Abstract

BackgroundEnterobacter cloacae is a major nosocomial pathogen causing bloodstream infections. We retrospectively conducted a study to assess antimicrobial susceptibility and phylogenetic relationships of E. cloacae bloodstream isolates in two tertiary university-affiliated hospitals in Shanghai, in order to facilitate managements of E. cloacae bloodstream infections and highlight some unknowns for future prevention.MethodsFifty-three non-duplicate E. cloacae bloodstream isolates were consecutively collected from 2013 to 2016. Antimicrobial susceptibility was determined by disk diffusion. PCR was performed to detect extended-spectrum β-lactamase (ESBL), carbapenemase and colistin resistance (MCR-1) gene. Plasmid-mediated AmpC β-lactamase (pAmpC) genes were detected using a multiplex PCR assay targeting MIR/ACT gene (closely related to chromosomal EBC family gene) and other plasmid-mediated genes, including DHA, MOX, CMY, ACC, and FOX. eBURST was applied to analyze multi-locus sequence typing (MLST).ResultsThe rates of resistance to all tested antibiotics were <40%. Among 53 E. cloacae isolates, 8(15.1%) were ESBL producers, 3(5.7%) were carbapenemase producers and 18(34.0%) were pAmpC producers. ESBL producers bear significantly higher resistance to cefotaxime (100.0%), ceftazidime (100.0%), aztreonam (100.0%), piperacillin (87.5%), tetracycline (75.0%), and trimethoprim-sulfamethoxazole (62.5%) than non-producers (p<0.05). PAmpC- and non-producers both presented low resistance rates (<40%) to all antibiotics (p>0.05). SHV (6/8, 75.0%) and MIR/ACT (15/18, 83.3%) predominated in ESBL and pAmpC producers respectively. Moreover, 2 isolates co-carried TEM-1, SHV-12, IMP-26 and DHA-1. MLST analysis distinguished the 53 isolates into 51 STs and only ST414 and ST520 were assigned two isolates of each (2/53).ConclusionThe antimicrobial resistance rates were low among 53 E. cloacae bloodstream isolates in the two hospitals. Multiclonality disclosed no evidence on spread of these isolates in Shanghai. The simultaneous presence of ESBL, carbapenemase and pAmpC detected in 2 isolates was firstly reported in Shanghai, which necessitated active ongoing surveillances and consistent prevention and control of E. cloacae.

Highlights

  • Enterobacter cloacae is an important emerging pathogen, causing various nosocomial infections, including respiratory infections, bloodstream infections (BSIs) and surgical site infections [1, 2]

  • The factors dominantly contributing to resistance among E. cloacae maybe the plasmidmediated AmpC β-lactamases, plasmid-encoded CTX-M family of extended-spectrum β-lactamases(ESBLs), the KPC family of carbapenemases, and metallo β-lactamases of the VIM, IMP, and NDM-1 types[6, 11]

  • E. cloacae was frequently implicated in nosocomial infections[1, 2], and the production of plasmidmediated AmpC β-lactamases (pAmpC), ESBLs and carbapenemases have led to the multidrug-resistance and high potential dissemination of clinical E. cloacae isolates[23, 24]

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Summary

Introduction

Enterobacter cloacae is an important emerging pathogen, causing various nosocomial infections, including respiratory infections, bloodstream infections (BSIs) and surgical site infections [1, 2]. BSIs due to multidrug-resistant (MDR) Enterobacteriaceae were related to high mortality, sometimes exceeding 50% depending on the study population[3]. The factors dominantly contributing to resistance among E. cloacae maybe the plasmidmediated AmpC β-lactamases (pAmpC), plasmid-encoded CTX-M family of extended-spectrum β-lactamases(ESBLs), the KPC family of carbapenemases, and metallo β-lactamases of the VIM, IMP, and NDM-1 types[6, 11]. 42% E. cloacae bloodstream isolates were screened as ESBL positive in Brazil with CTX-M-15 the most common type [13]. Enterobacter cloacae is a major nosocomial pathogen causing bloodstream infections. We retrospectively conducted a study to assess antimicrobial susceptibility and phylogenetic relationships of E. cloacae bloodstream isolates in two tertiary university-affiliated hospitals in Shanghai, in order to facilitate managements of E. cloacae bloodstream infections and highlight some unknowns for future prevention

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Conclusion

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