Enterococcus faecalis is an opportunistic pathogen that infects many animal hosts, including insects and mammals. It is an important human pathogen and is often highly drug resistant. 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-surface 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.
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