GENTECH archive 8.96-97


Mad Pigs in the USA

This Mad Pig Went to Market
In These Times (Chicago, Illinois) May 26, 1997
by Joel Bleifuss

Some pigs in the United States may be infected with a porcine form of mad cow
disease, according to an alarming study by U.S. Department of Agriculture
(USDA) scientists that has recently come to light. This previously
unrecognized form of the disease in swine may be infecting humans, according
to epidemiological studies that link pork consumption with mad cow's human
equivalent, Creutzfeldt-Jakob disease.

In late 1978, Dr. Masuo Doi, a veterinarian with the Food Safety and Quality
Service, observed signs of a mysterious central nervous system (CNS) disorder
in some young hogs that had arrived at the Tobin Packing Plant in Albany,
N.Y., from several Midwestern states. For the next 15 months, Doi studied 106
of the afflicted pigs. He described their symptoms this way: "Excitable or
nervous temperament to external stimuli such as touch to the skin, handling
and menacing approach to the animals is a common characteristic sign among
those affected with the disease." These symptoms, Doi now notes, are
strikingly similar to those of British cattle infected with mad cow disease,
which is scientifically known as bovine spongiform encephalapathy (BSE).

Doi sent the brain material from these pigs to Karl Langheinrich, the head
pathologist at the USDA's Eastern Laboratory in Athens, Ga. In a November
1979 report, Langheinrich noted that one pig's brain exhibited what the
veterinary reference work Pathology of Domestic Animals defined as "the
classical hallmarks of viral infection of the central nervous system."
Langheinrich went on to report that the damage in the pig's brain was similar
to the damage observed in the brains of sheep afflicted with scrapie and of
mink afflicted with transmissible mink encephalapathy, the two other variants
of transmissible spongiform encephalapathy (TSE) known at the time.

In March of this year, Dr. William Hadlow, a retired veterinary pathologist
who is one of the world's leading TSE researchers, examined the microscope
slides of pig brain from Doi and Langheinrich's 1979 investigation. The pig
"could have suffered from a scrapie-like disease," he reports, but adds that
such a conclusion cannot be "justified by the limited microscopic findings,
however suggestive of a TSE they may be."

The Government Accountability Project (GAP), a Washington-based organization
that supports public-sector whistleblowers, has been working with Doi to
alert the public that a porcine form of mad cow disease may be circulating in
the American pig population. In a March 27 letter to Secretary of Agriculture
Dan Glickman, GAP points out that if we assume a similar incidence of central
nervous system disorders in swine being slaughtered nationwide as that found
among swine at the Tobin Packing Plant, "it is reasonable to question
whether, since at least 1979, USDA has been allowing 99.5 percent of animals
with encephalitis, meningitis and other CNS disorders into the human food

And what happens once those thousands of diseased pigs are eaten by the
American public? Two epidemiological studies found pork to be a dietary risk
factor in Creutzfeldt-Jakob disease (CJD). A 1973 study published in the
American Journal of Epidemiology discovered that 14 of 38 CJD patients (36
percent) ate brains. Further, of those who ate brains, most (10 of the 14)
preferred hog brains. Another study published in the American Journal of
Epidemiology in 1989 looked at how frequently 26 CJD patients ate 45 separate
food items. Nine of these foods were found to be statistically linked to
increased risk of CJD. Of those nine, six came from pigs--roast pork, ham,
hot dogs, pork chops, smoked pork and scrapple. (The three that were not
pig-derived were roast lamb, raw oysters/clams and liver.) The authors of the
study concluded: "The present study indicated that consumption of pork as
well as its processed products (e.g. ham, scrapple) may be considered as risk
factors in the development of Creutzfeldt-Jakob disease. While scrapie has
not been reported in pigs, a subclinical form of the disease or a pig
reservoir for the scrapie might conceivably exist."

The number of Americans who develop CJD in a given year is in dispute. The
Centers for Disease Control (CDC) claims that the human form of mad cow
disease occurs at a rate of one in a million. Further, ignoring evidence of a
new variant of CJD found in Britain, the CDC maintains that people who eat an
infected animal cannot contract the disease. In January, CDC Assistant
Director for Public Health Lawrence Schonberger told a Congressional hearing,
"The bottom line from our perspective is that it's a theoretical risk... but
it is not as yet a real risk."

