From: JHTSAO at UGA.CC.UGA.EDU (jhtsao)
Path: UGA.CC.UGA.EDU!JHTSAO
Newsgroups: rec.food.veg
Subject: Re: MAD COW DISEASE TRANSMISSIBLE TO HUMANS VIA MEAT
Message-ID: <17BB29619S86.JHTSAO at UGA.CC.UGA.EDU>
Date: Mon, 21 Jul 97 10:39:42 EDT
Organization: University of Georgia
References: <17BAEF23DS86.JHTSAO at UGA.CC.UGA.EDU> <19970718174832655743 at mri2.mri.montana.edu>
In article <19970718174832655743 at mri2.mri.montana.edu>
umbjm at gemini.oscs.montana.edu (John Mercer) writes:
>>jhtsao <JHTSAO at UGA.CC.UGA.EDU> wrote:
>>> The following article appeared in Flagpole Magazine, Athens, GA, on July
>> 2, 1997, and is used by permission. Flagpole Magazine's Website is:
>> www.flagpole. com --E-mail: flagpole at negia.net Used by permission of
>> the editor.
>>>> "Modern Cannibalism" by Maureen McGinley Forget Clive
>> Barker, Dean Koontz and Stephen King. The most horrifying book of the
>> year is a non-fiction account of the uncovering of a new form of disease
>> about which you need to learn.
>>Yes, you certainly do!
>>> Part of my motivation in writing this column is to get you readers to
>> think more critically about the stuff that you eat. There are certain
>> basic ques- tions that are worth asking about food. Who raised this?
>> What part of the world did it come from? How was it grown? What was it
>> fed? There are some new possible answers about meat in general and beef
>> in particular in the book I just read that are deeply disturbing. The
>> name of the book is _Deadly Feasts: Tracking the Secrets of a Terrifying
>> New Plague._ Its author, Richard Rhodes, won a Pulitzer Prize for his
>> last book on the making of the atomic bomb. In this one, he tracks the
>> development of a new class of diseases called transmissible spongiform
>> encephalopathy (TSE), which includes kuru in New Guinea,
>> Creutzfeldt-Jakob disease, scrapie in sheep, transmissible mink
>> encephalopathy (TME), and bovine spongiform encephalopathy (BSE), a.k.a.
>> mad cow disease.
>>Rhodes never claims, as does the poster, that the disease is transmitted
>by eating meat. There is no evidence to date linking vCJD to
>meat-eating. Brain-eating, yes; meat-eating, no.
>>See the difference?
>>---snip---
>>>--
>John Mercer
>Scientist
>McLaughlin Research Institute
Ever heard of brains for breakfast? :-)
It's not vegetarian, but in some parts of the U.S. you find it on the
menus of small town restaurants. I was not vegetarian until after reading
Rhodes' book, but even back in those days the idea of scrambled brains as
a breakfast dish offended me.
Let me quote some passages from the book:
p. 208
...Dr. James Ironside is a pathologist with the British National CJD Sur-
veillance Unit in Edinburgh. In September 1995, studying a brain cross
section from the teenage boy who had recently died of Creutzfeldt-Jakob
disease, Ironside found amyloid plaques so large that they looked under the
microscope like chrysanthemum blooms. They were not confined to the cere-
bellum, the pathologist determined, but spread throughout the brain. They
stained for PrP. Unlike the smaller plaques of ordinary CJD, these florid
plaques were surrounded by a zone of spongiform change--a destructive
halo of holes.
Ironside had never seen this unusual pattern of damage before, but he
knew that sporadic CJD pathology varied widely from case to case. He was
startled, then, when another teenage case turned up almost immediately with
identical pathology. He alerted the director of the Surveillance Unit, Dr.
Robert Will. Will mobilized the Unit's staff. Staff members quickly
turned up six more suspect cases in young people. At first Will and Ironside
thought the youthfulness of the victims might be the reason for the similari-
ties in their pathology. When the physicians checked the medical literature,
however, they learned that the few rare cases of CJD in people under thirty
in Britain and Europe showed no such florid plaques widespread in the brain.
Late in 1995, Surveillance Unit staff began traveling the country interviewing
the victims' families to rule out familial CJD or iatrogenic CJD from growth
hormone or surgery.
By the end of February 1996, Will and Ironside knew they had an epidemiolo-
gical cluster: eight cases of CJD in young people that all showed a new neuro-
pathological profile of florid plaques, early loss of coordination and late
dementia. Will arranged to report the ominous new finding to the Spongiform
Encephalopathy Advisory Committee (SEAC), a group of scientists and physicians
appointed to advise the British government on BSE. A SEAC meeting was set for
March 8. Ironside opened the meeting with slides illustrating the unusual
pathology. The SEAC chairman, Dr. John Pattison, remembers the moment vividly:
"Before he said anything, we could see what it was. It was dramatically dif-
ferent." Another SEAC member, Dr. Jeffrey Almond, recalls near panic. "The
atmosphere became genuinely quite tense.Some of us were afraid that this really
maybe indicated a transmission (of BSE) to humans.
...Will and Ironside now had a tenth case to report. All ten showed the same
unique pathology All had what (Carleton) Gajdusek (Nobel Prize-winning
researcher) would later identify as kuru plaques: the florid plaques may not
have been seen in Britain and Europe, but they were diagnostic signs of kuru
in Papua New Guinea....SEAC finalized its recommendations the next morning.
