The Problem with Pigs: It's Not about Bacon

Abstract

In this issue of Clinical Infectious Diseases, Forgie et al [1] offer the most compelling documentation to date of the introduction of a human influenza virus into a pig herd and subsequent related influenza epidemics in both pig and human populations. Although their article could be criticized, because nasal swab specimens from pigs were not taken to prove that the virus was not already enzootic before the likely human index case, circumstances and investigational data strongly support the authors’ interpretation of the data. The event occurred at a closely monitored Canadian swine research facility, where biosecurity and laboratory support had protected the pig herd from other common swine respiratory infections. The authors’ position that this was an acute and explosive human introduction of pandemic influenza A (H1N1) virus (pH1N1) in a modern swine facility was supported by the chronology of the signs in the pigs and signs and symptoms in the swine workers, the serologic investigation in the workers, the molecular detection of pH1N1 in pigs and the workers, and the subsequent genomic comparisons of the influenza A isolates. The authors’ report is also remarkable because it demonstrates that preclinical asymptomatic shedding of influenza A virus can circumvent even our best policies and biosecurity infrastructure. As we have clearly seen with the rapid international and interspecies spread of pH1N1, nonpharmaceutical interventions may slow transmission of such novel influenza A virus strains, but in the long term, such strains beat our best efforts. The report reinforces our understanding that this particular strain is often associated with subclinical infections in both humans and pigs. The authors’ observation that 94% of pH1N1-infected pigs had no clinical signs is consistent with a recent report in which 64% of influenza A virus–naive Norwegian swine herds showed no signs of infection after pH1N1 was introduced[2]. Furthermore, pH1N1 infections in pigs are transient, and experts agree that they do not threaten the safety of meat consumption. This supports the US pork industry’s position that influenza A virus is not a substantial problem for the swine industry; infections are not reportable and, therefore, not a matter of their concern. In fact, misunderstandings of the public health risk of pH1N1 detection in pigs caused considerable fiscal damage to pork production at the beginning of the 2009 H1N1 pandemic. One can understand why the pork industry is unlikely to adapt influenza surveillance policies like those of the US poultry industry. The figure provided by Forgie et al [1] clearly documents what other reports have only hinted at—the explosive nature of viral transmission among pigs in modern, confined animal feeding operations (CAFOs). We know from limited veterinary studies of Canadian pigs that swine influenza virus strains are most prevalent in areas where large herds of pigs are densely confined [3]. This is biologically plausible, because large CAFOs with numerous pig barns have weekly introductions of young immunologically naive pigs necessary to sustain influenza A infection. Despite various biosecurity and animal husbandry measures in these large facilities (eg. ‘‘all in all out’’ cohorting), influenza A virus strains often are detected in these herds. Mathematical models and epidemiological studies of swine workers have suggested that workers can serve as a bridging population to introduce the influenza A virus strains that are being amplified in the CAFOs to their surrounding human communities [4–7]. With assumptions similar to that of the 1918 pandemic virus, Saenz et al [4] found that such bridging could markedly accelerate influenza virus Received 14 September 2010; accepted 17 September 2010. Correspondence: Gregory C. Gray, Dept of Environmental and Global Health, College of Public Health and Health Professions, University of Florida, Box 100188, Gainesville, FL 32610 (gcgray@phhp.ufl.edu). Clinical Infectious Diseases 2011;52(1):19–22 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. 1058-4838/2011/521-0001$37.00 DOI: 10.1093/cid/ciq051