Next time, DON'T PROCRASTINATE(sp?)!! here is some advise:
Bovine Spongiform Encephalopathy (BSE)
I INTRODUCTION
Bovine Spongiform Encephalopathy (BSE) or Mad Cow Disease, degenerative brain disease of cattle linked to a variant form of Creutzfeldt-Jakob disease (CJD), a fatal degenerative brain disease in humans. The clinical signs of BSE in cattle include loss of coordination, a staggering gait, difficulty in rising, decreased milk production, and weight loss. Affected animals also show signs of behavioral changes, such as nervousness, aggression, and a lack of interest in their surroundings. The period from exposure and infection to the onset of the disease, known as the incubation period, is from two to eight or more years. Once clinical signs develop, animals progressively deteriorate and die within several months.
II ORIGINS OF BSE
BSE was first identified in the United Kingdom in November 1986. By 2003 more than 185,000 cases of the disease had been confirmed worldwide, the vast majority of them in the United Kingdom. Studies have suggested that more than 1 million animals were likely infected during this period and entered the human food supply. These animals went undiagnosed or were slaughtered before clinical signs developed. The appearance of BSE in native-born cattle has been recorded in many other European countries, including Austria, Belgium, Czech Republic, Denmark, France, Germany, Greece, Ireland, Italy, Luxembourg, The Netherlands, Poland, Portugal, Slovakia, Slovenia, Spain, and Switzerland. Cases in native-born cattle outside of Europe, although rare, have been confirmed in Canada, Israel, and Japan. BSE has also been recorded in the Falkland Islands (Islas Malvinas) and Oman in cows imported from the United Kingdom. In 2003 the first case of BSE was confirmed in the United States in a dairy cow that originated in Alberta, Canada.
Autopsies of affected cattle reveal telltale holes in the brain tissue that give it a spongiform, or spongy, appearance resembling Swiss cheese. Similar spongiform brain changes have been recognized in humans, as in the case of CJD, for more than a century. Similar changes have been seen in sheep for more than 200 years due to the brain disease known as scrapie. Together these diseases and a few others are called the spongiform encephalopathies, and they are caused by prions, normal proteins that fold into abnormal shapes and become infectious and pathogenic (disease-causing). As prions accumulate in the brain, they cause in still largely unknown ways the spongiform change to neurons (nerve cells) and produce, also in largely unknown ways, the characteristic clinical signs of the disease.
Health officials identified animal feed containing recycled animal tissue as the source of the infection that led to the BSE cattle epidemic in the United Kingdom. This type of animal feed was routinely fed to dairy cows as a protein supplement for most of the 20th century. But in the 1980s rendering (the cooking method used to process hide, bones, and other inedible tissue after slaughter) changed in a way that may have enabled the survival of the BSE infectious agent.
There are two theories regarding the origin of the BSE prion. One is that scrapie prions were introduced into cattle feed from animal feed containing sheep brains and other sheep byproducts. Subsequently, brain tissue taken from cows infected with BSE was included in protein supplements, and this worsened the epidemic. The second theory is that the BSE prion originated via a spontaneous mutation. Such a mutation would have led to a protein that folded into the abnormal form. This abnormal prion protein would have built up in the central nervous system of the cow and then would have spread when tissues from this cow were included in protein supplements fed to other animals. The epidemic widened when the brains and other rendered products from infected cattle were used in protein supplements distributed throughout Britain and then elsewhere across Europe and in Japan and Canada.
III PREVENTIVE MEASURES IN BRITAIN
To prevent the spread of BSE, the British government introduced compulsory destruction of suspect animals and the burning of their carcasses beginning in 1988. The feeding of rendered animal tissue to cattle was banned in the United Kingdom in July 1988. As a result of these efforts, monitors working for the United Kingdom Ministry of Agriculture recorded a persistent decline in the incidence of BSE after 1992, when the number of confirmed cases peaked at more than 37,000. By 2002 fewer than 1,150 cases of BSE were confirmed in the United Kingdom, and by 2003 this number had fallen to 159.
After the initial report of the disease, there was fear and speculation that it might be transferable to humans through beef products. The medical community was aware of the similarity of CJD symptoms to those of BSE and was also aware that a related disease, known as kuru, was spread by ritualistic cannibalism among New Guinea tribes.
