Abstract
BackgroundTo clarify the molecular epidemiology of carbapenem-resistant Enterobacter cloacae complex (CREC) and the risk factors for acquisition of carbapenemase-producing E. cloacae complex (CPEC).MethodsUsing clinical CREC isolates detected in a Japanese university hospital over 4 years, carbapenemase production was screened with phenotypic methods. Carbapenemase genes were analysed by PCR and sequencing. Molecular epidemiological analyses were conducted with repetitive extragenic palindromic (REP)-PCR and multilocus sequence typing (MLST). CRECs were identified to the subspecies level by hsp60 sequencing. Whole-genome sequencing of plasmids was conducted. A case-control study was performed to identify risk factors for acquisition of CPEC among patients with CREC.ResultsThirty-nine CRECs including 20 CPECs carrying blaIMP-1 were identified. Patients with CPEC had longer hospital stay before detection (26.5 days vs. 12 days, p = 0.008), a urinary catheter (odds ratio [OR], 5.36; 95% confidence interval [CI], 1.14–30.9; p = 0.023), or intubation (OR, 7.53; 95% CI, 1.47–53.8; p = 0.008) compared to patients without CPEC. Four genetically closely related CPEC clusters were observed, which showed that three of four CPEC clusters corresponded to E. asburiae (ST 53), E. hormaechei subsp. steigerwaltii (ST 113 and ST 1047) and E. cloacae subsp. cloacae (ST 513) by MLST and hsp60 sequencing. Seven representative plasmids shared structures with class I integron containing blaIMP-1 and IncHI2A replicon type.ConclusionsA longer hospital stay, presence of a urinary catheter, and intubation are risk factors for CPEC acquisition. In addition to horizontal transmission of genetically indistinguishable CPECs, IncHI2A plasmid carrying blaIMP-1 appeared to be transferred among genetically different ECs.
Highlights
To clarify the molecular epidemiology of carbapenem-resistant Enterobacter cloacae complex (CREC) and the risk factors for acquisition of carbapenemase-producing E. cloacae complex (CPEC)
This study aimed to clarify the molecular epidemiology of CPEC isolates and their plasmids carrying carbapenemase genes detected in Nagoya University Hospital (NUH) and to analyse the risk factors for CPEC acquisition compared with CREC without carbapenemase production
Twenty CPECs among 39 CRECs were revealed with modified carbapenemase inactivation method (mCIM), and blaIMP-1 was identified in all CPEC isolates with negative PCR results for blaIMP-2, blaNDM-1, blaVIM-2, and blaKPC
Summary
To clarify the molecular epidemiology of carbapenem-resistant Enterobacter cloacae complex (CREC) and the risk factors for acquisition of carbapenemase-producing E. cloacae complex (CPEC). The emergence of carbapenem-resistant Enterobacteriaceae (CRE), especially carbapenemase-producing Enterobacteriaceae (CPE), has been increasing worldwide and is a clinical and public health threat [1]. The National Epidemiological Surveillance of Infectious Diseases and Japan Nosocomial Infections Surveillance (JANIS) by the Ministry of Health, Labor and Welfare of Japan have been implemented for CRE using the criteria of either meropenem-minimum inhibitory concentration (MIC) ≥2 μg/mL or cefmetazole-MIC ≥64 μg/mL, in addition to imipenem-MIC ≥2 μg/mL. The latest results of surveillance of Japanese CRE in 2017 revealed that 239 CPE strains (28%) were detected, and 227 CPE strains carried blaIMP, of which EC was the most common (74 strains). The IMP genotype was assessed in some strains, and IMP-1 (44%) and IMP-6 (56%) were detected [4]
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