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Mad
Cow Disease In 1985, cows in Britain began to die of a mysterious ailment that no one had ever seen before. The symptoms were strange. At first the cows staggered and drooled, their ears twitching. Then they began to show signs of fear, grinding their teeth, acting aggressively toward other animals. Soon they died. Farmers named the condition "mad cow disease" and the name stuck. The disease is now known formally as "bovine spongiform encephalopathy" or BSE for short. BSE is one of a small family of diseases called transmissible spongiform encephalopathies, or TSE’s. TSE’s destroy neurons, the main nerve cells in the brain, creating holes that leave the brain resembling a sponge (thus"spongiform"). BSE, like the other TSE’s, is an infectious disease, meaning that it can be transmitted from one cow to another. During the 13 years since it first appeared, mad cow disease has killed more than 167,000 cows in Britain [1] and many more became infected but were slaughtered for food before symptoms appeared. Symptoms take an average of 5 years to show up after a cow is infected. Until the late 1990s, there was no test that could detect whether a cow was infected -- only the appearance of symptoms and microscopic examination of the brain could provide a definitive diagnosis. (Even today, tests require brain tissue, so they cannot be conducted on live animals.) British-type BSE has now been observed in cows in Switzerland, the Netherlands, Ireland, Portugal, France, Oman and the Falkland Islands. To date, the disease has not been observed in cows in the U.S. When the disease first struck in Britain in 1985, health authorities insisted that British beef was safe to eat. For 10 years they defended that position aggressively, despite mounting evidence to the contrary. Then in 1996, the official story changed suddenly and the public was stunned. A panel of government scientists told Parliament in 1996 that the "most likely explanation" for 10 cases of a new TSE disease in humans was that BSE had moved from cows into people. That explanation is now widely accepted by most scientists, though airtight evidence remains elusive. By the time of the stunning announcement in 1996, some British experts calculated that more than a million infected cows had already been consumed in Britain. [2] In humans, the BSE-like disease is called "new variant Creutzfeld-Jacob disease," or nvCJD for short. Creutzfeld-Jacob disease (CJD) is a member of the TSE family, a brain-destroyer. CJD has been recognized for a long time as a rare disease of the elderly -- very similar to Alzheimer's disease -- but nvCJD is different. It has somewhat different symptoms, a different pattern of disintegration in the brain, and it strikes young people, even teenagers. Between 1995 and early 1998, at least 23 people died of nvCJD in Britain and at least one in France, [3] the oldest of them age 42 and the youngest 15. In January 1997, British epidemiologists tried to estimate how large the outbreak of nvCJD might become. They concluded that the data were not sufficient to allow a precise estimate: somewhere between 75 people and 80,000 people would eventually die of the new disease, they estimated. [4] Only time will tell. More precise estimates of the size of the problem are not possible because no one knows for sure how long nvCJD "incubates," how much time elapses between infection and the appearance of symptoms. An excellent recent book by Sheldon Rampton and John Stauber, MAD COW U.S.A.--CAN THE NIGHTMARE HAPPEN HERE? tells the story of the emergence of mad cow disease in Britain, and the scientific and political battles that have ensued. [5] Despite the evocative title, the book is thoroughly documented and carefully written. Without oversimplifying the details, the book recounts a complicated story of medical discoveries, strong-arm tactics by the beef industry, and waffling and cover-up by governments on both sides of the Atlantic -- yet it reads as easily as a detective story. As a piece of science writing -- a description of science as it plays out in the real world -- the book is an impressive accomplishment. By the end, the reader has absorbed several important lessons about public health policies distorted by big money, and about very serious threats to our first amendment right of free speech. Rampton and Stauber show that the U.S. beef industry will go to almost any lengths to try to prevent a public discussion of "mad cow" and the steps that the U.S. government still needs to take to prevent this disease from becoming an American problem. In a nutshell: Mad cow disease developed because of a little-known but very-widespread modern agricultural practice -- farmers feeding dead cows to their cows, thus turning a vegetarian species into meat-eaters. In Britain and the U.S., when a cow is slaughtered, about half of the animal cannot be sold for human uses -- the hide, bones, entrails, hooves, horns, fat, gristle and tough membranes are, by law, not permitted to be used in food. Obviously something else has to be done with these parts, to avoid creating a public health hazard. Then there are "downer
