 2002-11-30 11:05:49 PST
For those interested, there is a current article on Chronic
Wasting Disease in the Milwaukee Magazine on line at
http://www.milwaukeemagazine.com/122002/cwd.html It is long
and the slant in on the Wisc. deer herd, but is fairly well
researched and written in non-technical terms. Skip
-----------------
From: Thundercleese (dan@angband.org), Subject: Re: CRUISE
VIRUS- WHAT THE H... IS GOING ON?, Newsgroups: rec.boats,
Date: 2002-12-03 22:20:06
PST
Also Sprach Floyd in Tampa <Flooydomit@prodigy.net>:
> I'm not a vector specialist, but watching the crew rubbing >
> the ship
down with rags seems laughable, and what could > they possibly
be spraying that would affect a virus?
Most likely dilute chlorine bleach. Virii are pretty weak,
when outside a host. Now you want a tough infectious agent,
look at prions. Basically a distorted protein molecule, can
survive autoclaving, exposure to vacuum, and all kinds of
chemicals. They cause the Mad Cow Disease, Chronic Wasting
Disease, and Creutzfeldt-Jakob Disease (the human Mad Cow).
CJD has been transmitted to surgical patients from
contaminated surgical instruments even though they had been
cleaned and autoclaved. Scary stuff. Dan
---------------
Susan, Su_Texas my opinions
PP Some quotes from the article mentioned above:
If you ask the country's highest-ranking experts on prion
diseases like CWD, mad cow and human Creutzfeldt-Jakob disease
(CJD), they will tell you that only incineration, bleach and
chemical tissue digestors destroy the infectious agents that
cause the diseases and that serious public concern is
warranted.
"We have repeatedly underestimated these diseases, and we've
been wrong. People have died because of it," says Judd Aiken,
UW animal health and biomedical sciences researcher. "I'm not
an alarmist and I don't like having people mad at me, but it's
the truth when I say don't consume venison from an area where
CWD exists."
The group urged the state to adopt the steps Britain has taken
to stop mad cow disease and immediately ban venison handling
by meat processors who also prepare beef, chicken and other
meats. The nearly indestructible CWD disease prions, it said,
could contaminate equipment and pass into the rest of the food
chain. "People have the right to decide for themselves whether
they want to eat venison," says Olds. "They shouldn't have to
worry that other meat they eat is contaminated."
-------
Like elk, deer can carry the disease for years without
symptoms, infecting other animals. Until just recently, there
was no live-animal CWD test.
Symptoms: It takes an average of 15 months for a deer infected
with CWD to exhibit symptoms, but they can occur in as little
as six months or not show up for as long as eight years, says
Hauge. Then it will display abnormal behavior, stupor, head
tremors, staggering, lack of coordination, trouble judging
distance and difficulty swallowing. CWD-infected deer drink
lots of water, increasing urination, and slobber excess
saliva. They "waste away" until paralysis or pneumonia set in.
"It is not a pretty death," says Hauge.
Spread: Scientists believe nose-to-nose contact spreads CWD,
as well as environment and food contaminated by saliva, urine
and feces and by does who infect their offspring.
--------------
CWD's Family Tree
When Richard Race (a leading researcher on CWD and related
diseases with the National Institutes of Health's Rocky
Mountain Laboratories), heard Kazmierczak's comment about
eating deer brains, he was appalled. "That's irresponsible. Do
we want to have a repeat of what happened in Britain, where
for 10 years the government said BSE [mad cow disease] was
safe to eat, and so far we have 133 people dead because of
it?" asks Race. "It's not fair to say people either are or
aren't susceptible to CWD at this point. Not enough people
have eaten enough infected venison and lived long enough for
it to incubate."
TSEs & Chronic Wasting Disease in Deer (CWD): Researchers who
saw the first cases of CWD in Colorado deer in 1967, thought
it was a nutritional problem. By 1980, they realized it was
part of a family of deadly neurological disorders called
transmissible spongiform encephalopathies (TSEs), affecting
humans, sheep, mink, cats and other animals.
TSEs & Mad Cow Disease (BSE): The most famous TSE of all,
bovine spongiform encephalopathy (BSE), appeared in Britain in
1985. It killed nearly 200,000 cattle, then spread to humans
who consumed infected beef.
