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Background  The global spread and increasing incidence of carbapenem-resistant Enterobacteriaceae have resulted in treatment and public health concerns. Here, we present an investigation of the molecular mechanisms and clonality of carbapenem-non-susceptible  Escherichia coli  (CnSEC) based on a nationwide survey in Taiwan.    Methods  We collected 32 and 43 carbapenem-non-susceptible  E. coli  isolates in 2010 and 2012, respectively. The genes encoding cabapenemases and plasmidic AmpC-type and extended-spectrum β-lactamases (EBSLs) were analyzed by polymerase chain reaction (PCR). The major porin channels OmpF and OmpC were evaluated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Molecular typing was performed with pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST).    Results  The resistance rates of CnSEC isolates to cefazolin, cefotaxime, cefoxitin, ceftazidime, and ertapenem were all 100%, and most (94.7%) isolates were CMY producers. The main mechanism of CnSEC in Taiwan is via plasmidic AmpC β-lactamase CMY-2 and DHA-1 in combination with the loss of OmpC/F. In 2010, one isolate was confirmed to harbor  bla  IMP-8 ; a KPC-2 producer and an NDM-1 producer were detected in 2012. No isolate had VIM- or OXA-carbapenemases. ST131 was the predominant ST type (33.3%). PFGE revealed no large cluster in CnSEC isolates in Taiwan.    Conclusions  The co-existence of plasmidic AmpC β-lactamase and outer membrane protein loss is the main mechanism for CnSEC in Taiwan. The emergence of KPC-2 and NDM-1 in 2012 and the predominance of ST131 warrant close monitoring and infection control.

bmc infectious diseases

Updated molecular epidemiology of carbapenem-non-susceptible Escherichia coli in Taiwan: first identification of KPC-2 or NDM-1-producing E. coliin Taiwan