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 (CJD).
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 swine 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 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.
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 whistle-blowers, 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 supply."
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 really 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 Alzheimer's 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 of 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, 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."
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 already afflict the U.S.
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" each 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 Britain. 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, which is part of the USDA, 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 such a ban for seven years. But undercutting this important step, the FDA has played a taxonomic 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 food 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 this 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 its story, Marie Farris, had been employed at a packing plant where she handled slaughtered pigs.
Albion Monitor May 27, 1997 (http://www.monitor.net/monitor)
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