TSEs & Prions (Infectious Protein): Unlike most diseases,
which are caused by viruses or bacteria, the infectious agent
in TSEs is believed to be a normal protein that mutates,
becoming an infectious protein, or prion, and then causes the
misfolding of other proteins. The process creates sponge-like
brain lesions leading to physical and mental decline.
Although human cases are rare, TSEs are so significant that
two Nobel prizes for medicine have been awarded for prion
disease research.
-----------
When mad cow disease first appeared, officials said it was
"just like scrapie in sheep", the oldest known TSE, never
known to have infected humans. The disease is called scrapie
because infected sheep become so deranged, that they rub
themselves raw attempting to scrape off their fur.
The Spread of TSEs, From Sheep to Deer to Elk?: There is
unproven speculation that CWD originated when environmental
contamination passed scrapie from sheep to deer housed at
Colorado State University's Foothills Research Station, then
to wild deer and elk. That's one reason Wisconsin officials
say CWD is like scrapie. Of course, that's what the British
government thought, too, while nearly two million contaminated
cattle slipped into the human food chain.
TSEs in Cats: For more than a decade -- even after cats fed
infected beef meat and bone meal came down with a mad cow-like
disease -- the British government insisted that human beef
eaters were protected by a "species barrier."
Five years after some physicians and scientists started
sounding alarms about eating infected beef, then British Prime
Minister John Major was still reassuring the public: "There is
no scientific evidence that BSE can be transmitted to humans."
TSEs & Creutzfeldt-Jakob Disease in Humans (CJD): [In about
March 1996,] two dairy farmers, a butcher, a meat pie maker
and eight young people who had eaten contaminated beef were
dead from an Alzheimer's-like disease called new variant
Creutzfeldt-Jakob disease (nvCJD). It looked similar to the
rare sporadic CJD that affects only one person per million,
but when their brains were autopsied, they looked just like
the brains of mad cows. The government finally admitted
that the "species barrier" -- if it existed at all -- had
holes in it.
---------
TSEs Spread Through Meat: The World Health Organization now
says mad cow disease passed to humans when they ate infected
beef. Hamburgers and processed meats like sausage that
included bovine offal (by-products) -- brains, spinal chords,
eyes, lymph nodes, thymus and intestines -- areas with the
highest concentration of disease prions, are the chief
suspects, although laboratory scientists have since found TSE
disease agents in blood and muscle, too.
(Dr. Olds says Wisconsinites should forgo venison sausage even
if deer offal is left out and their deer tests negative
for CWD because there is no guarantee their deer won't be
mixed with others in the sausage-making process.)
No one knows how much infected meat you'd have to eat to get
new variant CJD or even whether a little now and then will
add up to infection. But as little as one-half gram of
BSE-infected brain -- the size of a good vitamin pill --
taken orally will infect a cow, NIH senior prion disease
researcher Paul Brown told the FDA's TSE Advisory Committee
on January 19, 2001.
Cooking at temperatures above 600 degrees C doesn't kill the
infectious agent in TSEs, nor do detergents and enzymes known
to kill most viruses. Radiation doesn't faze it, and even
after being buried in the soil for three years, enough prions
remain to spread the disease. Chlorine bleach is one of the
better disinfectants, in concentrations of 50 percent and
higher, but sometimes even that has diminished effectiveness.
Beef by-products are now banned from human consumption in
Europe (though not in the United States), but since human TSEs
incubate for decades, no one knows what the final human death
toll will be.
------------------
Autopsies: It's difficult to find a neurologist like Antuono,
willing to autopsy the brain of a patient suspected of dying
of a TSE. A splash in the eye of bodily fluid can carry the
disease straight to the brain.
Those who have already died shared one of three genetic
variations for the human prion protein, a genetic make-up seen
in 40 percent of the population. But "that doesn't mean others
are immune," says UW's Aiken. The disease may merely incubate
longer in people with other genes.
Research published in May 2000 in The European Molecular
Biology Organization Journal states: "CWD transmissions would
be similar to transmissions of mad cow disease," adding that,
"it would seem prudent to take reasonable measures to limit
exposure of humans (and cows and sheep) to CWD infectivity."
--------------
Wisconsin's TSE History
TSEs & Alzheimer's?: The original human TSE, classic
Creutzfeldt-Jakob disease, is often mistaken for Alzheimer's,
but it is a rare nervous system disease that results in
rapidly progressive dementia, a nightmare of madness and
terrifying hallucinations, loss of motor control, paralysis
and death.
