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Small‐colony variants and phenotype switching of intracellular S taphylococcus aureus in chronic rhinosinusitis
Author(s) -
Tan N. C.W.,
Cooksley C. M.,
Roscioli E.,
Drilling A. J.,
Douglas R.,
Wormald P.J.,
Vreugde S.
Publication year - 2014
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/all.12457
Subject(s) - staphylococcus aureus , virulence , intracellular , microbiology and biotechnology , phenotype , phenotypic switching , biology , secretion , chronic rhinosinusitis , intracellular parasite , biofilm , bacteria , immunology , gene , genetics , biochemistry
Background Chronic rhinosinusitis ( CRS ) has been linked to the gram‐positive bacteria Staphylococcus aureus ( S. aureus ) in its biofilm or intracellular forms. Recent evidence suggests that S. aureus also exists in a small‐colony variant ( SCV ) form as a mechanism of altering its virulence capabilities. The aim of this study was to investigate the presence of SCV s in sinonasal mucosa of CRS patients and whether the phenomenon of phenotype switching can be applied to intracellular epithelial infections. Methods Sinonasal specimens were examined for the presence of intramucosal S. aureus and characterized to the strain level. An airway epithelial cell culture infection model was utilized to investigate whether bacteria were capable of alterations in virulence phenotype. Results Intramucosal organisms harvested from sinonasal biopsies demonstrate phenotypic growth patterns and lack of coagulase activity consistent with SCV s. Intracellular infection of airway epithelial cell cultures with S. aureus led to decreased secretion of enterotoxins and phenotypic growth alterations consistent with SCV s. Conclusions Regulation of S. aureus virulence factors is a dynamic process, and exposure to the intracellular environment appears to provide the necessary conditions to enable these alterations in an attempt for the bacterium to survive and persist within host tissues. Further work is required to ascertain whether SCV s in CRS hold a clinically relevant pathogenic role in recalcitrant disease.