They included destroying all British cattle over thirty months of age.
p. 212. Robert Will would tell a London newspaper of these ten cases that
"their brain tissue displayed a distinctive disease pattern closer to the
damage inflicted on a cow's brain by BSE than the damage normal CJD inflicts
on humans."
At the SEAC session on March 19, senior members of the British Cabinet
tried to suppress any announcement of the new variant form of CJD, arguing
that the scientists might be wrong. The Secretary of State for Health,
Stephen Dorrell, insisted that the public had to be told. Wednesday, March
20, speaking in the House of Commons, Dorrell informed a stunned nation that
BSE had probably spread to humans from eating beef.
Wouldn't you know.
p.217. French and British researchers reported in June that they had success-
fully infected rhesus monkeys with BSE and that the resulting lesions looked
like the new-variant CJD (vCJD), with florid kuru plaques haloed with holes.
"It's the first experimental argument," the French researchers told the media--
"and a very strong one--in favor of a link" between the two diseases. BSE
transmission to macaques, reported the same month in _Nature_, gave further
evidence of a link: "...The pathological 'signature' of the BSE agent in...
kuru plaques were seen in tow macaques inoculated at the same time with
sporadic CJD. Interpreting those results, a Swiss neuropathologist found
"unsettling" the fact that the modest amounts of infected tissue inoculated
directly into the brains of the vCJD macaques were "well within the range
of brain tissue present in commercial food products for human consumption
until a few years ago." We can hope, the neurolopathologist observed, "that
the oral route of administration will be considerably less efficient."
But the six sheep Douglass Hogg had mentioned had each been fed only five
hundred milligrams of brain extract--about one-fiftieth of an ounce--and the
fact that so small an oral dose had infected one with BSE did not encourage
optimism.
p.220. ...Just as MAFF had restricted access to its animal studies and sta-
tistics, so did Robert Will of the CJD Surveillance Unit restrict information
on his ongoing investigation of new suspect cases of vCJD. But when French
scientists reported two additional, highly suspect French cases in spring
1996, Will refused to reciprocate wtih information on further British cases
he might be investigating. Someone leaked the information: the London
Sunday Times reported in June that beyond the eleven previously confirmed
in Britain and one in France, the CJD Surveillance Unit was following five
more suspect cases in the summer of 1996.
Carleton Gajdusek called me in mid-July sounding apocalyptic. .
"They don't have the least idea what caused the human cases," he told me.
"It's kuru and nothing but kuru, and any species could be carrying it--dairy
cows, beef cattle, pigs, chickens. They need to assess the risk and deal
with it realistically. All the pigs in England fed on this meat-and-bone
meal. The disease hasn't turned up in pigs only because you don't keep pigs
alive for seven or eight years; they're killed after two or three years at
most. When we kept pigs we'd inoculated in our laboratory for eight years,
they came down with scrapie. Probably all the pigs in England are infected.
And that means not only pork. It means your pigskin wallet. It means catgut
surgical suture, because that's made of pig tissue. All the chickens fed on
meat-and-bone meal; they're probably infected. You put that stuff in a chicken
and it goes right through. A vegetarian could get it from chickenshit that
they put on vegetables. It could be in tallow, in butter--how the hell am
I supposed to measure infectivity in butter? No one on earth knows how to
do that. These people who've come down with CJD have given blood. It's
undoubtedly in the blood supply. The answer in that case is, stop giving
anyone blood who doesn't really need it. Bob Will and those people don't
know anything about where it came from. But I'll tell you this. If it
turns up in one kid under fifteen, it's kuru. And by the way, it could
be in the milk. That hasn't been excluded either."
P.221....Dr. John Collinge, a neurologist at St. Mary's Hospital in London,
and colleagues including James Ironside reported in _Nature_ that the
molecular signature of BSE in cattle matched the molecular signature of
variant CJD.
p.220...With BSE, (Richard) Lacey pointed out, there was no certainty that
the source of infection had been cut off; indeed, there was evidence that
animals were still becoming infected with BSE and every reason to suspect
that animals incubating BSE were still entering the human food supply.
The consequences, he feared, could be dire for the British as they had
been dire for the Fore. "If it seems that the incubation-period average
for CJD in humans begins to be about twenty-five years, maybe thirty years,"
he told me grimly, "then the peak human epidemic will come around the year
2015. If the current numbers of variant CJD cases increase by fifty percent
per year compound, as they well might, that wuld take it to about two hundred
thousand cases a year by then." HUMAN cases, that is: 200,000 deaths PER
YEAR.
p. 230...The British government, by making the wrong public-health choices,
has conducted a frightening natural experiment, allowing a lethal disease
agent to spread through the human food supply, exposing the entire British
population. There is every reason to believe exposure is continuing, from
infected beef and possibly from infected lamb and mutton as well.
...The lack of vCJD deaths outside France doesn't mean that the rest of the
continent is free of human infection; the French deaths indicate merely
that exposure began there earlier. Nor do the limited number of vCJD
deaths identified so far offer any basis for assessing the future of the
disease agent. The ease with which BSE crosses species barriers and the fact
that it is easily transmissible orally in small doses suggest that it may
be an exceptionally virulent strain.
p.231. What about the rest of the world? If TSEs occur sporadically in
animal species, as CJD does in humans, then no population anywhere in the
world that eats meat is entirely free of risk.
------
Excerpts from the book _Deadly Feasts: Tracking the Secrets of a Terrifying
New Plague_, by Richard Rhodes (Pulitzer Prize winning author), published
by Simon and Schuster, New York, 1997.