cows" that must be dealt with. Cows that cannot stand up,
cows that collapse, and cows that die mysteriously are called
"downers." Every year in the U.S. about 100,000 cows
die of unknown causes. One day they are alive and the next day
they are dead, and no one knows why. Something must be done with
their carcasses. From the 1960s through the mid-1990s, rendering plants dried their rendered products, ground them into the consistency of brown sugar, and sold them for animal feed. Feed mills then mixed these animal by-products into various feed formulations – about one-third for cattle, one-third for pigs and chickens, and one-third for pets. Unfortunately, some of the animals sent to rendering plants (or abattoirs) are sheep killed by a disease called "scrapie." Scrapie is another TSE, a member of the same family as BSE, CJD, and nvCJD -- one of those diseases that eat holes in the brain and invariably kills its victims. Scrapie takes its name from the way sheep act once they get the disease -- they rub up against a fence or a barn until they scrape away their wool, leaving raw wounds. Then they die. Scrapie has been a well-known, though mysterious, disease of sheep for at least 200 years, but only recently have scrapie-infected sheep been fed to cows. Scientists who study mad cow disease believe that the illness crossed the species barrier from sheep to cows through contaminated feed. Indeed, the British in 1988 banned the practice of feeding animal carcasses to other animals and within seven years new cases of mad cow disease diminished quite dramatically from 900 to 1000 per week to 280 to 300 per week. [6] The U.S., however, has been slow to act. Scrapie is well established among sheep in this country. From October 1988, to June 1989, scrapie was diagnosed in 52 flocks of sheep in 20 states. [5,pg.104] Clearly, there was ample reason to ban the feeding of animal carcasses to animals in this country when the British took that action in 1988. However, the beef industry, and the rendering and feed industries, have generally opposed such precautionary measures. TSE’s have a very long incubation period. In cows, BSE takes three to eight years (average, five years) from the time of first infection to the appearance of symptoms shortly before death. CJD in humans has an incubation period of 10 to 40 years. Thus, by the time symptoms of BSE appear; many cows are likely to be carrying the infection silently. This was confirmed earlier this year in Switzerland when tests of brain tissues from 1761 cows revealed 8 infected animals without any symptoms, for a "silent" infection rate of 4.5 per 1000. This is 100 times as high as the rate of Swiss cows showing symptoms. [7] If this rate holds for Britain, it means that today there are about 460,000 British cows infected -- but symptom-free -- in a total herd of roughly 11 million. TSE diseases are characterized by a long incubation period, and they are always fatal. Furthermore, the infectious agent is incredibly resistant to deactivation. Cooking infected meat, or even rendering it at high temperature, does not completely eliminate its infectivity. Animals get TSEs by eating infected animals or parts of infected animals, especially nerve tissues. TSE diseases have now been identified in sheep, pigs, goats, cattle, deer, elk, mink, mice, hamsters, guinea pigs, domestic cats, puma, cheetah, eland, kudu, Arabian oryx, myland, marmosets, macaques, chimpanzees and humans. In addition, a TSE has been reported in ostriches in a German zoo. [8] Thus one might think the U.S. Food and Drug Administration (FDA) would prohibit the feeding of any animals to any other animals, as the British did in 1988. But that is not what the FDA has done. Under pressure from the beef, rendering, and feed industries, in 1997 FDA only prohibited the feeding of ruminants and mink to ruminants. [1,8] Ruminants are animals that chew their cuds, including cattle, sheep, goats, deer and elk. Mink are included in the ban because they can get a TSE similar to mad cow disease. FDA is still allowing the feeding of pigs to other animals, and the feeding of blood and gelatin from rendering plants to all animals. For example, many calves in the U.S. are being raised on a diet of dried blood taken straight from rendering plants. Pigs and chickens are still being fed rendered animal products. There are sound scientific arguments why this policy represents a form of Russian roulette being played with the health of the American public. Given that we are dealing with infectious diseases that invariably kill, the precautionary principle (see REHW #586) seems the only appropriate policy. · [1] Michael Hansen, "The Reasons Why FDA's Feed Rule Won't Protect Us from BSE," GENETIC ENGINEERING NEWS (July, 1997), pgs. 4, 40. See also Lawrence K. Altman, "F.D.A. Proposal Would Ban Using Animal Tissue in Feed," NEW YORK TIMES January 3, 1997, pg. A14, which says BSE has affected 165,000 British cows. · [2] John Darnton,
