Abstract
BackgroundThe emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains.ResultsThis study showed that the mechanisms of carbapenem resistance in this study are: 1. Generating carbapenemase (7 of 19); 2. The production of AmpC or ESBLs combined with decreased expression of out membrane protein (12 of 19). hsp60 sequence analysis suggested 10 of 19 the strains belong to colistin hetero-resistant clusters and the mechanism of colistin resistance is increasing expression of acrA in the efflux pump AcrAB-TolC alone (18 of 19) or accompanied by a decrease of affinity between colistin and outer membrane caused by the modification of lipid A (14 of 19). Moreover, an ECC strain co-harboring plasmid-mediated mcr-4.3 and blaNDM-1 has been found.ConclusionsThis study suggested that there is no overlap between the resistance mechanism of co-resistant ECC strains to carbapenem and colistin. However, the emergence of strain co-harboring plasmid-mediated resistance genes indicated that ECC is a potential carrier for the horizontal spread of carbapenems and colistin resistance.
Highlights
The emergence of carbapenem-resistant and colistin-resistant Enterobacter cloacae Complex (ECC) pose a huge challenge to infection control
5 ECC strains were resistant to meropenem, 6 ECC strains were resistant to imipenem, and 4 of them were resistant to 3 carbapenems
In the presence of efflux pump inhibitors carbonyl cyanide mchlorophenylhydrazone (CCCP) or omeprazole, the Minimum inhibitory concentrations (MIC) of colistin to 19 ECC strains or 17 ECC strains decreased significantly and returned to susceptible respectively, while almost all inhibitors of efflux pump activity showed no effect on the MICs of ertapenem
Summary
The emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains. When ECC is exposed to β-lactam drugs for a long period of time, it can further lead to the highly induced phenotypes of AmpC cephalosporin, producing resistance to third-generation cephalosporins [13]. The acquisition of a variety of plasmids mediated extended-spectrum β-lactamase (ESBL) genes conferred ECC resistance to most β-lactam drugs, making the treatment more difficult. Literature has shown that the resistance of Enterobacter cloacae to carbapenem can be mediated by AmpC expression and membrane permeability (the decrease in or loss of the outer membrane proteins OmpF and OmpC) changes, but it may be more common to obtain carbapenemase gene transferred by plasmids [14, 15]. The plasmid-mediated mechanism significantly increases the spread of carbapenem resistance, while further limiting the choice of effective antibacterial drugs
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