Abstract
SummaryEnterococcus faecalisis 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 generatedDrosophila-adaptedE. faecalisstrains, which exhibited immune resistance, resulting in increasedin vivogrowth 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 toDrosophila-adapted strains. Our results show that common mechanisms provide a route to resistance to both antimicrobials and host immunity inE. faecalisand demonstrate that the selection and emergence of antibiotic resistancein vivodoes not require antibiotic exposure.One sentence summaryHost interaction can promote antimicrobial resistance and antimicrobial treatment can promote virulence inE. faecalis.
Publisher
Cold Spring Harbor Laboratory
Cited by
2 articles.
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