Format

Send to

Choose Destination
See comment in PubMed Commons below
Cell. 2014 Aug 28;158(5):1060-71. doi: 10.1016/j.cell.2014.06.046.

Evolution of resistance to a last-resort antibiotic in Staphylococcus aureus via bacterial competition.

Author information

  • 1Research Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany.
  • 2Institute for Molecular Infection Biology (IMIB), University of Würzburg, Würzburg 97080, Germany.
  • 3Department of Zoology, University of Oxford, Oxford OX1 3QU, UK; Oxford Centre for Integrative Systems Biology, University of Oxford, Oxford OX1 3QU, UK.
  • 4Research Centre for Infectious Diseases (ZINF), University of Würzburg, Würzburg 97080, Germany; Institute for Molecular Infection Biology (IMIB), University of Würzburg, Würzburg 97080, Germany. Electronic address: daniel.lopez@uni-wuerzburg.de.

Abstract

Antibiotic resistance is a key medical concern, with antibiotic use likely being an important cause. However, here we describe an alternative route to clinically relevant antibiotic resistance that occurs solely due to competitive interactions among bacterial cells. We consistently observe that isolates of Methicillin-resistant Staphylococcus aureus diversify spontaneously into two distinct, sequentially arising strains. The first evolved strain outgrows the parent strain via secretion of surfactants and a toxic bacteriocin. The second is resistant to the bacteriocin. Importantly, this second strain is also resistant to intermediate levels of vancomycin. This so-called VISA (vancomycin-intermediate S. aureus) phenotype is seen in many hard-to-treat clinical isolates. This strain diversification also occurs during in vivo infection in a mouse model, which is consistent with the fact that both coevolved phenotypes resemble strains commonly found in clinic. Our study shows how competition between coevolving bacterial strains can generate antibiotic resistance and recapitulate key clinical phenotypes.

PMID:
25171407
PMCID:
PMC4163622
DOI:
10.1016/j.cell.2014.06.046
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center