Bovine spongiform encephalopathy historical perspective
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Adnan Ezici, M.D[2]
Overview
Overview
Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD. The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called prions developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of organophosphorus pesticides increased the susceptibility of cattle to the disease. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989. It is believed that the disease may be transmitted to human beings who eat infected carcasses. In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere with the number expected to rise because of the disease’s long incubation period.
Historical Perspective
Historical Perspective
- Publius Flavius Vegetius Renatus records cases of a disease with similar characteristics in the 4th and 5th Century AD.[1]
- A British inquiry into BSE concluded that the epidemic was caused by feeding cattle, who are normally herbivores, the remains of other cattle in the form of meat and bone meal (MBM), which caused the infectious agent to spread.[2][3] The origin of the disease itself remains unknown. The current scientific view is that infectious proteins called prions developed through spontaneous mutation, probably in the 1970s, and there is a possibility that the use of organophosphorus pesticides increased the susceptibility of cattle to the disease.[4] The infectious agent is distinctive for the high temperatures it is able to survive; this contributed to the spread of the disease in Britain, which had reduced the temperatures used during its rendering process.[2] Another contributory factor was the feeding of infected protein supplements to very young calves.[2][5]
- It is believed that the disease may be transmitted to human beings who eat infected carcasses.[6] In humans, it is known as new variant Creutzfeldt-Jakob disease (vCJD or nvCJD), and by June 2007, it had killed 165 people in Britain, and six elsewhere[7] with the number expected to rise because of the disease’s long incubation period. Between 460,000 and 482,000 BSE-infected animals had entered the human food chain before controls on high-risk offal were introduced in 1989.[8]
References
References
- ↑ Digesta Artis Mulomedicinae, Publius Flavius Vegetius Renatus
- ↑ 2.0 2.1 2.2 “BSE: Disease control & eradication – Causes of BSE”, Department for Environment, Food, and Rural Affairs, March 2007.
- ↑ “The BSE Inquiry”, led by Lord Phillips of Worth Matravers, report published October 2000.
- ↑ “Volume 1: Findings and Conclusions. Executive Summary of the Report of the Inquiry. 3. The cause of BSE”, Phillips Inquiry, October 2000.
- ↑ Harden, Blaine. “Supplements used in factory farming can spread disease”, The Washington Post, December 28, 2003.
- ↑ Commonly Asked Questions About BSE in Products Regulated by FDA’s Center for Food Safety and Applied Nutrition (CFSAN) US Food and Drug Administration. September 14 2005. Accessed August 21 2007.
- ↑ “Variant Creutzfeld-Jakob Disease, June 2007”, The National Creutzfeldt-Jakob Disease Surveillance Unit, Edinburgh University. The number of dead in the UK from Creutzfeld-Jakob Disease had reached 1,206 by June 4, 2007.
- ↑ “CJD deaths ‘may have peaked'”, BBC News, November 13, 2001.
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