Get access

Consumption of Bovine Spongiform Encephalopathy (BSE) Contaminated Beef and the Risk of Variant Creutzfeldt-Jakob Disease

Authors

  • Chu-Chih Chen,

    Corresponding author
    1. Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan
    • Address correspondence to Chu-Chih Chen, Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, 35 Keyan Road, Zhunan, 350, Taiwan; ccchen@nhri.org.tw. Kuen-Yuh Wu, Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, 17 Xu-Zhou Road, Taipei, 100, Taiwan; kuenyuhwu@ntu.edu.tw.

    Search for more papers by this author
  • Yin-Han Wang,

    1. Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan
    Search for more papers by this author
  • Kuen-Yuh Wu

    Corresponding author
    1. Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, Taipei, Taiwan
    • Address correspondence to Chu-Chih Chen, Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, 35 Keyan Road, Zhunan, 350, Taiwan; ccchen@nhri.org.tw. Kuen-Yuh Wu, Institute of Occupational Medicine and Industrial Hygiene, College of Public Health, National Taiwan University, 17 Xu-Zhou Road, Taipei, 100, Taiwan; kuenyuhwu@ntu.edu.tw.

    Search for more papers by this author

Abstract

To date, the variant Creutzfeldt-Jakob disease (vCJD) risk assessments that have been performed have primarily focused on predicting future vCJD cases in the United Kingdom, which underwent a bovine spongiform encephalopathy (BSE) epidemic between 1980 and 1996. Surveillance of potential BSE cases was also used to assess vCJD risk, especially in other BSE-prevalent EU countries. However, little is known about the vCJD risk for uninfected individuals who accidentally consume BSE-contaminated meat products in or imported from a country with prevalent BSE. In this article, taking into account the biological mechanism of abnormal prion PrPres aggregation in the brain, the probability of exposure, and the expected amount of ingested infectivity, we establish a stochastic mean exponential growth model of lifetime exposure through dietary intake. Given the findings that BSE agents behave similarly in humans and macaques, we obtained parameter estimates from experimental macaque data. We then estimated the accumulation of abnormal prions to assess lifetime risk of developing clinical signs of vCJD. Based on the observed number of vCJD cases and the estimated number of exposed individuals during the BSE epidemic period from 1980 to 1996 in the United Kingdom, an exposure threshold hypothesis is proposed. Given the age-specific risk of infection, the hypothesis explains the observations very well from an extreme-value distribution fitting of the estimated BSE infectivity exposure. The current BSE statistics in the United Kingdom are provided as an example.

Ancillary