Editorial Commentary:This Little Piggy Went to Market—but Perhaps Should Have Stayed Home (2015)

Influenza A is a zoonotic disease. Although some causative viruses have become adapted to humans and circulate exclusively in this host, the animal reservoirs are the source of all past and future pandemic strains. With this knowledge, there has been decades of research toward identifying the interfaces where infected animals and humans are most likely to interact. A particular target of these studies has been live bird markets, particularly in Asia. While the importance of these markets had been previously recognized [1], the H5N1 outbreak in Hong Kong in 1997, where 6 of 18 persons known to be infected with the virus died, refocused much of influenza’s public health attention [2]. Live bird markets provide a prime environment to support the evolution of influenza A viruses and promote human infection. Not only are different hosts of influenza—including humans— each with their own variants of the virus, brought together in unnatural proximity, but as fresh animals are introduced to replenish stocks, new susceptible hosts are made available, allowing the virus to spread and be maintained for prolonged periods. The importance of live bird markets in the ecology of influenza was again highlighted in 2013 when human H7N9 infections were detected in China [3]. The correlation between the closing of the market systems and the drop-off in human cases suggested markets as the likely source of infection. Although mammalian species have been present in some of the markets studied, the majority of influenza work has centered on the role of the avian species. In this issue of Clinical Infectious Diseases, Choi and colleagues have provided convincing evidence that animal markets that sell swine present another active interface in which infected animals and humans interact and where zoonotic infections occur [4]. Surprising to many will be the fact that these markets are located not in Asia, but in the United States. In what is a textbook example of collaboration between academia and veterinary and public health, this team of investigators undertook a 12-week surveillance program in 2 mixed-species markets in the state of Minnesota targeting swine, environmental surfaces, and employees. The 2 markets were selected based on epidemiologic evidence that suggested them as possible sources for prior zoonotic influenza infections. Although a number of interesting observations were made and detailed in the manuscript, one striking finding was the surprisingly high level of influenza virus detected in market employees. Eleven of the 17 employees tested positive at least once for the presence of influenza virus RNA during the 12-week period. Although half of these positive samples were unsubtypable due to viral load issues, 4 were confirmed to be H3N2 viruses of swine origin, with the remaining 7 being seasonal H3N2 influenza viruses. The relatively high detection of H3N2 viruses of swine origin in the employees is a challenge to interpret. Real-time reverse transcription polymerase chain reaction (PCR) cycle threshold values were all high, and it is possible that detections represented true viral infection or, alternatively, fomite contamination of the nasal cavity. Influenza viruses were detected in pigs, air samples, pen railings, and other environmental surfaces in the markets, and there was a marked lack of clinical symptoms reported, indicating that the latter is a real possibility. Regardless, the fact that virus genetic material was detected in nasal cavities demonstrates ample exposure and, at minimum, a threat of infection. Unfortunately, the high degree of antigenic similarity between many of Received 14 July 2014; accepted 19 July 2015; electronically published 29 July 2015. Correspondence: Richard Webby, PhD, Department of Infectious Diseases, St Jude Children’s Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105 (richard.webby@ stjude.org). Clinical Infectious Diseases 2015;61(9):1363–4 © The Author 2015. 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. DOI: 10.1093/cid/civ620