P. aeruginosa infection increases morbidity in experimental cholesteatomas.

OBJECTIVES: Clinicians have long noted that infected cholesteatomas are more aggressive than uninfected ones without data to support these observations. The purpose of this study is to determine the etiological role of biofilm forming P. aeruginosa (PA) and the virulence factor, type IV pili (TFP), in the pathogenesis of experimental cholesteatomas.
DESIGN: We evaluated three different PA strains and one Escherichia coli strain in cholesteatoma progression: PA14, a well-characterized wound isolate, OPPA8, an otopathogenic strain from a human cholesteatoma, OPPA8-NP, an isogenic TFP deletion mutant, and DH5α, an E. coli strain.
METHODS: Cholesteatomas were induced in gerbils. We inoculated the right ear with bacteria and the left with vehicle. After 6 weeks their cholesteatomas were evaluated by micro-CT scanning. Cholesteatoma size and bone resorption were analyzed digitally.
RESULTS: Results demonstrate that PA infection increases cholesteatoma size when compared to uninfected controls: OPPA8 showed an 8.9-fold increase, PA14 a 2.6-fold increase, OPPA8-NP a 1.9-fold increase, while DH5α was not increased over controls. Additionally, infected bullae showed 10 to 50% more cholesteatoma-induced bone resorption.
CONCLUSIONS: In this model, PA infected cholesteatomas enlarge more rapidly and are more destructive than uninfected controls. OPPA8, the strain from a human cholesteatoma, showed the greatest enlargement and bone destruction. Additionally, we demonstrate that TFP is a virulence factor in this model because the nonpiliated isogenic mutant, OPPA8-NP, was significantly less aggressive than the wild-type OPPA8 indicating that type IV pili may be a virulence factor in this disease.