You and your cat
and Mad Cow Disease

The following article is written by Eve Riser-Roberts, Ph.D. and was originally published in About.com

Rendering is the practice of converting waste animal parts into marketable products, such as meat and bone meal (MBM) for animal feed or as human food additives, cosmetics, leather products, etc., all of which provides a huge revenue for the livestock industry and avoids the problem of having to otherwise incinerate or land dispose of this enormous amount of material (53).Cows are fed "protein concentrates" made from rendered (ground-up) dead horses, dogs, cats, chickens and turkeys, as well as blood and fecal matter of their own species (6), and cattle too sick for human consumption. Maggot-infested grains, food contaminated by roaches, rodents, and bird excreta (59), outdated moldy meats, dogs and cats euthanized by vets and animal shelters; roadkill; noncommercial parts of cattle, sheep, pigs and horses—including offals, heads, and hooves; whole skunks; rats, raccoons, possums, deer, foxes, snakes, and even elephants end up in a pile on the floor of rendering plants, their decomposing carcasses swarming with maggots, covered with rat dung, waiting to be made into animal food. On top of that is added dehydrated food garbage, fats emptied from restaurant fryers and grease traps, cement-kiln dust, newsprint and cardboard, as well as cattle and hog manure. Chicken manure is popular, because it’s cheaper than alfalfa and hay (5, 20). Human sewage sludge is even used in some countries (19). The fur is not removed and the dead animals are cooked at 115°C for 20 minutes (5, 7, 19, 20). And this can legally go into your pet food.

"When you read pet-food labels and it says meat or bone meal, that's what it is--cooked and converted animals, including some dogs and cats," said Eileen Layne, of the California Veterinary Medical Association. Federal regulations mandate that brain and other nerve tissue be removed from cattle after they are slaughtered for human food, but nerve tissue is allowable in pet food. On the label it's listed as meat byproducts (1). One of the serious consequences of this practice is when Mad Cow Disease or a form of it in another animal is present in this cycle, it can be passed on to everything that follows in the food chain. Tara Parker-Pope, staff reporter of The Wall Street Journal, points out that, "it's possible that a cow with Mad Cow Disease could be fed to a pig or chicken that is, in turn, fed back to other cows, that are eventually eaten by people." (84) The FDA allows rendered materials from animals that have a mad cow type disease to be used in pet food, pig, chicken, and fish feed, simply requiring it to be labeled, ‘Do not feed to cattle and other ruminants’ (53). However, in spite of an FDA ban, the rendered cows and other ruminants, as well as the remains of other animals, are still being fed directly back to cattle. Quietly, behind the scenes, out of public view, this story is unfolding in the U.S. and around the world.

What's All the Fuss About

• TSEs (transmissible spongiform encephalopathy diseases)
• BSE (Bovine Spongiform Encephalopathy--Mad Cow Disease)
• CJD (Variant Creutzfeldt-Jakob Disease--the human form)
• FSE (Feline Spongiform Encephalopathy--the cat form)
• Scrapie (the sheep form)
• CWD (Chronic Wasting Disease—the deer and elk form)
• Kuru (a human cannibal form)

These diseases are all transmissible spongiform encephalopathy diseases (TSEs), which means they can be spread and that they cause the deterioration of the brain in their victims, turning them to sponges. The industrialized, cannibalistic practice of feeding animal remains back to other animals is now considered to be the cause of the spread of TSEs. (53) The suspected agent (a prion) that produces the disease cannot be destroyed. These diseases are always fatal.

“The initial symptoms of the human form of the disease (CJD) are subtle and ambiguous and can include insomnia, depression, confusion, personality/behavioral changes, strange physical sensations, balance disorders and/or memory, coordination and visual problems. Rapid progressive dementia and usually myoclonus (involuntary, irregular jerking movements) develop as CJD progresses. Also, language, sight, muscular weakness, swallowing and coordination problems worsen. The patient may appear startled and become rigid. In the final stage the patient loses all mental and physical functions. The patient may lapse into a coma and usually dies from an infection like pneumonia precipitated by the bedridden, unconscious state. The duration of CJD from the onset of symptoms to death is usually one year or less.” It is a horrible death. (55)

Kuru is the name given to a human disease that was discovered in the 1950s among New Guinea’s Highlander natives that practiced cannibalism (53, 85, 86). The symptoms were like those of CJD. The disease disappeared after cannibalism was outlawed by the Government. This disease showed the dangers of a species eating its own kind.