But does the CDC really know how many Americans contract CJD? Evidence
indicates that CJD may often be misdiagnosed, and thus go unreported.  A 1989
study at the University of Pittsburgh autopsied the brains of 54 patients who
had been diagnosed with Alzheimer's and discovered that three of the patients
(5.5 percent of the sample) actually had CJD.  A 1989 study at Yale
University reported similar findings.  Postmortem examination of 46 patients
who had been diagnosed with Alzheimer's revealed that six (13 percent of the
sample) actually had CJD.  The New York-based Consumers Union, which
publishes Consumer Reports, argued in a paper presented to the USDA, "Since
there are over 4 million cases of Alzheimers disease currently in the United
States, if even a small percentage of them turned out to be CJD, there could
be a hidden CJD epidemic."

Which brings us to the issue of what the Food and Drug Administration (FDA)
is doing to address this food-borne threat to public health.  In the past
several months, in response to questions about Doi's 1979 pig research, USDA
officials have put out a good deal of misinformation to public-interest
groups, the media and even the National Association ot Federal Veterinarians.
 On repeated occasions, officials have said that the slides of the pig brains
from the 1979 study were unavailable because they had been sent to scientists
in England who were studying mad cow disease.  But as it turns out, the USDA
never sent any slides to England.  

"Agency officials repeatedly misrepresented scientists' investigations and
conclusions to consumer groups and government employees and neglected to keep
other agencies also working on TSE issues informed," says Felicia Nestor of
GAP.  "The USDA had to be pushed to investigate scientific evidence which
only they had."

The USDA's lackluster response to this public health threat comes as no
surprise.  For years, the agency has done its best to ignore evidence that a
distinct American strain of mad cow disease may alrady afflict the U.S.
cattle population.  (See In These Times "The First Stone"  May 31, 1993 and
 April 15, 1996.)  Veterinary researchers in Mission, Texas in 1979 and Ames,
Iowa, in 1992 found that cattle injected with brain matter from
scrapie-infected American sheep developed BSE.  However the brains of these
infected cattle did not exhibit the spongy holes found in the brains of their
BSE-plagued British cousins.  Furthermore, cows afflicted with this American
strain of scrapie-induced BSE do not go mad; they simply collapse and die.

The distinction is important because the American strain of the disease leads
to symptoms that resemble what happens to the 100,000 American cattle that
succumb to "downer cow syndrome" every year. Veterinary researchers fear that
the widespread practice of feeding downer cows (in the form of rendered
protein feed supplements) to other cattle, sheep and hogs could already be
fueling a TSE epidemic in the United States like the one that plagued
Britian.  In fact, in 1979, before BSE was discovered in Britain, Doi pointed
out in his study of deranged pigs that "many animals have been found to be
'downers' at first observation."

On January 3, the FDA finally drafted a rule that would ban the fortifying of
animal feeds with "any Mammalian tissue." USDA researchers, critical of the
government's foot-dragging, have been calling for a ban for seven years. But
undercutting this important step, the FDA has played a taxonomical shell game
and arbitrarily removed pigs from the class "mammalia."  Consequently, if the
FDA's proposed rule is adopted, animals being fattened for slaughter will
stop eating cow renderings and instead eat only pig remains. Since mad cow
disease in Britain was spread by feeding mad cows to healthy cows, the FDA's
pigs-are-not-mammals proposal gives any porcine form of mad cow disease a
point of entry into the human food chain.

On April 28, Consumers Union filed comments with the FDA on the agency's
proposed regulations. The group advocates a complete ban on the use of all
mammalian protein in all feed intended for feed animals, as is now the case
in England. "The draft rule," says Consumers Union, "is not adequate to
protect public health, because it would continue to leave the door open for a
porcine TSE to contaminate pork and other meat."

It would be nice if the USDA were as concerned about protecting public health
as it is about the financial health of the $30 billion-a-year pork industry
and the $60 billion-a-year beef industry. Ditto for the Wall Street Journal,
where editors have put on hold a story by a staff reporter on mad pig disease
and the possible link between pork consumption and CJD.

ABC's World News Tonight has also sat on the information for a couple of
weeks. On May 12, the network did air a story that examined the fact that CJD
was being misdiagnosed as Alzheimer's. But the network failed to note that
CJD is the human form of mad cow disease. The network also neglected to
mention the possible connection to pork or the fact that the CJD patient
featured in the story, Marie Ferris, had been employed at a packing plant
where she handled slaughtered pigs.