23 February 2010
Pandemic (H1N1) 2009 outbreak on pig farm, Argentina

In June–July 2009, an outbreak of pandemic (H1N1) 2009 infection occurred on a pig farm in Argentina. Molecular analysis indicated that the virus was genetically related to the pandemic (H1N1) 2009 influenza virus strain. The outbreak presumably resulted from direct human-to-pig transmission. Swine influenza viruses (SIVs) occur worldwide; they usually cause asymptomatic infection but occasionally cause outbreaks of varying intensity. In North America, the landscape of swine influenza has changed substantially since the late 1990s, when human (H3N2) viruses were first isolated from swine and triple reassortant viruses carrying influenza genes (TRIG) of avian, swine, and human origin and showing great reassortment flexibility emerged concurrently. TRIGs of influenza subtypes H3N2, H1N1, H3N1, and H1N2 appear to be circulating in swine in North America. Coincidentally, 1 of these TRIG viruses led to emergence of the pandemic (H1N1) 2009 virus. Testing by the Canadian Food Inspection Agency identified pandemic (H1N1) 2009 virus in a swine herd in Alberta. The pigs may have been exposed to the virus by a farm worker who returned from Mexico with influenza-like symptoms. Affected pigs showed clinical signs of infection with SIV.

Young pigs are susceptible to pandemic (H1N1) 2009 as reported in Canada. Recently, experimental infections showed that the pandemic (H1N1) 2009 virus induced mild clinical signs, virus shedding, and gross and histopathologic lesions similar to those caused by SIV. Successful cross-species transmission usually requires a period of adaptation to the new host. However, phylogenetic analyses of pandemic (H1N1) 2009 virus showed that the HA and NA glycoproteins arose from the classical swine (H1N1) and avian-like Eurasian swine (H1N1) lineages, respectively, which might explain the high susceptibility and transmissibility among pigs. From an epidemiologic standpoint, the 25%–30% morbidity rate with few deaths agreed with the clinical presentation of SIV (H1N1) and was similar to the rates found in the outbreak in Canada. Clinical signs lasted 1 week. However, 5% of the bronchial swabs taken 15–18 days after onset of the outbreak from slaughter-weight pigs showed positive results. Virus shedding, detected by rRT-PCR, from nasopharyngeal samples peaked at 4 days postinoculation and ceased at ≈11 days postinoculation.

Epithelial cell necrosis, sloughing, and neutrophil infiltration with total or partial obstruction of bronchioles is the hallmark of SIV infection and was distinctive for influenza A virus (H1N1). However, IHC results were strongly positive for virus antigen in only those bronchioles that showed severe bronchiolitis. Our findings from field observation confirm findings from experimental studies with pandemic (H1N1) 2009 virus. The suspected human source of infection was not confirmed. This outbreak supports the belief that influenza cross-species transmission may occur between pigs and humans and vice versa.

Emerging Infectious Diseases
February 23, 2010

Original web page at Emerging Infectious Diseases