Mad cow disease has several different names. It is called Bovine Spongiform encephalopathy or BSE. Other names are New Variant Creutzfeldt-Jakob disease or vCJD (Morris). Transmittable Spongiform encephalopathy or TSE is another name. Spongiform encephalopathies are nervous system disorders which nerve cells of the brain die, causing the brain to assume a sponge-like appearance (Montague, Part 1). In 1985 a veterinarian found odd symptoms in a cattle (Morris). Cows in Britain began to die of mysterious ailments (Montague, Part 1). German physicians Hans Gerhard Creutzfeldt and Alfons Jakob first discovered vCJD in its natural form in the 1920’s (Shell, Part 2). In 1996 British government conceded that people were falling victim to a degenerate new brain disease linked to BSE (Morris).

Mad cow disease has a severe effect on animals. The infamous disease has increased 23 percent a year in Britain since 1994 (ABC News). As of June 30th 2000, 75 cases have been confirmed or suspected of having the disease. Of those 75 cases, 64 people have died (CNN News). Symptoms of the disease can vary. Loss or coordination, personality changes, mania and dementia are most common (Shell, Part 2). Symptoms may not even be seen. Many cows can be carrying the infection silently (Montague, Part 1). The disease can be unnoticed for thirty to forty years (Morris). It will eventually kill. Infected cows will stagger, drool, and show signs of fear, grind their teeth, exhibit aggressiveness toward other animals and their ears twitch (Montague, Part 1). A protein called Prion causes TSE. Prion is normal proteins, present in all mammals and some non-mammalian species. All TSE diseases have similar characteristics. They attack the central nervous systems, causing disintegration of the brain (Montague, Part 3). Mad cow disease has led to the slaughtering of 3.7 million cattle. It is leading to the near destruction of Great Britain’s cattle industry. A similar epidemic in the United States would be even more of catastrophic than Britain’s outbreak (Shell).

Bibliography Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD. Molecular Biology of the Cell, 3rd Edition. New York: Garland Publishing, Inc., 1994. Chesebro, B. 1998. BSE and prions: Uncertainty about the agent. Science 279: 42-43. Cousens, S. N., et al. 1998. Predicting the CJD epidemic in humans. Nature 385: 197-198. Harris DC. Quantitative Chemical Analysis, 5th Edition. New York: W.H. Freman and Company, 1999. Grolier. 1996. Ithaca, NY: GeoSystems Global Corporation, CD-ROM Karow, Julia. 2000. Stoppling Prions from Going Mad. Scientific American. Karp, Gerald. 1999. Cell and Molecular Biology: Concepts and Experiments 2nd ed., New York. John Wiley & Sons, Inc. Prusiner, S. B. 1995. The prion disease. Scientifique American. 271:77-83. (Oct.) Prusiner, S. B. 1997. Prion disease and the BSE crisis. Science 278: 245-251 Purves, William K., Orians, Gordon H., Heller, Craig. 1998. Life, the science of biology—5th ed, Salt Lake City. Sinauer Associates.

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