E. faecalis acquires resistance to antimicrobials and insect immunity via common mechanisms

Abstract

Enterococcus faecalis is a normal member of the gut microbiota and an opportunistic pathogen of many animals, including mammals, birds, and insects. It is a common cause of nosocomial infections, and is particularly troublesome due to extensive intrinsic and acquired antimicrobial resistance. Using experimental evolution, we generated Drosophila-adapted E. faecalis strains, which exhibited immune resistance, resulting in increased in vivo growth and virulence. Resistance was characterised by mutations in bacterial pathways responsive to cell envelope stress. Drosophila-adapted strains exhibited changes in sensitivity to relevant antimicrobials, including daptomycin and vancomycin. Evolved daptomycin-resistant strains harboured mutations in the same signalling systems, with some strains showing increased virulence similar to Drosophila-adapted strains. Our results show that common mechanisms provide a route to resistance to both antimicrobials and host immunity in E. faecalis and demonstrate that the selection and emergence of antibiotic resistance in vivo does not require antibiotic exposure. One sentence summaryHost interaction can promote antimicrobial resistance and antimicrobial treatment can promote virulence in E. faecalis.