650. Genomic Analysis of Shiga Toxin-producing Escherichia coli From Symptomatic Patients and Asymptomatic Carriers
Author(s) -
Hiroaki Baba,
Hajime Kanamori,
Hayami Kudo,
Yasutoshi Kuroki,
Seiya Higashi,
Kentaro Oka,
Motomichi Takahashi,
Yuko Makino,
Chihiro Oe,
Kengo Oshima,
Tetsuji Aoyagi,
Makiko Yoshida,
Kouichi Tokuda,
Mitsuo Kaku
Publication year - 2018
Publication title -
open forum infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.546
H-Index - 35
ISSN - 2328-8957
DOI - 10.1093/ofid/ofy210.657
Subject(s) - multilocus sequence typing , stx2 , genotyping , asymptomatic carrier , microbiology and biotechnology , virulence , escherichia coli , shiga toxin , typing , genotype , biology , phylogenetic tree , molecular epidemiology , medicine , virology , gene , genetics , asymptomatic , pathology
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. Disclosures All authors: No reported disclosures.
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