IV BSE AND HUMAN DISEASE
In March 1996 the British Ministry of Health announced the discovery of ten cases of a unique type of CJD, called variant CJD (vCJD). This type of CJD differed from the classical form in that all the patients were under the age of 42. (The classical form of the disease typically develops around age 65.) The patients displayed unusual psychiatric problems, distinct brain tissue changes identified during autopsies, and the patients had no family history of CJD. The British government found that the patients contracted the disease by eating BSE-infected meat products. The government had previously denied any possible link between BSE and human disease.
Since 1996 a number of studies have confirmed that BSE in cattle can be transmitted to humans and cause vCJD. By 2004 studies had linked BSE in cattle to more than 145 human cases of vCJD in Europe, mostly in Britain. Several lines of evidence confirmed this causal relationship: Molecular markers of vCJD prions from humans were shown to be the same as BSE prions from cattle. When scientists injected monkeys and mice with brain tissue from BSE-infected cows or brain tissue from vCJD-infected humans, the animals developed the same unique type of brain degeneration. This degeneration is distinguishable from the degeneration following injection with brain tissue from cases of the classical form of CJD.
V FURTHER PREVENTIVE MEASURES
Following the British government’s 1996 announcement that BSE may be transmitted to humans, beef consumption plummeted in the United Kingdom, and the European Union (EU) banned British beef imports. The British animal agricultural economy was devastated, as were related business such as restaurants and pharmaceutical and cosmetic companies that use animal products in the preparation of their products. To prevent similar economic losses, many countries decided to prohibit the use of animal products in animal feed.
In 1999, to further reduce the BSE risk in cattle, the British government began destroying all cattle at highest risk for BSE. This included all cattle that are more than 30 months of age at slaughter, regardless of their apparent health. Older animals are more susceptible to BSE. These and other precautions led the EU to lift the ban on British beef and beef products that met certain criteria. Among these criteria, animals must be more than 6 months of age and less than 30 months old at time of slaughter and be born after August 1, 1996. In addition, clear records of the lives of the slaughtered animals must be available, including the date and location of birth, the health records of the animal’s parents, and all movements prior to slaughter.
VI BSE IN THE UNITED STATES AND CANADA
To prevent BSE from infecting cattle in the United States, in 1989 the U.S. Department of Agriculture (USDA) banned the import of live cattle and beef products from countries—such as the United Kingdom—where BSE was known to exist. In 1997, amid concerns of persistent risk factors and inadequate surveillance in Europe, these import restrictions were extended to include all of the countries of Europe. These restrictions were further extended to include Japan in 2001 and Canada in 2003, after BSE was confirmed in a native-born animal in each of those countries. In another protective measure implemented in 1997, the U.S. Food and Drug Administration (FDA) banned the use of meat, bone, or fat from ruminants—cattle, sheep, goats, or deer—in cattle or sheep feed. These products can still be used in feed for other animals not affected by the BSE infectious agent, such as pigs and poultry.
To reduce the risk of cross-contamination from other animals, the USDA in 2000 prohibited imports from Europe of all rendered animal protein products, regardless of species. In addition, the USDA stepped up its surveillance for BSE throughout the United States.
The USDA surveillance program focuses on cattle that are at higher than usual risk for BSE. These are adult cattle with clinical signs of central nervous system disease and so-called downer, or nonambulatory, cattle—that is, cattle unable to walk. In the years before the decision was made to increase surveillance, few animals were tested, but in 2001 and 2002 about 20,000 animals were tested each year. This testing of 20,000 cattle brains represented a sample taken from an estimated 35 million cattle killed per year.
Critics of this testing program have charged that the sampling has been insufficient, noting that Europe tests some 200,000 cattle per day and that every bovine animal slaughtered in Japan is tested. The most exacting test involves the microscopic examination of sections of particular brain parts, often with a reacting chemical that detects a response by the animal’s immune system. This test is time-consuming and expensive. In Europe and Japan automated high-throughput tests produced by several companies are used. The USDA is investigating possible use of these tests.
After the discovery in December 2003 of BSE in a downer cow on a farm in eastern Washington, the USDA implemented a number of additional measures. It immediately banned the inclusion of downer cows as a source of meat for human consumption and required that all carcasses tested for BSE be withheld from the food supply until test results are complete. The USDA prohibited the use in the food supply of brains, skulls, spinal cords, vertebral columns, eyes, and certain nerve tissues from cattle older than 30 months. This is because older animals are most likely to harbor the prions suspected of causing BSE.
