BibTex format

author = {Wadhawan, A and Simoes, da Silva CJ and Nunes, CD and Edwards, AM and Dionne, MS},
doi = {10.1101/2022.08.17.504265},
title = {<i>E. faecalis</i>acquires resistance to antimicrobials and insect immunity via common mechanisms},
url = {},
year = {2022}

RIS format (EndNote, RefMan)

AB - <jats:title>Summary</jats:title><jats:p><jats:italic>Enterococcus faecalis</jats:italic>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<jats:italic>Drosophila</jats:italic>-adapted<jats:italic>E. faecalis</jats:italic>strains, which exhibited immune resistance, resulting in increased<jats:italic>in vivo</jats:italic>growth and virulence. Resistance was characterised by mutations in bacterial pathways responsive to cell envelope stress.<jats:italic>Drosophila</jats:italic>-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<jats:italic>Drosophila</jats:italic>-adapted strains. Our results show that common mechanisms provide a route to resistance to both antimicrobials and host immunity in<jats:italic>E. faecalis</jats:italic>and demonstrate that the selection and emergence of antibiotic resistance<jats:italic>in vivo</jats:italic>does not require antibiotic exposure.</jats:p><jats:sec><jats:title>One sentence summary</jats:title><jats:p>Host interaction can promote antimicrobial resistance and antimicrobial treatment can promote virulence in<jats:italic>E. faecalis</jats:italic>.</jats:p></jats:sec>
AU - Wadhawan,A
AU - Simoes,da Silva CJ
AU - Nunes,CD
AU - Edwards,AM
AU - Dionne,MS
DO - 10.1101/2022.08.17.504265
PY - 2022///
TI - <i>E. faecalis</i>acquires resistance to antimicrobials and insect immunity via common mechanisms
UR -
ER -