This paper examines Bovine Spongiform Encephalopathy (BSE), commonly known as Mad Cow Disease, tracing its origins in the United Kingdom during the 1980s and 1990s to its emergence as a global public health concern. Drawing on scientific explanations of prion biology and disease transmission, the paper covers BSE's link to Creutzfeldt-Jakob Disease (CJD) and its new variant (nvCJD), the international spread through contaminated animal feed, and the regulatory responses of British, European, and U.S. authorities. It also critically evaluates the adequacy of U.S. testing standards, slaughtering practices, and loopholes in animal feed regulations, arguing that the risk to American consumers may be greater than official assurances suggest.
The paper demonstrates the technique of moving from description to critical analysis: it first explains what BSE is and how it spreads, then uses that framework to evaluate the adequacy of official responses. By quantifying the scale of U.S. testing (e.g., only 5,000 of 99 million cattle tested in 2001) against European benchmarks, the author constructs a data-driven argument about regulatory insufficiency without overstating the claim.
The paper opens with the historical crisis context, then provides a scientific primer on BSE and prion biology. A mid-section covers international spread and economic consequences. The paper then transitions to regulatory responses before dedicating its longest section to critiquing gaps in U.S. safeguards — covering feed rules, testing frequency, slaughter techniques, dietary supplements, blood safety, and alternative causal theories. The conclusion is implicit, embedded in the accumulation of risk evidence rather than a separate closing paragraph.
During the 1980s and 1990s, an unknown but virulent cattle disease called "Mad Cow" destroyed 180,000 livestock in the United Kingdom and some other European countries, plunging major cattle-producing nations — including the United States — into global panic (Freudenrich 2004). Health experts initially assured the public that humans were not susceptible to it. Nonetheless, its symptoms resembled those of an already existing and similarly deadly human nervous condition called Creutzfeldt-Jakob Disease (CJD), believed at the time to afflict only those 50 years old and older. CJD was linked to Mad Cow Disease but was thought to be limited to older populations.
In the mid-1990s, however, several young British people died of a new variety of disease with symptoms similar to both Mad Cow and CJD — this time affecting the young, and designated as new variant CJD (nvCJD). Throughout those troubled years, contaminated British cattle were exported to numerous countries, including the United States, as animal products and by-products (University of Wisconsin Board of Regents 2001).
Bovine Spongiform Encephalopathy (BSE), commonly known as Mad Cow Disease, is a fatal brain disorder in cattle caused by a still-unknown agent (Freudenrich). When activated, this agent kills brain cells and leaves large spongy holes and large clumps of abnormal prion proteins, or plaques, similar to those found in Alzheimer's disease. The disease runs its course and kills the infected host in less than a year. The BSE agent can spread among species that ingest the brain or other nervous tissue of infected animals or animal by-products. Once taken in, the infectious agent can remain dormant in the body of the host for up to 10 to 15 years before it is activated (Freudenrich). Only then will symptoms manifest and control measures be taken. These symptoms include weight loss, abnormal behavior such as skittishness, paralysis, and ultimately death (Freudenrich).
Only a few things are known about BSE. It is smaller than a virus and requires temperatures far higher than those used in ordinary cooking or sterilization in order to be destroyed. Ordinary chemical disinfectants are not effective against it, and it appears to contain no genetic information (Freudenrich) — unlike infectious nucleic acids — that could provide a clue to its control.
A similar disease among sheep, called scrapie, occurring in the 1980s was initially blamed for BSE. Cattle feed was being made from ground meat and bone meal by-products from sheep. A later change in processing methods could have allowed scrapie to survive and contaminate cattle that fed on the resulting meal, leading to the emergence of BSE. Although neither scrapie nor BSE can directly affect people, unknowing ingestion of the nervous tissues of infected cows through the food supply led to the development of CJD in elderly people and nvCJD in younger people.
The disease spread to cattle in other countries through infected animal feed that the UK exported within that decade. European countries confirmed as having at least one infected cow included Belgium, Canada, the Czech Republic, Denmark, France, Germany, Greece, Ireland, Italy, Luxembourg, Liechtenstein, the Netherlands, Portugal, Spain, and Switzerland (Lohn). The UK also supplied animal feed to South Africa and other non-European countries during that period, extending the reach of Mad Cow beyond Europe and making it a global health scare.
The British health minister's shattering public admission in 1996 — that British beef infected with Mad Cow had probably caused the new variant of CJD — destroyed sales of British beef around the world (Lohn). The admission gave a significant economic and political advantage to the United States as a world-leading meat-exporting nation, provided the U.S. government could assure international markets that its cattle were free of Mad Cow Disease. As of December 2003, there were 153 reported cases worldwide; 149 of these were in the United Kingdom, with the remainder having acquired the disease while in the UK.
Biochemist Stanley Prusiner suggested that Mad Cow, scrapie, and nvCJD are all forms of transmissible spongiform encephalopathies (TSEs), which develop from abnormal proteins called prions (University of Wisconsin Board of Regents). His view soon gained broad acceptance. Prions are not nucleic acids and therefore do not possess DNA or RNA that could reveal their biological processes. Normal proteins are harmless (Lohn), but researchers believe that prions induce normal proteins to replicate their abnormal form. These prions accumulate in the lysosomes of nerve cells, which eventually die (Freudenrich). The death of many nerve cells leads to brain dysfunction and, ultimately, the death of the host.
A person contracts nvCJD by consuming the products and by-products of infected cattle, even from small parts such as the brain, spinal cord, gut, or bone marrow. These small parts may be added as ingredients in candies, cosmetics, shampoo, gelatin, yogurt, ice cream, mints, gummy candies, margarine, lotions, and bone meal used in gardening (Lohn).
UK reports also listed other animals as having been infected by TSEs, including domestic cats, mice, hamsters, goats, mink, monkeys, pigs, and some exotic members of the cat family. More than 80 domestic cats in the UK were reported to have been afflicted with the feline version of Mad Cow after being fed pet food made from animals with BSE or similar diseases (Lohn). This raises concern about how one infected domestic animal might pass the disease on to other animals in the home and neighborhood.
British neurologist John Collinge experimented on mice that were found to be infected with prions but showed no symptoms of disease. His findings drew attention to the danger posed by "silent carriers" of TSEs (University of Wisconsin Board of Regents) — animals that harbor the infection without yet manifesting their species' version of the disease.
You’re 45% through this paper. Sign up to read the remaining 3 sections.
Sign Up Now — Instant Access Already a member? Log inAlways verify citation format against your institution’s current style guide requirements.