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Human-to-swine transmission of seasonal influenza viruses has led to sustained human-like influenza viruses circulating in the U.S. swine population. While some reverse zoonotic-origin viruses adapt and become enzootic in swine, nascent reverse zoonoses may result in virus detections that are difficult to classify as "swine-origin" or "human-origin" due to the genetic similarity of circulating viruses. This is the case for human-origin influenza A(H1N1) pandemic 2009 (pdm09) viruses detected in pigs following numerous reverse zoonosis events since the 2009 pandemic. We report the identification of two human infections with A(H1N1)pdm09 viruses originating from swine hosts and classify them as "swine-origin" variant influenza viruses based on phylogenetic analysis and sequence comparison methods. Phylogenetic analyses of viral genomes from two cases revealed these viruses were reassortants containing A(H1N1)pdm09 hemagglutinin (HA) and neuraminidase (NA) genes with genetic combinations derived from the triple reassortant internal gene cassette. Follow-up investigations determined that one individual had direct exposure to swine in the week preceding illness onset, while another did not report swine exposure. The swine-origin A(H1N1) variant cases were resolved by full genome sequence comparison of the variant viruses to swine influenza genomes. However, if reassortment does not result in the acquisition of swine-associated genes and swine virus genomic sequences are not available from the exposure source, future cases may not be discernible. We have developed a pipeline that performs maximum likelihood analyses, a k-mer-based set difference algorithm, and random forest algorithms to identify swine-associated sequences in the hemagglutinin gene to differentiate between human-origin and swine-origin A(H1N1)pdm09 viruses. [ABSTRACT FROM AUTHOR]

On March 25, 2015, the Wisconsin Division of Public Health was notified of a possible respiratory syncytial virus (RSV) infection outbreak among infants hospitalized in a neonatal intensive care unit (NICU). On March 23, the index patient (neonate A), aged 3 days, had feeding intolerance and apnea. A nasopharyngeal swab specimen collected from neonate A was tested using a single-manufacturer rapid RSV antigen detection test (RRADT) at the hospital laboratory; the result was positive. The following day, because of concern about the possibility of more widespread RSV infection, RRADT was used to test nasopharyngeal swab specimens from neonate B, aged 1 month, who had resided in a different hospital room in the NICU and had developed an increased oxygen requirement, apnea, and poor feeding that day, as well as from two asymptomatic neonates who were hospitalized in the same room with neonate A; all three were positive. Later that day, nasopharyngeal swab specimens from the remaining 16 asymptomatic NICU patients were tested using the same RRADT; seven tests were positive, making a total of 11 positives. All 20 RRADTs were performed at the hospital laboratory.