Discovered in the 1920s, it seems to occur spontaneously
across the globe (300 per year in the United States),
attacking victims with a mean age of 68. Scientists refer to
it as "sporadic CJD." Another extremely rare type of CJD
occurs in families.
TSEs & Kuru: But in the 1950s, a human TSE called kuru was
discovered among the primitive Fore people of New Guinea, and
it was epidemic. American researcher Carleton Gajdusek
received the Nobel Prize in 1976 for showing that kuru was
spread by the Fore's ritual cannibalism of deceased
relatives, including eating the brains of those who died of
kuru. From kuru, scientists learned that a human TSE can
incubate 10 to 40 years.
------------
TSEs/TMEs in Mink: Transmissible Mink Encephalopathy, a
related disease, has a long Wisconsin history. Four of the
five known U.S. outbreaks since 1947 have occurred here. The
first killed every mink on the affected Wisconsin ranch.
TSEs/TMEs in Raccoons & Monkeys: In 1969, the late UW-Madison
researcher Dick Marsh discovered that TME could be transmitted
to raccoons and monkeys in the lab.
By the mid-1980s, both Marsh and Nobel laureate Gajdusek
believed all TSEs were really one disease altered by the
passage from one species to another, and that a single TSE
could have multiple strains that act differently.
(The CWD in Wisconsin and the CWD in Western states may turn
out to be distinct strains, but at present, scientists are
applying the little they know about the Western disease to
Wisconsin.)
TSEs in Mink & Cows: When mink TSE wiped out 60 percent of the
7,300 breeding mink on a Stetsonville, Wisconsin, ranch in
1985, Marsh traced the disease to the mink's feed, downer
dairy cows (cows unable to walk and considered unfit for human
consumption). Marsh injected some of the infected mink tissue
into the brains of two calves and waited. In less than two
years, the calves' rear legs collapsed under them just like
downer cattle. He injected some of the calves' brain tissue
back into healthy mink. After an incubation period identical
to that in the original infected mink, the new mink developed
the same disease.
Concluded Marsh: "If spontaneous cases of prion diseases can
occur in humans, they likely also occur in animals. Not
naturally transmitted to other members of the species, these
spontaneous incidents can still pose a danger because of the
unnatural act of cannibalism, as seen in kuru in humans or...
the feeding of animal protein produced by rendering ruminants"
back to other ruminants (sheep, cows, elk, goats and deer). In
effect, the then common practice made herbivore cattle into
cannibals. In 1995 alone, DNR records show that 26,488
road-killed Wisconsin deer were rendered into feed.
No case of mad cow disease has ever been confirmed in the
United States, but Marsh urged the USDA to ban the practice of
feeding processed bone and blood meal made from rendered
sheep, cows and deer to other ruminants. His suggestion would
have cost the agricultural industry dearly in substitute
protein, and the USDA took no action.
-------------
Frustrated, in 1993, Marsh repeated his concern in the state
Agri-View, warning Wisconsin dairy farmers they were feeding
cattle to cattle. He also talked to The New York Times.
Marsh's published comments ignited such a torrent of
complaints from the state's agri-business industry, which
underwrites much of the UW Agriculture School's research, that
the college's dean tried to silence Marsh.
Marsh was harassed and threatened with lawsuits, and the
university sponsored a symposium "whose only purpose seemed to
be arguing there was no need to change animal feeding
patterns," recalls Aiken, then a Marsh colleague, as was
Olander. (Both joined Marsh in pushing for a broad
ruminant-to-ruminant feeding ban.)
Marsh was "not allowed to speak, while everyone discredited
his work," says John Stauber, executive director of the
Madison-based Center for Media and Democracy, who dedicated
his book, Mad Cow, USA, to Marsh.
Despite the humiliation inflicted by the university, Marsh
would be vindicated. When protein feed from rendered downer
cows and scrapie sheep was identified as the cause of mad cow
disease in Britain in 1996, the university lionized Marsh in
its Wisconsin Alumni Magazine as the scientist who'd predicted
the disaster and tried to stop it.
"We were inundated. We had over 200 phone messages from CBS,
NBC and other people in the media who wanted to talk to
Dick," remembers professor Bruce Christenson, Marsh's
successor as chair of the department of animal health and
biomedical sciences. But by then, Marsh, 58, had cancer,
recalls Christenson. "He was a warrior even when he knew he
was dying."
-----------
like very scary stuff.