The Holstein recently discovered with Mad Cow Disease (BSE) in the United States in the state of Washington was introduced into the food chain, for both humans and animals. It would have ended up on many dinner tables (instead of just a few) in several states, if it had not been diagnosed in time for a recall of most of the meat from the animal. Quickly following this was a recall of meat from another cow from the same herd. It has now been announced that the infected cow was accompanied by 80 others from the same herd purchased from Canada, and only 19 of these have been accounted for (22). It is even possible there were actually 258 cattle in this shipment from Canada, only half of which have been located (23).

The most infectious parts of the diseased cattle -- the brain and spinal cord -- most likely went to a rendering facility, where these parts could be processed into pet and animal feed. If the FDA is able to trace where the parts went and whether they were converted into pet food, it might have the food recalled. The main threat among pets is cats because they "are susceptible to BSE," says Dr. Lester Crawford, FDA's deputy commissioner (3).

Even though we are placated by representatives from the Government and the cattle industry that there is nothing to worry about and that BSE has never been found before now in the U.S., this statement is actually untrue. (53) In spite of Government claims to the contrary, very little testing has been performed in the U.S. in the past to look for this disease. Also, the tests were conducted on specifically selected cattle and those from just a few states—not an even or representative distribution (75). Experts believe BSE has been in our food chain for many years. (26, 53) Former USDA veterinarians told UPI they have long suspected the disease was in U.S herds and there are probably additional infected animals. (28) A statement buried in FDA regulations confirms knowledge of this threat: “Perhaps the most egregious problem with the FDA rules is that they would permit known TSE-positive materials to be used in pet food, pig, chicken, and fish feed—FDA only requires that it be labeled ‘Do not feed to cattle and other ruminants.’” (53)

For years, there was a drive to initiate a total, enforceable ban of feeding animal remains to other animals in the U.S., but requests and warnings were ignored. (53) The FDA’s own TSE Advisory Committee knew the dangers of animal cannibalism in 1988, yet waited a decade to begin banning such practices, but with regulations containing plenty of loopholes to protect the industries involved. The USDA turned a blind eye to evidence of its own investigations. Finally, in 1997, the ground-up remains of cattle and other ruminants (animals that chew a cud) were ‘banned’ as ingredients for cattle supplements in the United States and Canada. But even the General Accounting Office, the investigative arm of Congress, has criticized U.S. enforcement of the ban as lax. (35) The FDA’s ban was ‘voluntary’ and was basically a symbolic gesture (44), a PR maneuver (49)."There is speculation . . . that a spongiform encephalopathy agent is present in the U.S. cattle population," notes a 1991 USDA report, pointing out that "prohibit[ing] the feeding of sheep and cattle-origin protein products to all ruminants, regardless of age. . . . minimizes the risk of BSE. The disadvantage is that the cost to the livestock and rendering industries would be substantial." (53) The ban has largely been ignored by farmers and feed manufacturers. (53) Over 300 feed manufactures have been found in violation of the 1997 feed ban for failing to guarantee that ruminant protein is kept out of cattle feed. Pigs and poultry have been fed ruminant protein and cattle have been fed the remains of pigs and poultry. The practice of feeding poultry manure directly to cattle could be another example of recycling undigested ruminant protein back to the cattle.

John Stauber is an investigative writer, executive director of the Center for Media and Democracy, and co-author of the 1997 book, "Mad Cow USA: Could the Nightmare Happen Here?" The so-called "fire wall" protecting American consumers from contaminated meat is "a farce," Stauber said. "The obfuscation and spin coming from the USDA is amazing." Stauber says it is preposterous that this is an isolated case. "The FDA said back in 1997 that by the time we saw one case of mad cow in the U.S. - even if there were an effective feed ban in place, which there isn't - over the next 11 years because of the invisible latency period we could expect to see 299,000 more cases," he said. (17)

Some 37 million cattle were sent to market in 2003, with an estimated 130,000 of them downed cattle. Yet only 20,526 cows in total were tested nationwide that year, which is like a blind person finding a needle in a haystack. (8, 9) Actually, the USDA claims to have tested approximately 20,000 cows for the disease in 2002 and 2003, but has been unable to provide any documentation in support of this to UPI. (28) In Europe, about 200,000 animals are tested each day, and in Japan, every bovine that enters the food supply is tested. (26)

The American system was never intended to keep sick animals from reaching the public's refrigerators, said Dr. Ron DeHaven, the Agriculture Department's chief veterinarian. It is "a surveillance system, not a food-safety test. Statistically, it is meant only to assure finding the disease if it exists in one in 1 million animals, and only after slaughter." (10) A 2001 study in Germany found that downed cows were up to 240 times more likely to test positive for BSE. Despite this known threat, an average of only 10 to 15 per cent of downers are tested for BSE in this country. (11) Older cattle, such as dairy cows, are more likely to exhibit symptoms of the disease. While little is known about its diet, the animal found to be infected with BSE in Washington state was a downer from a dairy herd.

