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

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 PrP(res) 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.

Estimation of the Exposure of the UK Population to the Bovine Spongiform Encephalopathy Agent through Dietary Intake During the Period 1980 to 1996

“…Based on the dose-response curve observed in mice, Fryer and McLean conclude that there is no evidence of the existence of such a threshold [38]. However, if this were the case in humans, the number of vCJD cases would have been far more than what has been observed to date, given our exposed individual estimate and the exponential growth rate of abnormal prions in the brain once infected [35]. The close model fitting to the observed vCJD cases justifies the threshold hypothesis.…”

A review of research on plant‐based meat alternatives: Driving forces, history, manufacturing, and consumer attitudes

“…Meat-borne infections are also a health concern associated with meat consumption, such as the variant Creutzfeldt-Jakob disease, which is believed to be caused by the transmission of pathogens from bovine spongiform encephalopathy-contaminated beef products to humans (Chen, Wang, & Wu, 2013). The outbreak of the viral African swine fever in countries such as China between 2018 and 2019 is another example of a potential infection from meat consumption (Zhang, Hayes, Ji, Li, & Zlong, 2019;Zhou et al, 2018).…”

Prion disease risk uncertainties associated with urine-derived and recombinant fertility drugs

“…Evidence suggests variant CJD (vCJD) may occur due to transmission of prions from cattle to human through the consumption of contaminated meat products derived from affected cattle in the food chain (Brown, 2001;Bruce, 2000;Chen et al, 2013).…”

“…Prion proteins were found to be excreted from infected animals through multiple routes including skin, feces, urine, saliva, blood, milk, placenta and nasal secretions (Gough and Maddison, 2010). Potential routes of transmission for developing human prion disease include surgical procedures, blood transfusion, injection of contaminated cadaveric human growth hormone and consumption of contaminated meat products (Chen et al, 2013;Hamaguchi et al, 2009;Puopolo et al, 2011;Croes et al, 2002).…”