Mad Cow Disease

Mad cow disease, also known as bovine spongiform encephalopathy is a brain wasting disease affecting cattle and humans. Once contracted, it is invariably fatal. The disease primarily affects cattle and is perpetuated by industrial animal husbandry practices; namely, feeding cattle by-products to other cattle. It is not thought to spread among livestock any other way. The disease has been observed in cattle in Britain since 1985, and as early as 1996 there were reported cases of a human disease, variant Creutzfeldt-Jakob disease (vCJD), which had many of the same symptoms but an unknown cause. The British government reassured the public that the two diseases were not related until 2000, when they reported a link between them: The newly described human disease was indeed likely caused by mad cow disease. That later announcement caused public panic. The human outbreak sparked conversations throughout Europe and North America about animal husbandry and food safety, elevating concern about food systems and ultimately changing international policies and trade practices. Because scientists and regulators had repeatedly assured the public that humans were not susceptible to the disease before announcing the opposite, the episode changed cultural ideas about the role and validity of scientific knowledge. The epidemic among both cattle and humans has been most sizable in the United Kingdom. As of December 2008, 210 people had been diagnosed with vCJD, the human form of the disease, and affected cattle have been found in most countries that have instituted monitoring programs.

Mad cow is in a class of diseases known as transmissible spongiform encephalopathies (TSEs). Other TSEs include scrapie in sheep and goats, kuru in humans, and chronic wasting disease in deer and elk. These diseases are communicable to varying extents, and some are able to affect other species. Unlike most communicable diseases, which are spread by viruses and bacteria, TSEs spread via exposure to a misshapen protein, called a prion. The way TSEs spread was initially disputed because it differs from standard explanations of disease, but scientists have gradually come to accept prion theory. Prions are found in all mammals and do not cause problems in most situations. When exposed to misshapen prions, however, healthy prions can change their folding pattern and themselves become misshapen. When this occurs, plaques of misshapen prions form in the central nervous system, creating holes in the brain material (thus the “spongiform” in the name).