‘Downer cow syndrome’ is a ‘garbage can’ category that refers to any animal that died or had to be put down after failing to stand on its own legs for 24 hours or more (53). It can include cows with arthritis, paralysis, grass tetany, bone fractures, ketosis, milk fever, and spongiform encephalopathies. BSE is generally a slow, progressive deterioration of the brain and central nervous system, with the cattle eventually becoming unable to walk or stand. But cattle will usually not display symptoms for three to eight years after becoming infected with BSE (1). Most animals are slaughtered before they would show symptoms. Thus many cattle, even though they were not yet downers, would go undiagnosed and be able to carry the disease into our diets and the diets of our cats. (27)

There has been no law to protect humans from the addition of downer cattle to our diet. On the other hand, those animals considered obviously too sick to be used for human food end up in pet food, no matter what they are infected with. (4) It is legal to use what the USDA calls 4-D meat, cattle that are dead, dying, disabled, or diseased, for this purpose. Condemned cattle that are contaminated with pesticides or antibiotics, as well as animals with transmissible spongiform encephalopathies, are also acceptable in pet food (21). This does not mean that all downer cattle carry the disease, but that this group of animals may be finally showing the symptoms. A more subtle danger is the cattle that are carrying the disease but are symptomless. If only downer cattle are tested for BSE the prion would be missed in cows that appear to be healthy.It was originally believed that the prion protein thought to be responsible for the disease would not cross from one species to another, but it has made the jump through the consumption of contaminated feed and adapted to new hosts (1, 2). In 1985, this principle was demonstrated when an outbreak of a spongiform disease occurred as a result of having fed BSE downer cattle to mink. (46, 48, 64) In a 1990 paper for the dairy publication, Hoard's Dairyman, the University of Wisconsin-Madison veterinarian Richard Marsh and Minnesota animal health consultant William Wustenberg announced that the evidence from the mink outbreak suggested a mad cow-like disease "is present but not recognized in the U.S." In fact, mink outbreaks traced to downer-cattle as feed were known as far back as the early 1960s. (51)

Experiments have shown that BSE can be transmitted to many animals, including goats, sheep, mice, monkeys, pigs, and mink (53).

• The deaths of domestic cats and a wide variety of other animals in Britain were associated with their diet of rendered animal feed containing BSE-contaminated cows. As of January 2000, around 100 domestic cats had died from FSE, the feline form of the disease, in that country (1). These were just the deaths that were confirmed, but there were most likely many more (63). John Bower, president of the British Veterinary Association said, “Vets are presented with cats showing nervous disorders like this one every day. Some can be treated, some can’t and have to be destroyed. But in 90% of cases when they do have to be put to sleep the owners don’t want us to carry out a post mortem
• In zoos, outbreaks of spongiform diseases among big cats, primates, antelope, and other species, have been associated with the feeding of BSE-infected material. One study in 2001 identified 82 cases having occurred in zoos (2).
• Research has confirmed it is possible to transmit scrapie (the sheep version of the disease) to cattle (51). Sheep scrapie could be transmitted to cattle and it could then be passed from cattle-to-cattle (47).
• BSE from contaminated cattle can infect mink (67).
• Material from BSE-contaminated cows also caused disease in macaque monkeys, which displayed brain characteristics of the new variant CJD (72).
• Brains from a mink that had died from eating downer cattle were injected into mink, ferrets, monkeys, hampsters, mice, and Holstein calves (65). Every species except the mice developed a TSE, including the cows. A critical observation from this experiment was that the infected cattle did not display the typical clinical symptoms of British-style BSE [i.e., the cows did not act "mad"[; rather, the symptoms were more like those seen in ‘downer cow syndrome’ (53, 66). Ultimately, the conclusion was reached that the U.S. has its own native version of Mad Cow Disease, the symptoms of which are not as extreme as those in the British outbreak, but can be observed in its ‘downer cattle.
• Paul Brown, medical director for the U.S. Public Health Service, believes that pigs and poultry could be harboring BSE and passing it on to humans, adding that pigs are especially sensitive to the disease. (30) Two epidemiological studies found pork to be a dietary risk factor in Creutzfeldt-Jakob Disease (the human form) (78, 79). In late 1978, Dr. Masuo Doi, a veterinarian with the Food Safety and Quality Service, studied a disorder in pigs that had arrived at a packing plant in Albany, N.Y. from several Midwestern states. The USDA's pathologist reported that the damage in the pig's brain was similar to the damage observed in the brains of sheep afflicted with scrapie (77). The conclusion was that a TSE disease has already infected pigs (53, 80). However, when the FDA finally drafted a rule that would ban the fortifying of animal feeds with "any Mammalian tissue," the FDA played a taxonomical shell game by arbitrarily removing pigs from the class of ‘Mammalia.’ They declared that a pig is NOT a mammal!

