Mad Cow Disease Essay ⋆ Environment Essay Examples ⋆ EssayEmpire

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Mad cow disease , or bovine spongiform encephalopathy (BSE), is a degenerative disease of the nervous system in cattle. It is always fatal. Cattle with BSE develop minute holes in their brains, have difficulty standing and walking, produce less milk, become irritable, and lose weight. The disease has an extended incubation period. Symptoms usually appear four to five years after infection, and death often occurs within weeks of symptom onset.

BSE belongs to a group of diseases called transmittable spongiform encephalopathies (TSEs). Other TSEs include scrapie in sheep, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob Disease in humans. TSEs can spontaneously arise in individual animals or can occur due to genetic mutations. They are believed to occur when certain cellular proteins, called prions, become misshapen. The misshapen prions then alter the shape of other prions. These proteins clump in the cells and damage nervous tissue. They are difficult to destroy: Heat, UV light, radiation, and disinfectants that destroy infectious agents such as bacteria and viruses do not destroy prions.

BSE was first seen in Great Britain in 1985 and was recognized as a disease in 1996. There are two lines of thought regarding its origin in Britain. Some researchers think the disease was passed to cattle in feed containing the remains of sheep infected with scrapie. Other researchers question this, because the prions of scrapie differ from those of BSE, and suggest the disease arose spontaneously in a single animal.

Whatever the origins of the disease, feeding practices in the United Kingdom (UK) allowed BSE to become established. Meat and bone meal, made from the remnants of animals after butchering, were routinely used as protein supplements in cattle feed. When meat and bone meal from infected animals entered this food chain, the disease spread throughout the UK. Changes in the processing methods for meat and bone meal in the early 1980s, which lowered the heat compared to that used in previous methods, may have led to a higher incidence of the prions in cattle feed. Cattle are not infected with BSE through contact with an infected animal.

The number of confirmed cases of BSE in the UK reached 14,000 by 1990, and 181,376 by 2002. In addition to the UK, infected cattle have been discovered in European, North American, and Asian countries. In 2003 the first cases of BSE were reported in both Canada and the United States.

To contain the outbreak, British cattle thought to be infected were slaughtered, and feeds containing remains of sheep and cattle were banned in the UK. Other countries took similar measures. In addition, some nations banned the import of cattle or beef from countries where BSE is known to have occurred. BSE is decreasing. The disease killed a reported 878 cattle worldwide in 2004 and 474 in 2005.

Since the mad cow epidemic began, a new TSE has been discovered in humans: variant CreutzfeldtJakob Disease (vCJD). It was first reported in 1996. It appears that vCJD is caused by eating beef from BSE infected cattle. Most infected individuals are known to have consumed tainted beef in Britain. The prions are similar, as are the patterns of brain damage seen in victims of BSE and vCJD. Victims of vCJD are usually young. The incubation period for vCJD can be as long as ten years. Death occurs, on average, 12-14 months after symptoms appear. Symptoms include depression, difficulty walking, shakiness, a sensation of sticky skin, dementia, and eventually muteness, the inability to move, and death. A cure for vCJD has not been found.

As of 2006, the UK’s National Creutzfeldt-Jakob Disease Surveillance Unit reported 158 confirmed and suspected vCJD deaths in the UK. An additional six living individuals are thought to be infected. Seven deaths have occurred in France, plus one death each in Canada, the United States, Ireland, and Italy. Other individuals may be incubating vCJD.

Bibliography:

Paul Brown, “Mad Cow Disease in Cattle and Human Beings,” American Scientist (July-August 2004);
Stanley Prusiner, “Detecting Mad Cow Disease,” Scientific American (July 2004).