650. Genomic analysis of Shiga Toxin-producing Escherichia coli from Symptomatic Patients and Asymptomatic Carriers
Session: Poster Abstract Session: Pathogenesis and Immune Response
Thursday, October 4, 2018
Room: S Poster Hall
  • IDWEEK2018poster180930.pdf (507.1 kB)
  • Background: Shiga toxin-producing Escherichia coli (STEC) causes serious gastrointestinal illness. Although O157 is predominant, non-O157 infections have been increasingly reported worldwide. We used whole genome sequencing (WGS) to investigate molecular characteristics and phylogeny of STEC isolates.

    Methods: A total of 22 STEC isolates from symptomatic patients (n=13) and asymptomatic carriers (n=9) in a Japanese region during 2016-2017 were used. Serogroups were O157, O26 and O103 (n=5, 12, and 5, respectively). WGS was performed using an Illumina Miseq. Genomic analysis was performed using web-based tools by the Center for Genomic Epidemiology. Single nucleotide polymorphism detection and construction of phylogenetic tree were performed using Mauve software.

    Results: Of 76 virulence genes, 32 (42%) were detected (Figure 1). Eighteen (82%) and 7 (32%) isolates contained stx1 and stx2, respectively. Twelve (91%) contained eae. stx2 was more frequent in isolates from patients (P < 0.05), whereas cba was more frequent in isolates from carriers (P < 0.05). stx2, etpD were more frequent in O157 isolates (P < 0.05, respectively), whereas stx1, efa1, cif, tccP, cba, lpfA were more frequent in non-O157 isolates (P < 0.05, respectively). Nine acquired resistance gene (aph(3’)-Ia, blaTEM-1b, dfrA5, dfrA8, strA, strB, sul2, tetA, tetB) were detected, while at least one was found in 6 (27%) isolates. Isolates from patients (5/13, 38%) were likely to have more resistance genes than isolates from carriers (1/9, 11%) (P = 0.33). Genotyping and multilocus sequence typing revealed all O26 isolates belonged to O26:H11 ST21, O103 belonged to O103:H2 ST17 and novel O103:H8 ST2836, while O157 belonged to O157:H7 ST11 and ST2966 (Figure 2). Phylogenetic tree showed O103:H8 ST2836 isolates clustered with O26, separated from O103:H2 ST17 (Figure 3). In a cluster of O26:H11 ST21 isolates, isolates from carriers formed a subcluster. O157 isolates clustered in a separate lineage. O157:H7 ST2966 isolates evolved from ST11.

    Conclusion: Of the non-O157 isolates, O26:H11 ST21, which contained as many virulence genes as O157, was prevalent among both patients and carriers in our region, highlighting the importance of monitoring genomic characteristics of non-O157 STEC.

    Macintosh HD:Users:HiroakiBaba:Dropbox:EHEC:IDWEEK2018:IDWEEK2018figures:Fig.1.jpeg

    Macintosh HD:Users:HiroakiBaba:Dropbox:EHEC:IDWEEK2018:IDWEEK2018figures:Fig.2.jpeg

    Macintosh HD:Users:HiroakiBaba:Dropbox:EHEC:IDWEEK2018:IDWEEK2018figures:Fig.3.jpeg

    Hiroaki Baba, MD1, Hajime Kanamori, MD, PhD, MPH1, Hayami Kudo, Mr1,2, Yasutoshi Kuroki, Mr2, Seiya Higashi, Mr2, Kentaro Oka, PhD1,3, Motomichi Takahashi, PhD1,3, Yuko Makino, MS1, Chihiro Oe, MD1, Kengo Oshima, MD, PhD1, Tetsuji Aoyagi, MD, PhD1, Makiko Yoshida, PhD, MPH1, Kouichi Tokuda, MD, PhD, MPH1 and Mitsuo Kaku, MD, PhD1, (1)Department of Infection Control and Laboratory Diagnostics, Tohoku University Graduate School of Medicine, Sendai, Japan, (2)Miyarisan Pharmaceutical Co., Ltd., Saitama, Japan, (3)Tokyo R&D Center, Miyarisan Pharmaceutical Co., Ltd., Saitama, Japan


    H. Baba, None

    H. Kanamori, None

    H. Kudo, None

    Y. Kuroki, None

    S. Higashi, None

    K. Oka, None

    M. Takahashi, None

    Y. Makino, None

    C. Oe, None

    K. Oshima, None

    T. Aoyagi, None

    M. Yoshida, None

    K. Tokuda, None

    M. Kaku, None

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