Targeting Biofilms in Translational Research

Biofilms underpin the disease etiology of nearly all opportunistic bacterial infections especially when integumentary barriers are surgically breached and foreign materials remain implanted. Endogenous spread from the patient’s own microbial flora is the likely source of most surgical site infections. Biomaterials potentiate infection by providing a substrate for biofilm formation. The biofilm protects these pathogens from both host immunity and clinical interventions in a variety of ways. Biofilm-forming bacteria excrete sticky exopolysaccharides to form cohesive communal aggregates and adhesive attachments to foreign surfaces like devitalized tissues and implanted biomaterials; this strategy deranges phagocytic clearance by host immune cells. Quiescent phenotypic variants in the biofilm cells are tolerant of antibiotic concentrations many orders of magnitude greater than would otherwise kill planktonic phenotypes, concentrations greatly exceeding toxic thresholds bounding safe systemic antibiotic concentrations. Biofilms are, thus, a nidus for infection as tolerant cells can outlast clinical antibiotic courses to subsequently reseed infection. Much emphasis has been placed on preventing biofilm infections from occurring as clinical strategies for eradicating established biofilm infections frequently fail. Biofilm infections usually require extensive surgical intervention to remove implanted biomaterials and debride affected tissues. These procedures are costly and usually accompanied by high patient mortality and morbidity. There is a pressing need for strategies that specifically target the biofilm because clinical measures to prevent infection still fail in this antibiotic era at great financial and physical expense.