The characteristics of intramucosal bacteria in chronic rhinosinusitis: a prospective cross-sectional analysis
Potential conflict of interest: None provided.
Presented orally at the Annual ARS Meeting on September 8, 2012, Washington, DC.
Correspondence to: Richard Douglas, Department of Surgery, Level 12, Auckland City Hospital, Park Road, Grafton, Auckland 1023, New Zealand; e-mail: firstname.lastname@example.org
We have observed subepithelial bacterial microcolonies within the mucosa of patients with chronic rhinosinusitis (CRS). These were predominantly Staphylococcus aureus and did not appear to elicit a local inflammatory response. We hypothesized that these microcolonies had made adaptations allowing them to exist apparently undetected within the mucosa. We sought to determine whether the tissue colonies had genotypic or phenotypic variations from the surface bacteria.
Mucosal swabs and tissue biopsies were taken from 31 patients with CRS undergoing functional endoscopic sinus surgery, and 9 with normal sinuses having transnasal pituitary surgery. Biopsied tissues were assessed histologically, by routine culture, and by culture techniques facilitating growth of small colony variants (SCVs). Genotypic typing compared isolates of S. aureus that were cultured from both swab and tissue samples. The activity of the accessory gene regulator (agr) gene, a global regulator of S. aureus virulence, was evaluated indirectly by determining the hemolytic activity of the colonies on blood agar.
SCVs were grown from 2 samples but these were found not to possess the nuc gene, specific to S. aureus. When S. aureus was recovered from both swab and mucosa, the genetic profiles were indistinguishable in all but 1 patient. All S. aureus cultured from mucosa demonstrated β-hemolysis, implying normal agr activity.
Intramucosal S. aureus are genetically closely related and phenotypically similar to surface S. aureus. Further studies are needed to explore the possible mechanisms by which intramucosal colonies become less immunogenic, and the role of the colonies in the pathophysiology of CRS.