Claims by the beef industry that only the cattle brains, nerve tissue, and spinal cord are infected and can cause disease are totally misleading. Published scientific studies have shown that the prion can also be present in many other tissues, including muscle (i.e., steak) (53) and blood (12), bone, eyes, tonsils, lymph, intestines, spleen, liver, and other organs, glands, and other tissues (13, 14). Organ transplants, surgical equipment, pharmaceuticals made from animal products, garden fertilizers, cosmetics, human growth hormone, and baby food can also carry the prions (53). The infectious agent for the sheep TSE (scrapie) can be found throughout the body of an infected sheep. It has been suggested that the brain, spinal cord, spleen, thymus, tonsils, and intestines of the cattle were chosen by both the British and U.S. Governments for their initial feed ban possibly because these parts had the least commercial value (62, 68).

Two broadcasts of the TV program, Dateline, in 1996 and 1997, covered BSE (47). They pointed out that while cows are supposedly not allowed to directly eat cow parts since a 1997 FDA voluntary ruling, cows and calves may still be fed bovine blood products. (26) This is a dangerous exception, because scientists have conclusively proved that blood and blood products can carry the disease-producing prion (53). The Red Cross will not accept blood from donors who have lived in Britain for three months or Europe for six months dating from 1980. Dateline’s commentator, Stone Phillips, stated point-blank that the American Red Cross had secretly sequestered 2 million units of various blood products, because of uncertain provenance with regard to donors and CJD (47).

Although there is a case description in the New England Journal of Medicine (1992) in which colostrum from a Creutzfeldt-Jakob diseased woman was found to be infectious to mice, cow's milk is considered "safe" by the World Health Organization. (30) Teamsters for dairy workers petitioned the U.S. Secretaries of Agriculture and Health & Human Services to immediately ban the distribution of milk associated with the BSE outbreak in the Pacific Northwest. (33) In Great Britain, the distribution of milk from any cows linked to the outbreak was banned. In 1993, the British medical journal, Lancet, reported the death of a 61-year-old dairy farmer from CJD (53). His herd of BSE-infected cattle had been destroyed in 1989, and he had been drinking milk from the herd for at least seven years. Four months later, another dairy farmer died, aged 65.

However, it’s not only the beef products that can be contaminated, but also the equipment used to process an infected cow. When other cows and other animals are then run through the machinery, their products will also become contaminated by picking up nerve debris and prions left behind by the infected cow. Many different types of animals pass through the same equipment. If one is infected with a TSE, the machines become infected. In 1990, Dr. Linda Detwiler, a USDA official, reported that U.S. sheep scrapie had been spread into cattle in Government tests. For decades scrapie-infected sheep have passed through U.S. rendering plants. (50) In 1990, the USDA produced a report titled, "BSE Rendering Research Priorities," which warned that rendering plants themselves may be contaminated with TSE disease agents: "If scrapie or BSE-infected animals are rendered, it may become necessary to disinfect the rendering facilities. Unfortunately, both the resistance of spongiform encephalopathy agents to many disinfectants and the need to avoid corrosive chemicals in rendering plants create major limitations on the choice of technology available." (53) Referring to the first acknowledged case of BSE in America in Washington state, Michael Hansen, of Consumers Union, the watchdog group in Yonkers, N.Y said, "All those rendering plants the infected cow material passed through will be contaminated.” Therefore, it was not just meat and various products from this cow, but also from other cattle and other animals that were processed after them in three different plants, and which will probably not be traced or recalled. (3) Also worth noting is that, depending on the equipment used, water may be drained from the rendering tanks to go to the water treatment facility (carrying prions with it). (53)

One process used on a cow carcass is to remove meat from the bone with machines using high-pressure water jets. (2) This method also strips off bone and spinal cord material, which is likely to be highly infectious in a sick cow. It is pooled into beef patties, meat pies, and pasta fillings; meat from as many as 60 animals may go into a hamburger mix. Each batch contains meat from about 1,000 animals, any one of which could infect the whole, and expose as many as 400,000 persons to the agent. An agency of the U.S. Department of Agriculture pointed out that about 35% of samples from advanced meat and bone separation machinery had ''unacceptable nervous tissues'' detected. Also, 29% and 10% of the samples had spinal cord tissue and dorsal nerve root ganglia tissue detected, respectively, according to the Food Safety and Inspection Service (FSIS). (15) Meat that is cut close to the bone, such as T-bones and ribs, can have traces of spinal cord tissue. (20) Processed beef products such as hamburger, hot dogs, sausage (believed to be the source of most human BSE infections in Europe), and pizza toppings can have traces of spinal cord tissue. Although brain and spinal cord material are banned from meat, a 2002 USDA survey found these tissues in beef products at 74 percent of the plants tested. The stun gun method that splattered brain material into the liver has just been banned (82).