The USDA also mandated changes in the use of advanced meat recovery (AMR) systems that use hydraulic pressure to force muscle tissue from bones. These muscle tissues are then used in processed foods, such as hamburgers, hot dogs, and pizza toppings. Spinal cord tissue has been found in such meat scraps when AMR systems were not handled properly. The new USDA rules required slaughterhouses to establish verification procedures to ensure that spinal cord and other nerve tissues do not get into meat products. Finally, the USDA banned the practice of air-injection stunning to render cattle unconscious before slaughter because the method can force skull tissue into meat tissue. See also Meatpacking Industry.
Although the USDA is responsible for inspecting meat and poultry processing in the United States, the FDA is responsible for the safety of other food products and for cosmetics. In February 2004 the FDA issued a set of interim rules designed to prevent the spread of BSE. It banned the use of any material from downer cattle in cosmetics and FDA-regulated human food, such as canned soups and pizzas and including dietary supplements. It also tightened regulations on animal feed given to cattle, prohibiting the use of mammalian blood or blood products in animal feed for ruminants. Blood from slaughtered cattle is given to calves as a substitute for cow milk so that the milk can be sold instead. The blood acts as a protein substitute, but the FDA cited scientific studies to support a claim that BSE can be spread through blood. For similar reasons the FDA banned the use of poultry litter in animal feed for ruminants. The litter consists of bedding, spilled feed, feathers, and feces collected from poultry yards and can contain ground-up tissues from slaughtered cattle.
An expert panel advising the FDA also recommended in February 2004 against using any animal remains to feed cattle, a rule that has been adopted by the EU. The rule is designed to prevent a cycle in which rendered (cooked) matter from cattle is fed to pigs and chicken that are then rendered into feed for cattle. The director of the FDA’s Center for Veterinary Medicine said there was no evidence that pigs or chicken could transmit BSE and that the advisory report conflicted with the recommendations of other experts. Consumer groups in the United States also have called for a ban on animal remains in cattle feed.
The first BSE case in the United States led about 30 nations to impose a ban on U.S. beef imports, including bans by the four top importers—Japan, Mexico, South Korea, and Canada. These nations account for 92 percent of U.S. beef exports. In late 2005 the principal importing nation, Japan, lifted its ban, but restored it almost six weeks later in January 2006 after the discovery of bone in a supply of veal from the United States.
The first U.S. BSE case was linked by DNA testing to a farm in Alberta, Canada. The first case of BSE in Canada, discovered in May 2003, also appeared in Alberta. Although the two animals originated on different farms, officials said it was likely they had eaten the same infected feed. USDA and Canadian officials noted that both animals had become infected prior to the feed ban imposed by the two countries. However, another cow in Alberta tested positive for mad cow disease in January 2006, and this cow was born after the 1997 feed ban. Canadian officials noted that no part of the cow had entered the human food system. United States officials said the discovery, the fourth confirmed case of mad cow disease in Canada since May 2003, would not lead to a new U.S. ban on Canadian cattle. In July 2005 a U.S. court had lifted the ban on importing Canadian beef from cattle younger than 30 months, although older animals continued to be prohibited.
VII QUESTIONS REGARDING THE SAFETY OF THE FOOD SUPPLY
Scientists continue to investigate whether prions can be found in animal tissue other than spinal cord, nerve, and brain tissue. In 2002 American neurologist Stanley B. Prusiner, who won the 1997 Nobel Prize in physiology or medicine for his discovery of prions, found prions in the muscles of mice infected with the scrapie prion. Prions have also been found in the muscle of hamsters and of humans with Creutzfeldt-Jakob disease. However, other experts have cited extensive testing in which muscle tissue from cows infected with BSE have been injected into other cows without passing along the infection. The future resolution of this important question depends upon the development of better tests, and such tests were in the advanced stages of development in 2004.
In November 2003 the Institute of Medicine of the U.S. National Academy of Sciences urged more funding for the study of prion diseases among animals and the threat they pose to humans. The institute emphasized the importance of developing new diagnostic tests to determine whether low levels of prions might be found in other species, such as pigs and chickens, that are fed cattle waste materials. Additionally, more research was called for to investigate the possible threat posed by the rise of chronic wasting disease, the most recently discovered prion disease, among deer and elk.
Reviewed By:
Frederick A. Murphy
Microsoft ® Encarta ® 2007. © 1993-2006 Microsoft Corporation. All rights reserved.
~Kristy~ 
