Chronic suppurative otitis media
Biofilms have a central role in the pathogenesis of chronic otitis media, resulting in a chronic refractory disease that is not able to be resolved by standard antimicrobial therapies or by the host immune response. The two most common, and likely most significant pathogens involved in the pathogenesis of CSOM are Staphylococcus aureus and Pseudomonas aeruginosa. Unfortunately the current available treatments are primitive and include intravenous or topical antibiotics and topical antiseptic flushes, which may have secondary ototoxic effects. Current therapies have some effect on the planktonic bacteria in the middle ear which cause the acute infections but do not resolve the biofilms which act as infectious reservoirs. The Santa Maria lab has developed a rodent CSOM model that now provides the opportunity to test new therapeutics for this indication.
The first step in developing the CSOM model was to create a chronic TM perforation model. An inhibitor of EGFR ligand shedding (KB-R7785) following surgery created a defect to induce a 3-month non-healing perforation. A surgical model was then used to obstruct the Eustachian tube using gutta percha. Pseudomonas aeruginosa was then inoculated into the middle ear and confirmed by PCR two weeks later.
Work is now being done to further characterize these biofilms in the in vivo model and to trial novel therapeutics that can disrupt these biofilms and reduce the burden of disease.