The suppression of this information and the lack of surveillance over the years could result in tremendous loss of human and animal life, as the disease eventually expresses itself. It can reportedly take an average of 13 years, and as much as 40 years before symptoms are seen in humans, and it is always fatal. (1) In the British outbreak, the disease was found to occur in people under 30, even teenagers, which is rare (53). In 1996, the death of two teenagers from CJD in America was reported in the English press (69). By 1995, more British farmers were being diagnosed as having the disease (53). Waiting until the first case of BSE is diagnosed in the United States will certainly be "closing the barn door after the horse is gone," says R. F. Marsh, DVM, PhD. (45) “With a disease having a 3- to 6-year incubation period, thousands of animals would be exposed before we recognize the problem and, if that happens, we would be in for a decade of turmoil” (60).

As of 2002, there were 830 deaths in Great Britain due to CJD (55). The number of definite or probable variant CJD (BSE-caused) cases were 122. Other European countries also report human deaths from BSE-contaminated meat. One problem emerging is that when a country announces that it has a BSE problem, it loses its international trade markets, which can be financially devastating (53). So, many countries appear simply not to be reporting their cases of BSE. This then allows their contaminated products to be imported into other countries, such as the U.S., that are ostensibly dealing only with BSE-free nations.

If this hypothesis of the disease transmission proves correct, the man-made cycle of using dead animals as feed for other animals ensures that the disease will be perpetuated. Our pets would play an important role in this cycle, as they are fed the contaminated food and are in turn used as contaminated food themselves.

It is believed that this is a pandemic disease, an epidemic that is worldwide. (29) And a quiet one, because the cause and effect are not easily linked, because the symptoms do not appear until years after the initial infection, because the existence of the disease and its transmissibility are being denied by Governments, because the disease is not being adequately monitored, because interests of countries and meat industries are taking precedence over human lives, and because too little is being done too late to prevent it.

What Is Causing the Disease?

It is now believed that a newly discovered, mutant protein (called a prion) present in nerve tissue is responsible for all the transmissible spongiform diseases (TSEs) and that it is contracted through eating contaminated food (43). Human cases have been strongly linked to the BSE agent (70, 72). This was confirmed with the development of a new test that provided molecule markers to distinguish the TSE from different sources. It was able to show that the new variant CJD occurring in people who ate BSE-contaminated beef was like BSE, and not like the common form of CJD (53, 54, 73, 74).The hypothesis is that proteins, called prions, present in nerve tissue can be turned into lethal prions that become deformed and convert other prions in an unstoppable process that gradually riddles the brain with holes like a sponge until it results in death (53). The destruction of neurons, the main cells responsible for carrying nerve impulses throughout the body is what leads to the symptoms observed with the TSEe, as described earlier. The prion cannot be destroyed.

It has been proposed that every mammalian species normally has the disease at a rate of about one in a million, and every species should have its own, but rare, form of TSE. (53) However, if that one diseased animal ends up as feed, the infectious agent can be passed to the animals consuming that feed. Then when those contaminated animals are fed to others, the disease can spread rapidly among the susceptible species. The fact that TSEs can be spread between species increases the odds of infected animals entering the system. The ‘species barrier,’ which usually protects one species from another’s diseases, is more like a sieve with the TSE prions. USDA’s Linda Detwiler said that testing for that one in a million cow would be too expensive. “You just have to do all the preventions. You can’t stop the one-in-a-million from occurring” (76).

How much of the prion does it take to cause the disease? British scientists have determined that a cow can get BSE by eating one gram of infected material - a speck the size of a peppercorn - from another cow. Even a minute trace of the material in meat and bone meal (MBM), the protein supplement produced from rendered animal remains, can infect a cow. (2) According to the European Union's Standing Scientific Committee, "the minimal infective dose considered to be valid for animals should also be applied for humans." The minimum dose is unknown, but British scientists discovered that a piece of wire that had been in contact with the pathogen for five minutes became as infectious as a solution made from infected brain. (2)

What Makes the Prion Lethal?

