254. Application of Whole-Genome Sequencing to Investigation of a Prolonged Outbreak Caused by Multidrug-Resistant Acinetobacter baumannii at A Large Academic Burn Center
Session: Poster Abstract Session: Diagnostics: Typing and Sequencing
Thursday, October 8, 2015
Room: Poster Hall
Posters
  • 150915AcinetoWGS_poster_IDWeek2015.pdf (1.3 MB)
  • Background:

    Whole-genome sequencing (WGS) has emerged as a promising method for molecular epidemiology in investigations of healthcare-associated outbreaks. Here we investigated prolonged hospital outbreaks of multidrug-resistant Acinetobacter baumannii (MDRAB) during a three-year period at a large academic burn center and examined transmission dynamics of MDRAB strains through WGS and comparative analysis.

    Methods:

    Forty-two nonduplicate clinical isolates of MDRAB between 2007 and 2010 at the burn center were analyzed. Short-read libraries from DNA of all samples were pooled and sequenced on a single Illumina MiSeq run, then were mapped to a PacBio-generated reference genome of the outbreak index case (A3). Acquired resistance genes were identified using ResFinder v2.1. Multilocus sequence typing (MLST) was performed using MLST v1.7 and the Pasteur MLST database. A neighbor-joining tree was constructed on the basis of single-nucleotide variants (SNVs), and a corresponding heatmap representing genome-wide variants was calculated. Bayesian transmission-chain reconstruction was performed using Outbreaker software.

    Results:

    These sequential MDRAB outbreaks were caused by three clones based on SNVs differences; the first outbreak of 13 strains starting from A3 (August 2007 - November 2008), the second outbreak of 3 strains starting from A15 (June 2008 - August 2009), and the third outbreak of 24 strains starting from A20 (August 2008 - March 2011) (Figure 1). Two strains (A32 and A42) were not related to these sequential outbreaks. In the second outbreak (A15, A25, and A36), WGS identified a recombination of A18 from the first outbreak. The first outbreak was caused by ST2, and then the second outbreak was by a combination of ST 2 and ST391. In contrast, the third outbreak was primarily ST79. The transmission network for the three outbreaks is provided in Figure 2. Distribution of resistance genes varied among three outbreaks. The first and second outbreak strains possessed blaOXA-23-like group, while the third outbreak strains harbored blaOXA-40-like group.

    Conclusion:

    WGS and comparative analysis enabled us to conduct outbreak tracing and transmission pathways as well as detect recombination events and resistance genes among MDRAB strains.

    Hajime Kanamori, MD, PhD, MPH1,2, Christian Parobek, BSc3, David Weber, MD, MPH1,2, William Rutala, PhD, MPH1,2 and Jonathan Juliano, MD, MSPH2, (1)Hospital Epidemiology, University of North Carolina Health Care, Chapel Hill, NC, (2)Division of Infectious Diseases, University of North Carolina School of Medicine, Chapel Hill, NC, (3)University of North Carolina School of Medicine, Chapel Hill, NC

    Disclosures:

    H. Kanamori, None

    C. Parobek, None

    D. Weber, None

    W. Rutala, None

    J. Juliano, None

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