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As a precaution against an outbreak of "mad cow disease" and related human illness in the United States, the U.S. Food and Drug Administration issued regulations on June 5, 1997 that would prohibit the use of the remains of all mammals except pigs and horses in ruminant (sheep and cow) feed. Consumers Union believes that to protect public health this proposal should be made stronger, consistent with regulations now in effect in the United Kingdom (UK).
Consumers Union believes that the FDA should ban the use of all mammal protein from the feed of all animals intended for human consumption.
What is "mad cow" disease?
"Mad cow disease" is one of many related progressive degenerative diseases affecting the central nervous system, known as transmissible spongiform encephalopathies (TSEs). Over 150,000 cows have contracted the disease in the UK, and new cases are still occurring there.
TSEs have been found in many mammals including humans, cows, sheep, cats, goats, deer, mink and certain zoo animals. Pigs are not immune. A TSE has been experimentally induced in pigs.
"Mad cow disease" refers to bovine spongiform encephalopathy (BSE). A related disease known as Creutzfeldt-Jacob disease (CJD) affects humans.
What are some characteristics of TSEs?
TSEs get their technical name from the fact that the brains of infected animals usually develop sponge-like holes. "Mad cow disease" owes its name to the fact that infected cows often act nervous, aggressive, and jumpy in the later stages of the disease.
Mammals can contract TSEs by eating infected animals.
TSEs have a long latency period — 10-20 years in humans.
There is no known treatment or cure for TSEs, and they are invariably fatal.
What is the infectious agent?
While the cause of TSEs has not been definitively established, the most widely accepted theory is that the infectious agent is an abnormal form of a naturally occurring protein, called a prion. Prion proteins normally occur on the surface of nerve cells and lymphocytes. When an abnormal prion comes in contact with a normal prion the normal one converts to the abnormal form. This can continue in a kind of domino effect. The conversion of many prions damages the nervous system. The gene that results in animals producing prion protein has been identified, and has been found in all mammals looked at so far.
Most experts believe some TSEs occur naturally as a result of spontaneous mutation in the prion gene. If a spontaneous mutation occurred in a food animal, the practice of feeding the remains of slaughtered animals back to other food animals could result in a single diseased animal infecting many additional animals.
Infectious prions are extremely stable, and are not destroyed by cooking, or by any common disinfectants like formaldehyde or alcohol.
Can a TSE in one species infect other animals and humans?
There is strong suggestive evidence that a new strain of CJD that recently appeared in Great Britain and has claimed more than 15 lives is linked to a form of BSE among cows. Researchers have found that the new variant form of CJD is highly distinct from other forms of CJD in humans and very similar to the type seen in cows infected with BSE. It is suspected that the humans became sick by eating infected beef.
The strain of TSE that occurred in Great Britain (BSE) has proven particularly adept at crossing species barriers. The occurrence of a spongiform encephalopathy in more than 70 domestic cats and various exotic animals in zoos in the United Kingdom has been linked to animal feed containing rendered animal remains.
What led to the outbreak of "mad cow disease" in Great Britain?
Epidemiological evidence suggests that British cattle first became sick in the 1980s after eating protein feed supplements made of either sheep or cattle remains infected with a TSE. Change in cattle farming in the last several decades may have contributed to the emergence of "mad cow disease."
- Animals were increasingly fed meat and bone meal to increase output, and;
- Rendering facilities (which process dead animals and discarded animal parts into meat and bone meal and other products) stopped using powerful solvents and high heat in processing. Experts suspect that the new techniques, which use lower temperatures and less toxic solvents, failed to deactivate the infectious agent and allowed it to spread to the animals.
Similar changes have been made in rendering and feeding practices in the cattle industry in the United States.
What should FDA do?
FDA has instituted a partial ban on feeding mammal remains to ruminants, exempting swine and horses, as well as all blood, milk and gelatin. This is inadequate. In a number of studies, blood has been shown to carry the infectious agent. Under FDAs' proposed rule, rendered remains of cows and other food animals could be fed to pigs, and vice versa. Even animals known to harbor at TSE infection could be fed to swine and poultry. Thus an infectious agent could circulate among food animals.
CU recommends that FDA prohibit feeding any mammal protein to any food animal, thus greatly reducing the possibility of a TSE disease circulating among food animals.
The UK banned feeding of ruminant remains to ruminants in 1988. Subsequently BSE in UK cattle declined but was not eliminated. In 1996, the UK banned feeding of all mammal protein to all food animals.
If infectious prions were circulating in the food supply, wouldn't we know it?
Because TSE's have relatively long incubation periods during which animals show no symptoms, farmers and meat inspectors would not necessarily know if an animal were infected. Most food animals are slaughtered at an early age before any obvious disease symptoms would appear.
The U.S. Department of Agriculture (USDA) has looked at more than 5,000 cattle brains since 1993 and not detected BSE. However, the majority of the brains were only examined visually for signs of disease, and were not subjected to a more sensitive biochemical test. The animals may have the disease and be infectious for several years before any visible symptoms appear and even before molecular tests could detect the disease. The USDA's surveillance systems thus will not pick up cows in the early stages of infection. USDA has no program for monitoring swine brains.
What research is needed?
While more research is urgently needed on many aspects of TSE diseases, CU believes research on whether TSEs occur in swine must be a top priority. In addition, although poultry have so far not contracted TSEs in British experiments, the continued use of poultry protein in animal feed raises some concern. A high priority should be additional efforts to determine if any form of TSE can be experimentally induced in poultry.
Consumers Union believes that considering what we know -- and don't know -- about "mad cow disease" and other TSEs, the FDA should act conservatively to prevent the spread of TSE disease. To protect public health, it should ban the use of all mammal protein from any feed intended for a food animal.