Normal prions in nerve tissue of cattle, humans, cats, or other animals have to be deformed as the initial stage of spongiform encephalopathies. As discussed above, the mutant prion could occur spontaneously in a population at a rate of one in a million. The predilection for it can also be an inherited trait, which is related to the gene sequence for the prion protein and can be found in 38% of the human population (53). The other 62% ‘might’ be resistant to the disease. However, other research suggests that those in the ‘resistant’ group might simply develop the disease much later (57).But what causes a normal or susceptible prion to turn into a lethal one? One hypothesis that has been put forth is that this could be caused by organophosphates. Nerve damage is known to be caused by exposure to these potent chemicals, which were originally developed by the Nazis during the war as a toxic nerve agent.

If organophosphates are involved, the highly reactive free radicals in the chemical could deform normal or susceptible prions. According to some researchers, the deformed prions would become more prone to binding with manganese, and it is this combination that makes them dangerous. (One form of organophosphate even contains magnesium.) It is postulated that manganese-bound prions then become rogue prions that have the ability to deform other normal prions in a chain reaction that eventually destroys the brain.

This hypothesis contends that TSEs are likely linked to environmental conditions rather than prion-contaminated feed. The researchers discovered that prions require copper to develop properly. If copper is low and exposure to high levels of manganese occurs, the prion may bind to manganese and turn into the fatal form that eventually burns holes in the brain.

A small cluster of scientists argues that the environmental imbalance of copper and manganese are common factors among TSE cases around the world. This could explain the observance of scrapie in sheep and chronic wasting disease in deer in Colorado and Wyoming, where the deer feed on copper-starved soil. The deer could also have been exposed to the insecticide and then obtained the manganese from their diet of pine needles, which contain this element. The Colorado Division of Wildlife denies that the deer were fed meat products. (52) On the other hand, the researchers advocating spread of TSE by contaminated feed, have found evidence that scrapie may be passed among sheep by their feeding on TSE-contaminate grass (53).

Manganese poisoning could be linked to the soil, water or even industrial emissions. In cattle, the damaged prions would be capable of binding with manganese present in animal feeds (especially chicken manure), feeds grown on copper-depleted soil, or in mineral licks, or manganese sprayed on the land. This would convert normal prions into the rogue prions that cause the neurological damage of BSE. Therefore, the spongiform encephalopathies may be linked to modern industrial development. Manganese emissions from steel or petrochemical refinery processing may also have a connection.

The cases of spongiform disease in Britain occurred in cows, humans, cats, and other animals during the same time period. The country had been using an aggressive organophosphate program to kill the warble fly at the time of the BSE/CJD outbreak there. During the 1980s and early 1990s, cattle and cats were exclusively treated with systemically acting forms of organophosphate insecticide that were designed to penetrate the entire physiological system of the animal, transforming the bloodstream into a toxic medium that would kill off any unwanted parasites present. The entire cow carcass would become toxic to warble fly. Farmers were ordered by the Government to apply the insecticide on the backs of their cows. This could have caused nerve damage in the coated area, deforming the normal prions along the spinal cord and making them susceptible. The systemic form of the chemical would have caused extensive damage. This chemical is also commonly used on humans as a treatment for scabies and head lice and has been sprayed in the environment. Humans who worked with the chemical or lived near the chemical plants had a higher incidence of the disease. Cattle, cats, and humans exposed to the insecticide could thus have been primed for the disease. Then, when their damaged prions came into contact with manganese, the disease was expressed. Soils with increased manganese levels equated with scapie (a transmissible spongiform disease in sheep) and chronic wasting disease in deer. The original BSE farms in England lie directly in a manganese hot spot. (37)The authors of this hypothesis do not believe that the prion is an infectious agent, but rather that the disease is caused directly by the organophosphate-damaged prions binding with manganese. This combination would then produce the chain reaction leading to disease. It is suggested that the transmissible 'infective agent' observed in laboratory tests may be the free radicals from the pesticide.

A similar view is supported by other researchers who propose a link to dioxins, accompanied by a change in procedures for rendering animal carcasses to produce the meat and bone meal for animal and pet feed (39, 40). In the past, excess fat was removed from this ground-up compound by subjecting it to a solvent wash. The solvent then underwent high temperature solvent blow-off, which also helped remove the toxic residues. This solvent fat-removing process was discontinued in England, and the new process increased the final fat content, which now also contained the previously removed toxic residues. These were in the form of bioaccumulated free radicals, such as dioxins and insecticide. Now, cattle are chronically ingesting this poisonous residue through eating feed containing other animals, and this may have triggered the BSE epidemic in Britain. Fat-laced milk in the suckling feed is also implicated as it comes from the same source. The major sources of dioxin are in our diet. Since dioxin is fat-soluble, it bioaccumulates in humans and in animals, climbing up the food chain, and it is mainly (97.5%) found in meat and dairy products (beef, dairy products, milk, chicken, pork, fish and eggs) in that order. (41, 53)

