Open AccessFunctional screening for triclosan resistance in a wastewater metagenome and isolates of Escherichia coli and Enterococcus spp. from a large Canadian healthcare region
Author(s) -
Andrew Cameron,
Ruth Barbieri,
Ron Read,
Deirdre L. Church,
Emelia H Adator,
Rahat Zaheer,
Tim A. McAllister
Publication year - 2019
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0211144
Subject(s) - triclosan , microbiology and biotechnology , enterococcus faecium , biology , enterococcus faecalis , escherichia coli , antibiotic resistance , enterococcus , drug resistance , teicoplanin , resistome , vancomycin , antibiotics , bacteria , genetics , medicine , staphylococcus aureus , integron , pathology , gene
The biocide triclosan is in many consumer products and is a frequent contaminant of wastewater (WW) such that there is concern that triclosan promotes resistance to important antibiotics. This study identified functional mechanisms of triclosan resistance (TCS R ) in WW metagenomes, and assessed the frequency of TCS R in WW-derived and clinical isolates of Escherichia coli and Enterococcus spp. Metagenomic DNA extracted from WW was used to profile the microbiome and construct large-insert cosmid libraries, which were screened for TCS R . Resistant cosmids were sequenced and the TCS R determinant identified by transposon mutagenesis. Wastewater Enterococcus spp. ( N = 94) and E . coli ( N = 99) and clinical Enterococcus spp. ( N = 146) and vancomycin-resistant E . faecium (VRE; N = 149) were collected and tested for resistance to triclosan and a comprehensive drug panel. Functional metagenomic screening revealed diverse FabV homologs as major WW TCS R determinants. Resistant clones harboured sequences likely originating from Aeromonas spp., a common WW microbe. The triclosan MIC90s for E . coli , E . faecalis , and E . faecium isolates were 0.125, 32, and 32 mg/L, respectively. For E . coli , there was no correlation between the triclosan MIC and any drug tested. Negative correlations were detected between the triclosan MIC and levofloxacin resistance for E . faecalis , and between triclosan and vancomycin, teicoplanin, and ampicillin resistance for E . faecium . Thus, FabV homologs were the major contributor to the WW triclosan resistome and high-level TCS R was not observed in WW or clinical isolates. Elevated triclosan MICs were not positively correlated with antimicrobial resistance to any drug tested.