-------------
From: The Rock Garden (hensler@povn.com), Subject: CWD
article, Newsgroups: misc.rural, Date: 2002-11-30 11:05:49 PST
For those interested, there is a current article on Chronic
Wasting Disease in the Milwaukee Magazine on line at
http://www.milwaukeemagazine.com/122002/cwd.html It is long
and the slant in on the Wisc. deer herd, but is fairly well
researched and written in non-technical terms. Skip
-----------------
From: Thundercleese (dan@angband.org), Subject: Re: CRUISE
VIRUS- WHAT THE H... IS GOING ON?, Newsgroups: rec.boats,
Date: 2002-12-03 22:20:06
PST
Also Sprach Floyd in Tampa <Flooydomit@prodigy.net>:
> I'm not a vector specialist, but watching the crew rubbing >
> the ship
down with rags seems laughable, and what could > they possibly
be spraying that would affect a virus?
Most likely dilute chlorine bleach. Virii are pretty weak,
when outside a host. Now you want a tough infectious agent,
look at prions. Basically a distorted protein molecule, can
survive autoclaving, exposure to vacuum, and all kinds of
chemicals. They cause the Mad Cow Disease, Chronic Wasting
Disease, and Creutzfeldt-Jakob Disease (the human Mad Cow).
CJD has been transmitted to surgical patients from
contaminated surgical instruments even though they had been
cleaned and autoclaved. Scary stuff. Dan
---------------
Susan, Su_Texas my opinions
PP Some quotes from the article mentioned above:
If you ask the country's highest-ranking experts on prion
diseases like CWD, mad cow and human Creutzfeldt-Jakob disease
(CJD), they will tell you that only incineration, bleach and
chemical tissue digestors destroy the infectious agents that
cause the diseases and that serious public concern is
warranted.
"We have repeatedly underestimated these diseases, and we've
been wrong. People have died because of it," says Judd Aiken,
UW animal health and biomedical sciences researcher. "I'm not
an alarmist and I don't like having people mad at me, but it's
the truth when I say don't consume venison from an area where
CWD exists."
The group urged the state to adopt the steps Britain has taken
to stop mad cow disease and immediately ban venison handling
by meat processors who also prepare beef, chicken and other
meats. The nearly indestructible CWD disease prions, it said,
could contaminate equipment and pass into the rest of the food
chain. "People have the right to decide for themselves whether
they want to eat venison," says Olds. "They shouldn't have to
worry that other meat they eat is contaminated."
-------
Like elk, deer can carry the disease for years without
symptoms, infecting other animals. Until just recently, there
was no live-animal CWD test.
Symptoms: It takes an average of 15 months for a deer infected
with CWD to exhibit symptoms, but they can occur in as little
as six months or not show up for as long as eight years, says
Hauge. Then it will display abnormal behavior, stupor, head
tremors, staggering, lack of coordination, trouble judging
distance and difficulty swallowing. CWD-infected deer drink
lots of water, increasing urination, and slobber excess
saliva. They "waste away" until paralysis or pneumonia set in.
"It is not a pretty death," says Hauge.
Spread: Scientists believe nose-to-nose contact spreads CWD,
as well as environment and food contaminated by saliva, urine
and feces and by does who infect their offspring.
--------------
CWD's Family Tree
When Richard Race (a leading researcher on CWD and related
diseases with the National Institutes of Health's Rocky
Mountain Laboratories), heard Kazmierczak's comment about
eating deer brains, he was appalled. "That's irresponsible. Do
we want to have a repeat of what happened in Britain, where
for 10 years the government said BSE [mad cow disease] was
safe to eat, and so far we have 133 people dead because of
it?" asks Race. "It's not fair to say people either are or
aren't susceptible to CWD at this point. Not enough people
have eaten enough infected venison and lived long enough for
it to incubate."
TSEs & Chronic Wasting Disease in Deer (CWD): Researchers who
saw the first cases of CWD in Colorado deer in 1967, thought
it was a nutritional problem. By 1980, they realized it was
part of a family of deadly neurological disorders called
transmissible spongiform encephalopathies (TSEs), affecting
humans, sheep, mink, cats and other animals.
TSEs & Mad Cow Disease (BSE): The most famous TSE of all,
bovine spongiform encephalopathy (BSE), appeared in Britain in
1985. It killed nearly 200,000 cattle, then spread to humans
who consumed infected beef.
