The multiplicity of Staphylococcus aureus in chronic rhinosinusitis: Correlating surface biofilm and intracellular residence


  • This work was funded by The University of Adelaide and the European Rhinologic Society. Dr. Wormald receives royalties from Medtronic for instrument design and is a consultant for Neilmed Pty. Ltd. The authors have no other funding, financial relationships, or conflicts of interest to disclose.



The biofilm paradigm of chronic rhinosinusitis (CRS) is increasingly understood to play a key role in the pathophysiology of this disease. The role of intracellular infection of sinonasal epithelial cells has been suggested as a potential reservoir of pathogenic organisms that can lead to recalcitrant disease despite maximal medical and surgical treatment. Could a surface biofilm play a role in allowing intracellular infection to occur, and what are the factors associated with potential intracellular infections? The aim of this study was to investigate these questions.

Study Design:

A prospective study including 36 CRS patients undergoing endoscopic sinus surgery and five control patients undergoing endonasal pituitary surgery.


Sinonasal mucosa harvested at the time of surgery was examined with a Staphylococcus aureus fluorescence in situ hybridization probe and propodium iodide counterstain using the confocal scanning laser microscope for both biofilm status and evidence of intracellular organisms.


Intracellular S aureus was identified in 20/36 (56%) CRS patients compared to 0/8 (0%) control patients. CRS patients with intracellular infection were significantly more likely to harbor surface biofilm (20/20, P = .0014) and have a S aureus-positive culture swab (12/20, P = .0485).


This study gives further evidence supporting a role of intracellular S aureus in CRS. In all cases intracellular infection was associated with surface biofilm, suggesting a potential relationship between the two. Further work is required to delineate the true mechanisms of intracellular persistence and also the role that it plays in the recalcitrant nature of CRS. Laryngoscope, 2012