Phenotypic Changes in a Laboratory-Derived Ertapenem-ResistantEscherichia coliStrain

Abstract

The aim of this study was to identify phenotypic changes in a laboratory-derived strain of ertapenem-resistant Escherichia coli (Ec-ERT) when compared to its susceptible parent strain (Ec-WT). In both strains, we assessed both the effects of ertapenem via time-kill curves and the occurrence of cross resistance with other beta-lactams. The strains were compared based on growth pattern, biochemical-physiological profile and changes in the subproteome using 2D-DIGE followed by MALDI-TOF/TOF MS. To assess virulence, we employed a murine model of intraperitoneal infection in which we investigated the invasiveness of both strains. Growth persistence of the laboratory-derived resistant strain was observed via the time-kill curve assay, but cross resistance was not observed for other beta-lactams. We also observed a slower growth rate and changes in the biochemical and physiological characteristics of the drug-resistant bacteria. In the resistant strain, a total of 51 protein spots were increased in abundance relative to the wild-type strain, including an outer membrane protein A, which is related to bacterial virulence. The mouse infection assay showed a higher invasiveness of the Ec-ERT strain in relation to the Ec-WT strain. In conclusion, the alterations driven by ertapenem in E. coli reinforce the idea that antimicrobial agents may interfere in several aspects of bacterial cell biology, with possible implications for host-bacteria interactions.

Comparative Proteomics of Inner Membrane Fraction from Carbapenem-Resistant Acinetobacter baumannii with a Reference Strain

“…The rationale for selecting RS307, is to compare ‘naturally induced’ resistance in RS307 with that of ATCC19606. Comparative proteomics has been used as an approach to understand the resistance mechanism in the microorganisms where the ATCC strain was considered as a reference (susceptible) strain [31], [32], [17], [11]. We have also performed proteomics of clinical resistant strains with lower MICs: RS122 with MIC, 32 µg/ml and RS259 with MIC, 1 µg/ml.…”

Molecular epidemiological survey of bacteremia by multidrug resistant Pseudomonas aeruginosa: the relevance of intrinsic resistance mechanisms

“…Many studies examining the mechanisms of carbapenem-resistance have involved controlled laboratory-derived strains; however, studies involving clinical isolates have not clearly defined the contributions of the MBL, AmpC cephalosporinase, alterations of the OprD porin or efflux systems to carbapenem-resistance [11,15]. In this report, we analyzed the mechanisms of carbapenem-resistance in clinical isolates of multidrug-resistant P .…”