2057. Increased detection of blaKPC in Enterobacter cloacae at a New York City Hospital including two emerging clones, ST171 and ST78
Session: Poster Abstract Session: Antimicrobial Resistant Infections: Treatment
Saturday, October 29, 2016
Room: Poster Hall
  • IDweek_poster_10_16ac2.jpg (145.0 kB)
  • Background: The proliferation of carbapenem-resistant Enterobacteriaceae (CRE) signifies an escalating threat to modern healthcare, but has been driven largely by Klebsiella pneumoniae. However, recent studies support the emergence of carbapenem-resistant Enterobacter cloacae (CREC), including at our New York City tertiary care hospital. Though likely due to uptake of plasmid-mediated blaKPC, CREC population structure and risk factors remain poorly understood.

    Methods: We performed a case-control study of patients with CREC (cases) and 3rd-generation cephalosporin-resistant E. cloacae (Ceph-R) (controls) collected at our hospital since 2010, matched by age, sex, and year of culture, to identify clinical and molecular factors associated with CREC. Isolate sensitivities were determined by Vitek2; genotyping was performed using multi-locus sequence typing (MLST). Select CREC and Ceph-R isolates underwent whole genome sequencing using Illumina HiSeq, and MLST, resistance gene, and plasmid types were extracted using SRST2.

    Results: Clinical data were obtained from 68 cases and 68 matched controls. Patients were older (median age 59) and 66% were male. CREC was more likely than Ceph-R to occur >2 days after admission (82% versus 54%, p = 0.0004), and to be cultured from the respiratory tract compared to the blood or urine (overall p = 0.003). We typed 58 CREC and 48 Ceph-R isolates and identified 26 and 20 different STs, respectively. ST171 was the most common CREC ST (n=26) followed by ST78 (n=6) which was also the dominant Ceph-R ST (n=21). blaKPC-3 (n=30), blaKPC-2 (n=12), and blaKPC-4 (n=2) were the putative mechanisms of carbapenem resistance in CREC isolates. WGS analysis revealed a single blaKPC-3-harboring ST171 clone present since 2010, suggesting persistent colonizing or environmental reservoirs, whereas ST78 consisted of several clades. ST171 and ST78 occurred in both CREC and Ceph-R but did not share potential blaKPC-harboring plasmids.

    Conclusion: CREC appeared to be due to both sporadic acquisition of blaKPC-encoding plasmids and spread of dominant clones ST171 and ST78. However, ST78 and ST171 also occurred among Ceph-R isolates, implicating a more complex dynamic of plasmid uptake and clonal expansion in this organism.

    Angela Gomez-Simmonds, MD, MS1, Yue Hu, BS2, Sean Sullivan, MPH1, Zheng Wang, PhD1, Susan Whittier, PhD3 and Anne-Catrin Uhlemann, MD, PhD1, (1)Columbia University Medical Center, New York, NY, (2)Columbia University, New York, NY, (3)NewYork-Presbyterian/Columbia University Medical Center, New York, NY


    A. Gomez-Simmonds, None

    Y. Hu, None

    S. Sullivan, None

    Z. Wang, None

    S. Whittier, None

    A. C. Uhlemann, None

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