The potential role of biofilm biofilm phenotypes in Chronic Otitis Media with Effusion (COME)

Livjot Sachdeva, Jason G. May, Michael Hoa, Richard S. Berk, James M. Coticchia

Research output: Contribution to journalArticle

Abstract

Hypothesis: Middle ear pathogens (MEPs) originating from nasopharyngeal biofilms play a significant role in the pathogenesis of Chronic Otitis Media with Effusion (COME). Objective: The role of bacterial infection in chronic suppurative otitis media and Acute Otitis Media (AOM) has been well established. There continues to be debate pertaining to the role of middle ear pathogens in COME. Work in our lab has previously demonstrated dense biofilms in the nasopharynx of patients with recurrent AOM. Through this study, we sought to elucidate the impact of biofilm phenotypes in COME. Study Design: Adenoid specimens obtained from 7 COME patients were evaluated using Scanning Electron Microscopy (SEM). Obstructive Sleep Apnea (OSA) patients were used as controls. Biofilm density analysis was performed with Carnoy image analysis software. Polymerase Chain Reaction (PCR) analysis was performed on a subset of nasopharyngeal specimens obtained from COME patients and their matched middle ear fluids (MEFs). Results: COME specimens had 31.80% mean biofilm density versus 0.04% in OSA controls. All MEFs demonstrated the presence of DNA from middle ear pathogens which included S. pneumoniae, M. catarrhalis, H. influenzae. Any MEP identified in MEF was also identified in matched adenoid specimen. Conclusion: These data suggest that MEFs from patients with COME contain MEPs and the source for these MEPs may be resistant adenoid mucosal biofilms.

Original languageEnglish (US)
Pages (from-to)S315
JournalLaryngoscope
Volume119
Issue numberSUPPL.3
DOIs
StatePublished - Dec 1 2009

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Otitis Media with Effusion
Middle Ear
Biofilms
Phenotype
Adenoids
Otitis Media
Obstructive Sleep Apnea
Suppurative Otitis Media
Nasopharynx
Bacterial Infections
Electron Scanning Microscopy
Human Influenza
Pneumonia
Software
Polymerase Chain Reaction

All Science Journal Classification (ASJC) codes

  • Otorhinolaryngology

Cite this

Sachdeva, Livjot ; May, Jason G. ; Hoa, Michael ; Berk, Richard S. ; Coticchia, James M. / The potential role of biofilm biofilm phenotypes in Chronic Otitis Media with Effusion (COME). In: Laryngoscope. 2009 ; Vol. 119, No. SUPPL.3. pp. S315.
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abstract = "Hypothesis: Middle ear pathogens (MEPs) originating from nasopharyngeal biofilms play a significant role in the pathogenesis of Chronic Otitis Media with Effusion (COME). Objective: The role of bacterial infection in chronic suppurative otitis media and Acute Otitis Media (AOM) has been well established. There continues to be debate pertaining to the role of middle ear pathogens in COME. Work in our lab has previously demonstrated dense biofilms in the nasopharynx of patients with recurrent AOM. Through this study, we sought to elucidate the impact of biofilm phenotypes in COME. Study Design: Adenoid specimens obtained from 7 COME patients were evaluated using Scanning Electron Microscopy (SEM). Obstructive Sleep Apnea (OSA) patients were used as controls. Biofilm density analysis was performed with Carnoy image analysis software. Polymerase Chain Reaction (PCR) analysis was performed on a subset of nasopharyngeal specimens obtained from COME patients and their matched middle ear fluids (MEFs). Results: COME specimens had 31.80{\%} mean biofilm density versus 0.04{\%} in OSA controls. All MEFs demonstrated the presence of DNA from middle ear pathogens which included S. pneumoniae, M. catarrhalis, H. influenzae. Any MEP identified in MEF was also identified in matched adenoid specimen. Conclusion: These data suggest that MEFs from patients with COME contain MEPs and the source for these MEPs may be resistant adenoid mucosal biofilms.",
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The potential role of biofilm biofilm phenotypes in Chronic Otitis Media with Effusion (COME). / Sachdeva, Livjot; May, Jason G.; Hoa, Michael; Berk, Richard S.; Coticchia, James M.

In: Laryngoscope, Vol. 119, No. SUPPL.3, 01.12.2009, p. S315.

Research output: Contribution to journalArticle

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