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

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.

• Authors: Hannah McCarthy, Elaine M Waters, Jeffrey L Bose, Simon Foster, Kenneth W Bayles, Eoghan O'Neill, Paul D Fey, James P O'Gara
• Journal: FEMS microbiology letters (FEMS Microbiol Lett) Vol. 363 Issue 9 (05 2016) ISSN: 1574-6968 [Electronic] England
• PMID: 27044299 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © FEMS 2016. All rights reserved. For permissions, please e-mail: [email protected].

Chemical References

• N-Acetylmuramoyl-L-alanine Amidase

Topics

• Animals
• Biofilms
• Catheter-Related Infections (microbiology)
• Disease Models, Animal
• Mice
• N-Acetylmuramoyl-L-alanine Amidase (genetics, metabolism)
• Staphylococcal Infections (microbiology)
• Staphylococcus aureus (genetics, growth & development, metabolism, pathogenicity)
• Virulence