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Keywords:

  • chronic rhinosinusitis;
  • CRS;
  • interstitial bacteria;
  • resistant;
  • small-colony variant;
  • chronic inflammation

Background

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.

Methods

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.

Results

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.

Conclusion

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.