Updated molecular epidemiology of carbapenem-non-susceptible Escherichia coli in Taiwan: first identification of KPC-2 or NDM-1-producing E. coli in Taiwan
1 National Institutes of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli, Taiwan
2 Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan
3 Department of Clinical Pathology, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan
4 Section of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
5 Division of Infectious Diseases, Department of Medicine, National Taiwan University Hospital, Taipei, Taiwan
6 Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Tzyou 1st Road, Kaohsiung City, Taiwan
7 College of Medicine, Kaohsiung Medical University, 100 Tzyou 1st Road, Kaohsiung City, Taiwan
8 Department of Internal Medicine and Medical Research, Chi Mei Medical Center, Tainan, Taiwan
9 Department of Internal Medicine, Chi Mei Medical Center, Liouying, Tainan, Taiwan
BMC Infectious Diseases 2013, 13:599 doi:10.1186/1471-2334-13-599Published: 20 December 2013
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.
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).
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 blaIMP-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.
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.