"Britain Ties Deadly Brain Disease to Cow Ailment,"
NEW YORK TIMES March 21, 1996, pgs. A1, A7. Mad cow disease appeared for the first time in Britain in 1985. Since that time it has killed roughly 170,000 cows in Britain, and it has spread to humans. [1] In humans the disease is called "new variant Creutzfeld-Jakob disease," or nvCJD for short. At this point nvCJD has killed 24 people in Britain and one in France. More human deaths are expected in Britain [2] because several million people ate diseased beef before the British government (or the beef industry) acknowledged that mad cow disease could infect people. From a U.S. perspective,
the obvious question is, how can an outbreak of mad cow disease
be prevented here? Mad cow disease is a member of a family of
rare diseases called transmissible spongiform encephalopathies,
or TSE’s. TSE’s have different names in different
animals (for example, scrapie in sheep, chronic wasting syndrome
in deer and elk, and bovine spongiform encephalopathy or BSE in
cows). However all TSE’s share a few common features: they
attack the central nervous system, causing disintegration of the
brain; they have a long incubation period between the time when
infection first occurs According to modern biology, a prion should not be able to reproduce itself, and therefore should not be able to cause disease, because prions contain no DNA. Without DNA, reproduction should not be possible. However, it is now becoming widely accepted that prions do reproduce themselves and do cause disease. Somehow a normal prion goes bad --it gets folded into an abnormal shape and in its abnormal shape it can destroy nerve cells in the central nervous system. The abnormal prions also cause other nearby prions to become folded into the same shape, thus creating more abnormal prions by a domino effect. After a long period of time (months or years, or even decades) the symptoms of disease appear, followed a few weeks or months later by death. Thus animals and humans can be carrying an infectious prion disease for months or years without showing any symptoms. The prion theory of disease is still not accepted by 100% of the scientific community, but the inventor of the theory, Stanley B. Prusiner of the University of California at San Francisco, received the Nobel Prize for his work in 1997. [3] In this country, the government agency with primary responsibility for preventing an outbreak of mad cow disease or its human variant, nvCJD, is the U.S. Food and Drug Administration (FDA). The FDA in 1997 issued a rule declaring it illegal for farmers to feed animal protein from ruminants or mink to other ruminants –a preventive step that had been taken by the British government in 1988. Ruminants are animals that chew their cuds, including cattle, sheep, goats, deer and elk. Mink are included in the FDA's ban because they can get a TSE similar to mad cow disease. When cows, pigs, and chickens are slaughtered, much of the animal cannot be used for food and is sent to a rendering plant to be ground up, boiled down, dried to the consistency of brown sugar and sold as feed for cows, pigs, chickens, and pets. It is this rendered "animal protein" derived from ruminants (and mink) that FDA has banned from feeding to ruminants. The FDA's ruminant-to-ruminant ban still allows animal protein of all kinds to be fed to pigs and chickens, and it allows animal protein derived from pigs and chickens to be fed to ruminants. The FDA ban also allows blood and gelatin derived from ruminants to be fed to other ruminants. In the U.S., many newborn calves are fed a high-protein diet consisting mainly of dried blood. Blood cells carry prions just as nerve cells do. [4] A small group of scientists, led by Dr. Michael Hansen of Consumers Union, has challenged the adequacy of FDA's ruminant-to-ruminant rule. [5] They argue that the FDA ban does not go far enough, "does not adequately protect human health, and is not scientifically defensible." [6] Consumers Union is the publisher of CONSUMER REPORTS magazine. Scientists on both sides of the controversy agree that mad cow disease probably developed in Britain in one of two ways. Possibly cows ate parts of sheep that had been infected with the TSE called scrapie, and the scrapie, once in cows, evolved into mad cow disease. Or, alternatively, a prion spontaneously went bad (via genetic mutation of the gene that produces normal prions) in a cow, and that cow was fed to other cows, which were fed to other cows until the disease was amplified into an epidemic. In either case, it was cows (which are vegetarians by nature) being forced to eat animals that created the