TSEs & Prions (Infectious Protein): Unlike most diseases,
which are caused by viruses or bacteria, the infectious agent
in TSEs is believed to be a normal protein that mutates,
becoming an infectious protein, or prion, and then causes the
misfolding of other proteins. The process creates sponge-like
brain lesions leading to physical and mental decline.
Although human cases are rare, TSEs are so significant that
two Nobel prizes for medicine have been awarded for prion
disease research.
-----------
When mad cow disease first appeared, officials said it was
"just like scrapie in sheep", the oldest known TSE, never
known to have infected humans. The disease is called scrapie
because infected sheep become so deranged, that they rub
themselves raw attempting to scrape off their fur.
The Spread of TSEs, From Sheep to Deer to Elk?: There is
unproven speculation that CWD originated when environmental
contamination passed scrapie from sheep to deer housed at
Colorado State University's Foothills Research Station, then
to wild deer and elk. That's one reason Wisconsin officials
say CWD is like scrapie. Of course, that's what the British
government thought, too, while nearly two million contaminated
cattle slipped into the human food chain.
TSEs in Cats: For more than a decade -- even after cats fed
infected beef meat and bone meal came down with a mad cow-like
disease -- the British government insisted that human beef
eaters were protected by a "species barrier."
Five years after some physicians and scientists started
sounding alarms about eating infected beef, then British Prime
Minister John Major was still reassuring the public: "There is
no scientific evidence that BSE can be transmitted to humans."
TSEs & Creutzfeldt-Jakob Disease in Humans (CJD): [In about
March 1996,] two dairy farmers, a butcher, a meat pie maker
and eight young people who had eaten contaminated beef were
dead from an Alzheimer's-like disease called new variant
Creutzfeldt-Jakob disease (nvCJD). It looked similar to the
rare sporadic CJD that affects only one person per million,
but when their brains were autopsied, they looked just like
the brains of mad cows. The government finally admitted
that the "species barrier" -- if it existed at all -- had
holes in it.
---------
TSEs Spread Through Meat: The World Health Organization now
says mad cow disease passed to humans when they ate infected
beef. Hamburgers and processed meats like sausage that
included bovine offal (by-products) -- brains, spinal chords,
eyes, lymph nodes, thymus and intestines -- areas with the
highest concentration of disease prions, are the chief
suspects, although laboratory scientists have since found TSE
disease agents in blood and muscle, too.
(Dr. Olds says Wisconsinites should forgo venison sausage even
if deer offal is left out and their deer tests negative
for CWD because there is no guarantee their deer won't be
mixed with others in the sausage-making process.)
No one knows how much infected meat you'd have to eat to get
new variant CJD or even whether a little now and then will
add up to infection. But as little as one-half gram of
BSE-infected brain -- the size of a good vitamin pill --
taken orally will infect a cow, NIH senior prion disease
researcher Paul Brown told the FDA's TSE Advisory Committee
on January 19, 2001.
Cooking at temperatures above 600 degrees C doesn't kill the
infectious agent in TSEs, nor do detergents and enzymes known
to kill most viruses. Radiation doesn't faze it, and even
after being buried in the soil for three years, enough prions
remain to spread the disease. Chlorine bleach is one of the
better disinfectants, in concentrations of 50 percent and
higher, but sometimes even that has diminished effectiveness.
Beef by-products are now banned from human consumption in
Europe (though not in the United States), but since human TSEs
incubate for decades, no one knows what the final human death
toll will be.
------------------
Autopsies: It's difficult to find a neurologist like Antuono,
willing to autopsy the brain of a patient suspected of dying
of a TSE. A splash in the eye of bodily fluid can carry the
disease straight to the brain.
Those who have already died shared one of three genetic
variations for the human prion protein, a genetic make-up seen
in 40 percent of the population. But "that doesn't mean others
are immune," says UW's Aiken. The disease may merely incubate
longer in people with other genes.
Research published in May 2000 in The European Molecular
Biology Organization Journal states: "CWD transmissions would
be similar to transmissions of mad cow disease," adding that,
"it would seem prudent to take reasonable measures to limit
exposure of humans (and cows and sheep) to CWD infectivity."
--------------
Wisconsin's TSE History
TSEs & Alzheimer's?: The original human TSE, classic
Creutzfeldt-Jakob disease, is often mistaken for Alzheimer's,
but it is a rare nervous system disease that results in
rapidly progressive dementia, a nightmare of madness and
terrifying hallucinations, loss of motor control, paralysis
and death.
