A 7-month-old boy was admitted to the hospital on September 10, 2006, with a 3-day history of fever, rhinitis, and cough. He had had no previous contact with ill persons. The child was born at term and was hospitalized for 21 days at 5 weeks of age when he received ventilation for 6 days for pneumonia due to respiratory syncytial virus. He lived on a communal farm (90 occupants) with horses, cows, swine, sheep, dogs, cats, turkeys, geese, ducks, and chickens but had no direct contact with the animals. The swine were contained in barns and did not mix with the other animals. His household contacts did not work directly with animals, but his father occasionally spent time in the barns, and his uncle, who lived next door, worked in the swine barns.

On admission, the child was afebrile with a heart rate of 120 beats/min, respiratory rate 56/min, and oxygen saturation of 85% on room air. Diffuse wheeze was noted. Chest radiograph results were unremarkable. Direct fluorescent antibody testing on a nasopharyngeal aspirate was positive for influenza A, and the virus was isolated in rhesus monkey cell culture. The isolate was sent to the National Microbiology Laboratory for influenza subtyping as a requirement of the Canadian influenza surveillance program, where it was subsequently designated A/Canada/1158/2006. The child stayed in the hospital for 2 days and then made an uneventful recovery at home. A cough and rhinitis developed in his 19-month-old brother on the day the index patient was admitted to the hospital, but the brother was not assessed by a physician.

We describe an infant with virologic and serologic evidence of infection with SIV (H3N2) and an ILI. Serologic evidence of infection with the same strain was found in 4 of 7 household members and in 3 of 46 nonhousehold contacts, with only 1 of the seropositive patients having a history of an ILI within the preceding year, which demonstrated unrecognized human infection with SIV. This relatively high seroprevalence is in contrast to a recent outbreak of avian influenza (H7N3) in which seropositivity was not documented in 91 persons exposed to infected poultry, including 2 poultry workers from whom the virus was isolated (12). The difference in the apparent incidence of infection may be explained in part by the fact that culling of infected poultry occurred immediately; in our study, infection of swine was not recognized and long-term human exposure may have occurred.

Infection of swine with human influenza viruses has been recognized for decades (2); in a recent US study, 22.8% of pigs were seropositive for human influenza viruses, although some may have had vaccine-induced immunity (13). Swine influenza (H3N2) emerged in 1998 in the United States, where subtype H1N1 viruses had predominated for 60 years (2). The isolate from this current study is closely related to triple reassorting genotype viruses that spread rapidly throughout the US swine population and have HA, NA, and RNA polymerase (PB1) genes of human influenza virus lineage; nucleoprotein, matrix, and nonstructural genes of classic swine influenza (H1N1) lineage; and RNA polymerase (PA and PB2) genes of North American avian virus lineage (8). However, triple reassortant SIV was not documented in swine in Canada until 2005 (8), which makes it unlikely that human cases occurred before that year and that seroreversion had occurred in any of the persons in the current serosurvey.

A previous study showed cross-reactivity in HI assay between the vaccine strain A/Panama/2007/99 reference antiserum and the triple reassortant A/swine/Minnesota/593/99, which is not unexpected since the HA gene of the triple reassortant viruses is a descendant of human viruses that circulated in 1995 (14,15). However, no cross-reactivity was observed between the reference human strain antiserum and the isolate from this study, which suggests that the seroconversion observed was indeed due to infection with swine influenza (H3N2) and not to cross-reactive antibody to human influenza (H3N2) infection. The low rate of seropositivity to recently circulating strains of human influenza in the study is likely explained by the fact that the farm is a relatively closed community. The child who was seropositive for both human and swine influenza viruses was likely exposed to both viruses. The HA protein of A/Canada/1158/2006 diverges significantly from the one of A/Wisconsin/67/2005, and antiserum against A/Wisconsin/67/2005 does not inhibit A/Canada/1158/2006 in HI assay.

Swine influenza (H3N2) has recently reassorted with H1N1 strains to produce H1N2 subtypes and has spread to turkeys in the United States (16) and Canada (8). A 4-aa deletion was found in the HA protein of A/Canada/1158/2006 when compared with similar swine influenza (H3N2) strains currently circulating in North America. This region of the protein has been assigned to antigenic sites (17) and has been associated with adaptation to growth in eggs (18). Phylogenetic analysis showed that each of the 8 viral genes of A/Canada/1158/2006 clustered with A/swine/Ontario/33853/2005 (H3N2) and other swine/turkey Canadian isolates from 2005. Although the HA gene of these isolates were shown to be closely related to American viruses that were first isolated from pigs in 1999, they represent a new distinct cluster (2). The NA genes are phylogenetically distinct from the US swine isolates and are represented by human influenza (H3N2) isolates from Asuncion, Paraguay (2001), and New York (2003) (2).

A recent review described 50 cases of symptomatic human infection with SIV, documented in the literature through April 2006; 46 cases were infected with subtype H1N1 and 4 were infected with subtype H3N2 (19). The spectrum of pathogenicity of SIV infection ranges from asymptomatic infection (6) to death; 7 of these 50 patients died (5,20–24). Laboratory-confirmed swine influenza in humans may be “the tip of the iceberg.” Diagnosis of the current case was serendipitous because typing was performed only because the case occurred outside of influenza season.

The mode of spread of SIV in humans is not established. Because of his young age, the index patient was not likely to have had unrecognized direct contact with swine. That aerosolization of influenza virus occurs is increasingly recognized (25), but the child was reportedly never in the barns that housed the swine. However, other members of the farm reported that infants were sometimes taken for walks through the barn. The child also may have acquired the virus from person-to-person spread or from fomites. All 13 patients in the Fort Dix outbreak and 15 of 37 previously reported civilian case-patients also had no swine contact (19,20).

The Fort Dix outbreak of SIV in humans lasted only 21 days and never spread outside the military base. The calculated basic reproductive rate (R₀) was only 1.1 to 1.2. This suggests that person-to-person spread of the implicated H1N1 strain was not efficient enough to produce a major epidemic (26). However, future strains of SIV could have a higher R₀, and documentation of a case of swine influenza (H3N2) in a child with unrecognized transmission within the community adds another possible mechanism by which major epidemics of influenza could arise. Swine influenza infection in humans most commonly results in either no symptoms or a self-limited illness (6). However, routine surveillance for cases among swine workers may enable early detection of a strain with the potential for person-to-person transmission, prompting institution of infection control measures and vaccine development.