problem. FDA officials say they are confident that their ruminant-to-ruminant ban has prevented, and will continue to prevent, an epidemic of mad cow disease in this country because (a) mad cow has never been observed in cows in the U.S., and (b) Creutzfeld-Jakob (CJD) disease is not increasing in the U.S. [7] If mad cow were occurring in U.S. cows, some form of CJD should be increasing, and it isn't, the FDA argues. Michael Hansen of Consumers Union offers evidence that the government may be wrong on both counts. Here are his arguments: Mad cow may have already appeared in U.S. cows. Hansen offers evidence from seven studies that some "downer" cows may have a form of mad cow disease, though with symptoms somewhat different from those in British cows. Downer cows are cows that cannot stand up, cows that collapse, and cows that die mysteriously. About 100,000 cows die each year in the U.S. with "downer" symptoms, and most of them end up in rendering plants, turned into animal feed. In 1961, an outbreak of transmissible mink encephalopathy (TME) --a brain-destroying TSE of mink --occurred on six mink farms in Wisconsin. Because all the farms used the same ready-mix feed which came from the same feed plant, investigators assumed that the feed was the source of the infectious agent. [8] Two years later, in 1963, an outbreak of TME occurred on two more Wisconsin mink farms. Based on the 1961 outbreak, scientists suspected feed and they examined the two farms' feed records carefully. They learned that "downer" cows from farm A had been fed to mink on Farm A and Farm B. The researchers wrote, "Since mink on both farms developed the disease almost simultaneously, we believe this feed component has to be incriminated."[9] In 1985 an outbreak of TME occurred on a mink ranch in Stetsonville, Wisconsin. Dr. Richard Marsh of the University of Wisconsin investigated and found that the mink had been fed 95% downer cows and 5% horsemeat. [10] When brains from infected mink were injected into two calves, within 19 months both calves had a bovine TSE but they did NOT exhibit the symptoms of Britain's mad cows. The Stetsonville cows simply became lethargic and then fell over. In other words, they exhibited typical "downer cow" symptoms. When brains from these cows were injected into mink, the mink got TME, confirming the kind of disease that had killed the cows. Marsh and his colleagues concluded, "These results suggest the presence of a previously unrecognized scrapie-like infection in cattle in the United States."[10] Marsh's cattle inoculation experiments have been repeated and, again, mink TME was transmitted to cows and back to mink and the cows exhibited "downer" symptoms, nothing like British mad cow disease. [8] Furthermore, in 1979 U.S. Department of Agriculture researchers in Mission, Texas, inoculated 10 cows with sheep scrapie. Three of the 10 cows developed neurological symptoms, but they were more like "downer cow" syndrome than British mad cow disease: "progressive difficulty in rising, a stiff-legged gait, incoordination, abnormal tail position, disorientation, and terminal recumbency [lying down]," according to Dr. Clarence Gibbs, Acting Chief of the Laboratory of Central Nervous System Studies at the National Institutes of Health. [11] Ten years later, when a test for mad cow disease became available, Dr. Gibbs confirmed a bovine TSE disease in the three cows, whose brains had been preserved. [11] Dr. Gibbs concluded, "Susceptibility of cattle to scrapie further suggests the possibility that sporadic cases of BSE [mad cow disease] may have occurred in the United States under the clinical picture of the downer cow syndrome...."[11] After Gibbs confirmed that the Mission, Texas cows had indeed died of a TSE, the U.S. Department of Agriculture repeated the experiments at Ames, Iowa under the direction of Randall Cutlip. [12] Dr. Cutlip described the results: "All calves kept longer than one year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis [partial paralysis], general weakness, and permanent recumbency [lying down]." In other words, cows infected with a sheep TSE had all the signs and symptoms of downer cows. Thus Hansen argues, there is considerable evidence that a TSE has been present in some U.S. cattle for several decades. But if mad cow disease is already present in some number of cows in the U.S., where are the human victims? People should be getting some form of CJD [Creutzfeld-Jakob disease], and this disease is thought to be vary rare and not increasing in the U.S. population. So where are the victims? Hansen argues that CJD may be more prevalent in the U.S. population than is presently thought. The official figures say that CJD is exceptionally rare --one case in every million people. In the U.S. this would mean there are 250 CJD cases at any given time. Hansen points to two studies in which people diagnosed with Alzheimer's were examined after death. In one study, among 54 presumed Alzheimer's victims, 3 (or 5.5%) were found to actually have CJD. [13] A Yale University study of 46 victims of Alzheimer's found that 6 (or 3%) actually died of CJD, not Alzheimer's. [14] There are 2 million people with Alzheimer's in the U.S. [8] If 5.5% of them actually have CJD; there are 110,000 cases of CJD in the U.S., not 250 cases. If 13% of the 2 million have CJD, then there are 260,000 cases of CJD in the U.S., not 250. If even 1% of the 2 million had CJD, it would mean there was an epidemic of 20,000 cases of CJD masquerading as Alzheimer's. Thus the FDA's argument that CJD is very rare, and not increasing, needs to be re-examined. · [1] John Collinge