he early methods of disposing of contaminated cattle in the outbreak in Britain were to incinerate the bodies in massive pyres, and this may even have exacerbated the condition. Beef incineration generates dioxin, and the ashes and smoke may well have carried the indestructible prion over the English countryside (81). Another opinion for the mutant prion activity is that the normal prions combine with sugars and go through different stages, with internal attractions that cause the prion to fold (53). The folded prions may attract other normal prions to them, perhaps in the manner that crystals are formed.Yet another hypothesis suggests these diseases may be caused by the actual conversion of normal prions into rogue prions—that the act of the conversion may produce a toxic byproduct, an intermediate form, or may deplete a factor that is crucial to brain-cell survival (36, 37). Giovanna Mallucci and colleagues at the Institute of Neurology in London have suggested that the accumulation of rogue prions does not kill nerve cells but is a symptom of the diseases. Their studies claim to have found a method of halting this conversion process, which would offer great potential for the development of a diagnostic test and a vaccine against the diseases. Their studies found that shutting off conversion actually allows brains to recover. These researchers and Adriano Aguzzi’s team at the University Hospital Zurich in Switzerland are now looking for the fatal factor.

Could the cases of BSE or CJD have come from eating contaminated meat? Could they have resulted from insecticide and manganese or dioxin exposure, either directly or after passage through animal products? Could chemical exposure and contaminated food have interacted to produce the disease? If people know they have been exposed to a chemical, such as organophosphates (or dioxin), or maybe lived in an area that had been sprayed, or used it as a pesticide around the house or as a product on their cats or dogs, they should consider avoiding food that might be contaminated and also avoid manganese. Their prions may possibly have been primed for the disease.

Conclusion

There is extensive evidence to support that TSEs are transmissible diseases, that they are spread to animals and humans by eating contaminated animal material, that they have been in the food chain in the U.S. for decades, that there have been Government denial and cover-ups at every stage, that big business interests are more important to protect than the lives of a country’s citizens, and that there will be many unnecessary deaths as a result of the lack of protective measures in the coming years (53).If this agent is truly indestructible and transmissible, and as long as the current cannibalistic practice of feeding animals to other animals continues, it will be passed on through the food chain and make its way to cats and other animals, then to cows, then from cows (and possibly pigs and sheep) on to humans. (53) Although chickens have not been found with the disease, they could still be spreading it. It has been shown that an intermediate host can pass on the disease without displaying symptoms itself (58). There also appears to be more than one BSE-derived prion strain that might infect humans; it is therefore possible that some patients with what was thought to be sporadic CJD (considered the usual, normally occurring form) may actually have the disease arising from BSE exposure (56).

It is believed that many of the cases assumed to be Alzheimer’s Disease may be the human form of BSE, Creutzfeldt-Jakob Disease (CJD), which is difficult to distinguish from Alzheimer’s (27). The most common misdiagnosis of CJD is Alzheimer's disease. (53) Hidden cases of 1 to 13% are CJD. Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, conducted a 1989 study that found 13 percent of Alzheimer's patients actually had CJD. That percentage could add up to 120,000 or more CJD victims a year going undetected and not included in official statistics, instead of the 250 reported (53). And since the disease could occur at any time up to 40 years, the number of people affected in future years could be astronomical.

The U.S. public has not been able to depend on protection by its Government. A 10,000 pound batch of beef that included cuts and bones from the single infected dairy Holstein was distributed in December to six states, including California. (31) Officials with the FDA said they knew where most of the recalled meat and bones had been sold but maintained that information was considered proprietary and was not available to the public. "It is inexcusable that the USDA forbids California from informing consumers where the meat is," said Caroline Smith Dewaal, Director of Food Safety for the Center for Science in the Public Interest, a Washington, D.C., advocacy group. "This policy is proof positive that the USDA voluntary recall system is more concerned about protecting the beef industry than protecting the public health," she added. Dangerous toys and cars must be recalled in this country and the public informed, but this is not the case with potentially fatal food. Because Japan has refused to import American beef, as a result of the current finding of BSE, the U.S. Government has agreed to test every animal exported to that country, in an effort to win back this revenue. However, this Government has not agreed to test every animal meant for consumption by Americans. (32) Even though the U.S. Government knew that the epidemic in Britain was spread through the use of rendered animal feed, it took no measures to ensure it could not happen here, even when Britain withdrew its rendered animal feed policy in 1988 (53). This country chose not to learn from the experiences of Great Britain and other European countries. The Government and food industry are more interested in ‘crisis management’ and PR for their products. Their reaction to this situation has been obstruction, deception, denials, lies, procrastination, and rules full of loopholes (53).

