Ebola Virus as a Foodborne Pathogen? Cause for Consideration, but Not Panic

Abstract

In this issue of the Journal, Kobinger et al [1] report on experimental infection of common domestic pigs with Ebola virus (EBOV). What possessed them to perform this seemingly odd experiment? The answer lies in a closer look at various species of the virus and recent findings from the field. There are 5 species of EBOV with a range of pathogenicity in humans; on one end of the spectrum is Zaire EBOV (ZEBOV), the quintessential ‘‘hot zone’’ EBOV, associated with case fatality ratios up to 90%. On the other end is Reston EBOV (REBOV), which does not appear to be pathogenic to humans. REBOV has always been the outlier among EBOVs, genetically distinct, with .40% nucleotide sequence divergence from ZEBOV for the glycoprotein gene [2, 3], which is thought to play a crucial role in pathogenesis [4]. Although ZEBOV and the other species are endemic in Africa, until 2008 all REBOV infections had been traced to monkeys in or imported from a single breeding facility in the Philippines [5–8]. The site was finally shuttered in 1997, and REBOV disappeared until 2008, when it resurfaced in domestic pigs on 2 Philippine farms within a few hundred miles of the closed monkey breeding facility [9]. The pigs had a respiratory disease but were coinfected with porcine reproductive and respiratory syndrome virus, so it was not possible to definitely attribute their disease to REBOV. It is not known how the pigs became infected, but it is reasonable to suppose that is was from exposure to fruit bats, the likely reservoir for EBOV [10]. The REBOV epizootic in pigs effectively answers some lingering questions, including whether this virus is truly endemic in the Philippines (apparently so), rather than somehow introduced from Africa, and whether REBOV is pathogenic to humans (apparently not, with some caveats discussed below). As is usually the case in science, however, answers bring about new questions. The pig epizootic was the first recorded instance of any EBOV in livestock [11]. What does this finding mean about the safety of our food and the people providing it? The work of Kobinger et al [1] provides some answers, showing that (1) domestic pigs can be infected with ZEBOV via the nasogastric mucosa; (2) infection in pigs causes a respiratory disease that can be severe; (3) virus replicates in cells of the upper airway and is shed in respiratory secretions; (4) sick pigs can transmit the virus to naive animals; and (5) histopathologic findings in the experimentally ZEBOV-infected pigs are very similar to those found in the pigs coinfected with REBOV and porcine reproductive and respiratory syndrome virus in the Philippines [9]. What are the ways in which EBOV might pose a threat to us through our food chain? Pigs are unlikely to be an integral part of the natural maintenance of EBOVs, but could they serve as accidental hosts transmitting REBOV or even ZEBOV to humans? Serologic evidence of past REBOV infection in 6 workers on the pig farms in the Philippines [9], all of whom denied any contact with bats or monkeys, strongly suggests this possibility [12]. The parallels are striking with the 1998–1999 outbreak of Nipah virus in Malaysia and Singapore, in which infected pigs developed a respiratory syndrome and transmitted the virus to humans, who developed the now well-described Nipah virus encephalitis [13]. The pigs were presumed to be infected through direct or indirect contact with Pteropus bats, later shown to be the Nipah virus reservoir [13]. What might be the risk from infected meat? ZEBOV transmission to humans has been clearly documented in central Africa through the hunting, butchering, Received 9 November 2010; accepted 9 November 2010. Potential conflicts of interest: none reported. Correspondence: Daniel G. Bausch, MD, MPH&TM, Department of Tropical Medicine, SL-17, 1430 Tulane Ave, New Orleans, LA 70112-2699 (dbausch@tulane.edu). The Journal of Infectious Diseases The Author 2011. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com 0022-1899 (print)/1537-6613 (online)/2011/00-0001$14.00 DOI: 10.1093/infdis/jir201