Discovered in the 1920s, it seems to occur spontaneously
across the globe (300 per year in the United States),
attacking victims with a mean age of 68. Scientists refer to
it as "sporadic CJD." Another extremely rare type of CJD
occurs in families.
TSEs & Kuru: But in the 1950s, a human TSE called kuru was
discovered among the primitive Fore people of New Guinea, and
it was epidemic. American researcher Carleton Gajdusek
received the Nobel Prize in 1976 for showing that kuru was
spread by the Fore's ritual cannibalism of deceased
relatives, including eating the brains of those who died of
kuru. From kuru, scientists learned that a human TSE can
incubate 10 to 40 years.
------------
TSEs/TMEs in Mink: Transmissible Mink Encephalopathy, a
related disease, has a long Wisconsin history. Four of the
five known U.S. outbreaks since 1947 have occurred here. The
first killed every mink on the affected Wisconsin ranch.
TSEs/TMEs in Raccoons & Monkeys: In 1969, the late UW-Madison
researcher Dick Marsh discovered that TME could be transmitted
to raccoons and monkeys in the lab.
By the mid-1980s, both Marsh and Nobel laureate Gajdusek
believed all TSEs were really one disease altered by the
passage from one species to another, and that a single TSE
could have multiple strains that act differently.
(The CWD in Wisconsin and the CWD in Western states may turn
out to be distinct strains, but at present, scientists are
applying the little they know about the Western disease to
Wisconsin.)
TSEs in Mink & Cows: When mink TSE wiped out 60 percent of the
7,300 breeding mink on a Stetsonville, Wisconsin, ranch in
1985, Marsh traced the disease to the mink's feed, downer
dairy cows (cows unable to walk and considered unfit for human
consumption). Marsh injected some of the infected mink tissue
into the brains of two calves and waited. In less than two
years, the calves' rear legs collapsed under them just like
downer cattle. He injected some of the calves' brain tissue
back into healthy mink. After an incubation period identical
to that in the original infected mink, the new mink developed
the same disease.
Concluded Marsh: "If spontaneous cases of prion diseases can
occur in humans, they likely also occur in animals. Not
naturally transmitted to other members of the species, these
spontaneous incidents can still pose a danger because of the
unnatural act of cannibalism, as seen in kuru in humans or...
the feeding of animal protein produced by rendering ruminants"
back to other ruminants (sheep, cows, elk, goats and deer). In
effect, the then common practice made herbivore cattle into
cannibals. In 1995 alone, DNR records show that 26,488
road-killed Wisconsin deer were rendered into feed.
No case of mad cow disease has ever been confirmed in the
United States, but Marsh urged the USDA to ban the practice of
feeding processed bone and blood meal made from rendered
sheep, cows and deer to other ruminants. His suggestion would
have cost the agricultural industry dearly in substitute
protein, and the USDA took no action.
-------------
Frustrated, in 1993, Marsh repeated his concern in the state
Agri-View, warning Wisconsin dairy farmers they were feeding
cattle to cattle. He also talked to The New York Times.
Marsh's published comments ignited such a torrent of
complaints from the state's agri-business industry, which
underwrites much of the UW Agriculture School's research, that
the college's dean tried to silence Marsh.
Marsh was harassed and threatened with lawsuits, and the
university sponsored a symposium "whose only purpose seemed to
be arguing there was no need to change animal feeding
patterns," recalls Aiken, then a Marsh colleague, as was
Olander. (Both joined Marsh in pushing for a broad
ruminant-to-ruminant feeding ban.)
Marsh was "not allowed to speak, while everyone discredited
his work," says John Stauber, executive director of the
Madison-based Center for Media and Democracy, who dedicated
his book, Mad Cow, USA, to Marsh.
Despite the humiliation inflicted by the university, Marsh
would be vindicated. When protein feed from rendered downer
cows and scrapie sheep was identified as the cause of mad cow
disease in Britain in 1996, the university lionized Marsh in
its Wisconsin Alumni Magazine as the scientist who'd predicted
the disaster and tried to stop it.
"We were inundated. We had over 200 phone messages from CBS,
NBC and other people in the media who wanted to talk to
Dick," remembers professor Bruce Christenson, Marsh's
successor as chair of the department of animal health and
biomedical sciences. But by then, Marsh, 58, had cancer,
recalls Christenson. "He was a warrior even when he knew he
was dying."
-----------