Hostname: page-component-586b7cd67f-2plfb Total loading time: 0 Render date: 2024-11-24T23:58:20.130Z Has data issue: false hasContentIssue false

The Role of Persistent Infection in the Pathogenesis of Cholesteatoma

Presenting Author: Richard Chole

Published online by Cambridge University Press:  03 June 2016

Richard Chole*
Affiliation:
Washington University in St. Louis School of Medicine
Rights & Permissions [Opens in a new window]

Abstract

Type
Abstracts
Copyright
Copyright © JLO (1984) Limited 2016 

Learning Objectives: To understand the significance of chronic, recalcitrant infections in cholesteatomas. Processes including biofilm formation and bacterial persistence.

Acquired and sometimes congenital cholesteatomas, often become chronically infected. The most common organisms associated with infected cholesteatomas are Pseudomonas aeruginosa and Staphylococcus aureus. Other gram negatives are common associated pathogens, such as Klebsiella, Proteus and E.coli. Infected cholesteatomas are more aggressive and destructive than uninfected cholesteatomas as evidenced by clinical observation and studies in experimental models of cholesteatoma.

The eradication of bacterial infections within cholesteatomas has proven difficult. Treatment with systemic and topical antibiotics often fails to eradicate the infection even though the involved organisms are sensitive to the antibiotics used. The mechanisms of bacterial resistance intolerance in cholesteatomas are complex. There are several possible mechanisms for the tolerance of chronic clinically bacteria in chronically infected cholesteatomas. These include: 1) sequestration of the cholesteatoma matrix from the general circulation; 2) ineffeective penetration of topically applied antimicrobials; 3) formation of microbial biofilms within the cholesteatoma with the resultant change in phenotype to be tolerant to host defenses and antibiotics; and 4) formation of persister cells in bacterial colonies. These cells while viable at a very low metabolic rate and low levels of replication. This change makes this persister cell type highly resistant to antimicrobials.

Strategies to eradicate biofilm infections and the presence of persister cells will be discussed.