EfrEF and the transcription regulator ChlR are required for chlorhexidine stress response in Enterococcus faecalis V583 [PublishAheadOfPrint]

Enterococcus faecalis is an opportunistic pathogen and leading cause of healthcare-associated infections. Daily chlorhexidine gluconate (CHG) bathing of patients is generally regarded as an effective strategy to reduce the occurrence of healthcare-associated infections. It is likely that E. faecalis are frequently exposed to inhibitory and sub-inhibitory CHG in clinical settings. The goal of this study was to investigate how the vancomycin-resistant strain E. faecalis V583 transcriptionally responds to and tolerates stress from CHG. We used transcriptome (microarray) analysis to identify genes up-regulated by E. faecalis V583 in response to CHG. The genes efrE (EF2226) and efrF (EF2227), encoding a heterodimeric ABC transport system, were the most highly up-regulated genes. efrEF expression was induced by CHG at concentrations several two-fold dilutions below the MIC. Deletion of efrEF increased E. faecalis V583 susceptibility to CHG. We found that ChlR, a MerR-like regulator encoded upstream of efrEF, mediated the CHG-dependent up-regulation of efrEF, and deletion of chlR also increased chlorhexidine susceptibility. Overall, our study gives insight into E. faecalis stress responses to a commonly used antiseptic.

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