Agriculture Secretary, Ann Veneman, has just announced additional safeguards against Bovine Spongiform Encephalopathy in the U.S. (81). These include:

1. Immediate ban on downer animals entering the human food chain.
2. Cattle tested for BSE will no longer be marked as "inspected and passed" until confirmation is received that the animals have, in fact, tested negative for BSE.
3. Skull, brain, trigeminal ganglia, eyes, vertebral column, spinal cord and dorsal root ganglia of cattle over 30 months of age and the small intestine of cattle of all ages, are prohibited from the human food supply.
4. Immediate ban on air-injection stunning to ensure that portions of the brain are not dislocated into the tissues of the carcass.
5. Prohibit use of mechanically separated meat in human food.
6. Immediate implementation of a verifiable system of national animal identification.

The Government will likely deem it too expensive for the meat industries and the country’s meat export revenues to institute a comprehensive program that would provide total protection (53). The next most important step would be to break the cycle that allows any rendered animals to end up as feed for animals eaten by humans, not just a ban on feeding ruminants back to ruminants. And to find an effective means of enforcing the ban. A soybean meal could be substituted for the meat and bone meal. Ideally, the ban should be comprehensive to prohibit feeding of rendered animals to any other animal. A method of disinfecting contaminated rendering plants is necessary to protect pets and other animals not consumed by humans, if rendering for their food continues. There are also many byproducts from rendering that could be made from infected animals that could still carry the prion, such as the gelatin around your vitamin capsules and sugar whitened by cow bones. It is still unknown what prions could do if present in products made from animal hides, say if they came in contact with broken skin. The current rendering practice has been shown to be risky (53). The extent of that risk is yet to be determined.And what about grills used to grill those beefsteaks? They could be contaminated by a BSE cow and spread the prion to grilled chicken or to the grilled vegetables the vegetarian has carefully ordered to avoid animal products, since the prion would not be killed by the heat. Hopefully, a rapid, inexpensive diagnostic test can be developed soon to identify contaminated animals while they are still alive and before they are sent to slaughter. Neurologist, Neil Cashman, a professor of medicine at the University of Toronto, has identified an antibody specific to a portion of the rogue prions (42). Researchers hope this can lead to development of a vaccine or therapy to prime the immune system to destroy the misfolded clumps of prions and a diagnostic test for living animals.

So, would eating meat containing the prion be a problem?

Some researchers hold that damaged prions and manganese are the cause of the disease but have rejected the idea of transmission through consumption of contaminated food. Others attribute the TSEs to something emitted or depleted during the process of the formation of rogue prions, but whatever that is, it is transmissible. However, the consensus from the bulk of research conducted on the disease is that BSE can be spread from contaminated animals to many other species of animals, including humans, and the means of transmission is food. Whatever is creating the rogue prions or the disease, it appears to be passed on in an active state to the next recipient in the food chain. Brain and nerve tissue have been identified as the most contagious part of an infected animal, and cheaper forms of meat are considered more dangerous (53). However, the body is laced with nerves and blood, and this includes muscle meat, and pretty much the whole cow.

There are still many questions to be answered. But if you wish to play it safe and reduce your risk of future exposure to possibly ‘contaminated’ material, you could choose to eat organic meat or become a vegetarian, although even vegetarians would have a hard time avoiding all contact with prion-containing products (53). But until more is known about the disease and the extent to which an infectious agent may already be widespread in our food stock, it’s a matter of how much risk you want to take for yourself and your pets while you wait for the results.

In any case, now that you know what goes into many of the commercial cat foods (as meat byproducts), you may want to consider at least giving your cat a healthier diet with food that does not include the ingredients mentioned at the beginning of this article. You may also want to reconsider eating beef or pork, based on the research results implicating that these animals do harbor TSEs and also knowing what they have been fed on, whether this meat is contagious with the spongiform disease or not. You may also wish to reconsider chicken because of its diet of potentially contaminated feedstock, and its ability to pass on the disease. Research is needed to determine if poultry are silent carriers of the disease themselves. And you should be sure to take plenty of anti-oxidants (e.g., Vitamin C, Vitamin E) yourself, which will help inactivate hazardous free radicals.

“If an evil force could devise an agent capable of damaging the human race, he would make it indestructible, distribute it as widely as possible in animal feed so that it would pass to man, and program it to cause disease slowly so that everyone would have been exposed to it before there was any awareness of its presence,” British microbiologist, Richard Lacey (61).

Source

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