and others, "Molecular analysis of prion strain variation
and the aetiology of 'new variant' CJD," NATURE Vol. 383
(October 24, 1996), pgs. 685-690. See also Adriano Aguzzi and
Charles Weissmann, "A suspicious signature," NATURE
Vol. 383 (October 24, 1996), pgs. 666-667. Descriptor terms: mad cow disease; emerging diseases; creutzfeld-jacob disease; new variant creutzfeld-jacob disease; nvcjd; cjd; great britain; consumers union; bse; tse; transmissible spongiform encephalopathies; scrapie; Britain; Michael Hansen; prions; prion theory of disease; fda; Stanley Prusiner; bans; ruminants; pigs; chickens; cows; consumers union; Richard Marsh; Clarence Gibbs; Randall Cutlip; Alzheimer’s disease; For the past several years, the U.S. Food and Drug Administration (FDA) has been considering ways to prevent an epidemic of "mad cow disease" in the U.S. In Britain, where the disease has killed 170,000 cows and at least 24 people since 1985, the beef industry has been crippled and confidence in government has plummeted because no one took adequate measures to control the disease. Additional human deaths are now expected in Britain because millions of people ate contaminated beef for a decade before authorities acknowledged that mad cow disease could endanger public health. (See REHW #606, #607.) Could such a thing happen in the U.S.? When animals are slaughtered
for human food, at least half of the carcass --hide, hooves, entrails,
and so forth --cannot be sold for human food and must be sent
to a "rendering" plant where it is ground up, boiled
down, dried into the consistency of brown sugar and sold as feed
for cows, pigs, chickens, and pets. Cows FDA says its ban is adequate because no cows in the U.S. have ever been confirmed with mad cow disease, nor is there evidence that any humans in the U.S. have been affected. However, last week we reviewed indirect evidence indicating that some cows in the U.S. may already have mad cow disease and that some people in the U.S. may already have a human version of the disease. In Britain, mad cow disease is thought to have infected some people with a variant of an age-old, but very rare, disease called Creutzfeld-Jakob disease, of CJD for short. In this country, there is some evidence that CJD may not be as rare as was once thought because some cases of CJD may have been misdiagnosed as Alzheimer’s disease. (See REHW #607.) Mad cow disease is one of a family of diseases called transmissible spongiform encephalopathies, or TSE’s for short. In sheep, the disease is called scrapie; in deer and elk it is called chronic wasting syndrome. In cows, it is called BSE [bovine spongiform encephalopathy] and in mink it is TME [transmissible mink encephalopathy]. TSE diseases all have similar characteristics: they attack the central nervous system, causing disintegration of the brain; they have a long incubation period --months or years (even decades) can pass between the initial infection and the time when symptoms appear; TSE’s are invariably fatal; and they are transmitted by eating animals or animal parts, especially brains and spinal cords. TSE’s are now thought to be caused by a protein called a prion (pronounced PREE-on). Prions are normal proteins, present in all mammals and some non-mammalian species such as salmon and ostriches. According to the prion theory of disease, some prions can fold abnormally and then they can kill nerve cells. Furthermore, according to the theory, abnormal prions can cause normal prions to fold abnormally, thus causing a chain reaction leading eventually to disease and death. [2] Prions are remarkably hardy. They are not destroyed by the digestive system of humans or other animals and they are very heat resistant. A scientific committee of the European Union says that heating prions to 271 degrees Fahrenheit (133 Celsius) less than three atmospheres of pressure will deactivate most, but not necessarily all of them. Prions also resist destruction by ultraviolet light and by radiation, and they are not affected by prolonged immersion in formalin, a potent disinfectant made from formaldehyde and alcohol. [3] Prions are hard to stop. Under FDA's rule, ruminants can be fed to pigs and pigs can be fed to ruminants. Under the rule, even ruminants that are known to be infected with a TSE can be fed to pigs. FDA allows this because, the agency says, no "naturally occurring" TSE has ever been confirmed in pigs. However, Dr. Hansen notes that British researchers have managed to infect pigs with a TSE by exposing them to high doses of contaminated brains from cattle. [4] This does not answer the question whether pigs can be infected through their normal diet, but it indisputably establishes that pigs, like many other species, are susceptible to TSE’s. Hansen offers evidence
