Pandemic (H1N1) 2009 Virus on Commercial Swine Farm, Thailand

A swine influenza outbreak occurred on a commercial pig farm in Thailand. Outbreak investigation indicated that pigs were co-infected with pandemic (H1N1) 2009 virus and seasonal influenza (H1N1) viruses. No evidence of gene reassortment or pig-to-human transmission of pandemic (H1N1) 2009 virus was found during the outbreak.


I n April 2009, a novel swine origin infl uenza A (H1N1)
virus, now referred to as pandemic (H1N1) 2009 virus, emerged in humans in Mexico and the United States and spread worldwide (1). In May 2009, pandemic (H1N1) 2009 was confi rmed in 2 patients in Thailand who had a history of travel to Mexico. Shortly after emergence of this virus, reports of transmission from humans to pigs on pig farms were documented (2,3). Human-to-pig transmission of this virus was reported in Thailand on December 17, 2009 (www.dld.go.th/dcontrol/Alert/Ah1n1/H1N1%20 update22_12_2009.pdf). Pigs showed mild respiratory signs; only 1 pandemic (H1N1) 2009 virus was isolated from 80 nasal swab specimens.
Swine infl uenza virus (SIV) was reported in Thailand in 1981 (4). All 3 subtypes (H1N1, H3N2, and H1N2) of this virus are circulating in Thailand (5). A recent pathogenesis study demonstrated that subtype H1N1 induces typical SIV-like illness and slightly more severe gross lesions than illness induced by subtype H3N2 (6). Genetic data indicate that SIV (H1N1) in Thailand differs from pandemic (H1N1) 2009 virus. SIV (H1N1) in Thailand contains surface proteins of infl uenza viruses from North America and Eurasia, which are also found in pandemic (H1N1) 2009 virus; SIV (H1N1) in Thailand contains internal proteins of viruses from Eurasia; and pandemic (H1N1) 2009 viruses contain swine, human, and avian virus gene segments (5,7).
We report an outbreak of infection with pandemic (H1N1) 2009 virus during November 2009-March 2010 on a commercial pig farm in Thailand. The outbreak presumably resulted from human-to-pig transmission because 1 of the workers on this farm had infl uenza-like clinical signs at the beginning of the outbreak. Infection in this worker was not confi rmed because he quit his job on the farm after the start of the outbreak and could not be located.

The Study
In early November 2009, a small commercial pig farm in central Thailand reported respiratory problems in pigs (morbidity rate 50%, mortality rate 10%) in nursery pigs. The farm contained 3,235 pigs (700 sows, 35 boars, 1,000 piglets, 1,000 nursery pigs, and 500 fi nishing pigs). It has a conventional open-house production system in which both sides of the unit have natural air fl ow ventilation. The farm also has continuous nursery herd fl ow in which new pigs are continuously added when they are old enough. This process results in pigs of different ages being in the same unit. Sick pigs had clinical signs (fever, cough, nasal discharge, edematous eyelids, and conjunctivitis) of infection.
Nasal swabs from 20 nursery pigs (4-9 weeks of age) were submitted to Chulalongkorn University Veterinary Diagnostic Laboratory. All samples were positive for porcine circovirus type 2 and porcine reproductive and respiratory syndrome virus (these viruses are major causes of swine respiratory disease), and 2 samples were positive for infl uenza A virus by reverse transcription-PCR (RT-PCR) with primers for each specifi c pathogen (8)(9)(10).
Because respiratory problems in nursery pigs continued, nasal swabs specimens from 20 nursery pigs and fi nishing pigs, gilts (young females), and sows (10 per group) with clinical signs were submitted to the diagnostic laboratory by the end of December 2009. Two samples from nursery pigs were positive for infl uenza virus A (H1N1) by multiplex RT-PCR (11). Both samples were subjected to virus isolation in MDCK cells (12) and designated RA20 and RA29 (Table 1). Genome characterization identifi ed RA20 as SIV and RA29 as pandemic (H1N1) 2009 virus (Table 2; Figure). SIV-positive nasal swabs obtained in November were then characterized. Results showed that isolates RA4 and RA9 were pandemic (H1N1) 2009 virus, which indicated that pigs on the farm were infected with this virus.

Conclusions
Consistent with fi ndings of previous reports (2,3), our fi ndings demonstrate that young pigs are susceptible to infection with pandemic (H1N1) 2009 virus. Infection in pigs substantiates the hypothesis that the clinical outcome caused by infection with pandemic (H1N1) 2009 virus differs from that of infection with SIV (H1N1), which currently circulates in pigs in Thailand. Serologic results demonstrated that uninfected populations are susceptible to infection with pandemic (H1N1) 2009 virus. Results of genome analysis did not show gene reassortment between the 2 different infl uenza (H1N1) viruses. However, a previous report showed that reassortment of infl uenza virus genes occurs in pigs (15). Continued monitoring, characterization of SIVs, and serologic surveillance of pigs are necessary for future infl uenza pandemic preparedness.