The major autolysin is redundant for Staphylococcus aureus USA300 LAC JE2 virulence in a murine device-related infection model

Hannah McCarthy, Elaine M. Waters, Jeffrey L. Bose, Simon Foster, Kenneth W. Bayles, Eoghan O'Neill, Paul D. Fey, James P. O'Gara

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

The major Staphylococcus aureus autolysin, Atl, has been implicated in attachment to surfaces and release of extracellular DNA during biofilm formation under laboratory conditions. Consistent with this, polyclonal antibodies to the amidase and glucosaminidase domains of Atl inhibited in vitro biofilm formation. However, in a murine model of device-related infection the community-associated S. aureus strain USA300 LAC JE2 established a successful infection in the absence of atl. These data indicate that Atl activity is not required for biofilm production in this infection model and reveal the importance of characterizing the contribution of biofilm phenotypes to virulence under in vivo conditions.

Original languageEnglish (US)
Article numberfnw087
JournalFEMS Microbiology Letters
Volume363
Issue number9
DOIs
StatePublished - Apr 3 2016

Keywords

  • Autolysin
  • Biofilm
  • Device infection
  • Staphylococcus

ASJC Scopus subject areas

  • Microbiology
  • Molecular Biology
  • Genetics

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