that some pigs in the U.S. may be infected with a TSE. [5] In
1979, Dr. Masuo Doi, a U.S. Department of Agriculture (USDA) hog
inspector, began noticing pigs with central nervous system (CNS)
disorders arriving at a swine slaughterhouse, the Tobin Packing
Plant, in Albany, New York. There are 83 million pigs slaughtered in the U.S. each year. [6] They are killed at an average age of only 5 months --long before symptoms of a TSE would ordinarily become apparent. [1] Therefore, if pigs were infected with a TSE, they still might end up in food products for humans and in animal feed. Even if a pig had the behavioral symptoms of a TSE disease, USDA inspectors might not notice it. To see the symptoms of such disorders, one must observe an animal in motion. The way they walk, turn corners, and hold their tails and heads can all be important clues to their condition. Most pigs are so jammed into pens with other pigs that they have no room to move. If the animals are not in motion, symptoms of TSE’s (or other CNS disorders) can go unnoticed. At present, USDA observes only 5% to 10% of pigs while they are in motion. [6] Thus USDA’s inspection program seems inadequate to detect symptoms of TSE diseases in pigs. And, as we have noted, even if a pig were identified with a TSE, FDA's rule would allow it’s infected carcass to be fed to all non-ruminant animals, including pets, chickens, fish, and pigs. Do humans who eat pork and other pig products have high rates of CJD, the human TSE associated with mad cow disease in Britain? There have been two epidemiological studies on this point. [7,8] Both were suggestive, though not definitive. The first study, in 1973, examined 38 patients with Creutzfeld-Jakob disease. The control group consisted of the nearest relatives of the CJD patients, often their spouses. These controls then selected a friend of the patient of the same age and sex to act as a second control. The study revealed that this group of people had an unusual diet. More than one-third of the CJD patients ate brains "and the great majority of patients had a specific preference for hog brains," the authors wrote. [7] One-third of the control group also ate brains, but not necessarily hog brains. Obviously the control group, composed of close relatives and close friends, shared dietary habits with the patients, reducing the power of the study to discern differences between the two groups. [7] The second study, in 1985, compared 26 patients with Creutzfeld-Jakob disease with 18 of their family members and 22 other people selected from a hospital population. [8] Compared to the control group, the CJD patients had an unusually high consumption of roast pork, ham, hot dogs, pork chops, smoked pork, and scrapple. Scrapple is made by adding cornmeal to the liquid derived by boiling pig bones and meat (usually from the head, feet and internal organs). Compared to controls, CJD patients also had an excess consumption of roast lamb, rare meats [meaning not thoroughly cooked], and raw oysters and clams. Could TSE-infected meat enter the human food chain from other sources besides pigs? The state of Colorado requires deer hunters to turn in the heads of any deer they kill. In 1996, 6% of the deer in northeastern Colorado were found to have a TSE. In 1997, 4% of the deer there had a TSE. [9] Diseased deer in Colorado are usually incinerated or buried in a landfill (where the prions remain infective for an unknown period). However, if any diseased roadkill deer were sent to a rendering plant, they could become animal feed for pigs and chickens. It is not known at
this time whether chickens can become infected by TSE diseases.
However, even if it turns out that chickens cannot get a TSE disease
themselves, they still might carry such a disease if it were in
their feed. As we have noted, the FDA rule allows chickens to
be fed rendered animal protein even if it’s --Peter Montague (National Writers Union, UAW Local 1981/AFL-CIO)
Descriptor terms: mad
cow disease; emerging diseases; creutzfeld-jacob disease; new
variant creutzfeld-jacob disease; nvcjd; cjd; Great Britain; consumers
union; bse; tse; transmissible spongiform encephalopathies; scrapie;
Britain; Michael Hansen; prions; prion theory of disease; fda;
bans; ruminants; pigs; chickens; cows; consumers union; Clarence
Gibbs; Alzheimer’s disease;
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