(153b) Targeted Disruption of Dual Species Interfacial Films of P. Aeruginosa and S. Aureus

Chronic lung infection with bacterial biofilms is one of the leading causes of death in cystic fibrosis (CF) patients. Among many species colonizing the lung airways, Pseudomonas aeruginosa and Staphylococcus aureus are two of the most prevalent pathogens responsible for recalcitrant infections. These pathogens contribute to a mechanically robust biofilm that is difficult to eradicate using methods such as lung lavage and airway clearance techniques. Disrupting agents such as glycoside hydrolase-based compounds are commonly employed to target and break down the biofilm matrix components, and subsequently increase cell susceptibility to antibiotics. In this study, we utilized an interfacial system to study the effect of disrupting agents on the biomechanics of interfacial films. We hypothesize that our system will serve as a standardized platform to characterize and predict the effects of disrupting agents on the mechanical properties of interfacial films. We aim to characterize the effect of generic and targeted biofilm disrupting agents on the mechanical properties of single and dual species interfacial biofilms of P. aeruginosa and S. aureus. Specifically, we assessed viscoelasticity and mechanical properties of the interfacial films using pendant drop tensiometry and pendant capsule elastometry followed by the treatment with disrupting agents. Generic enzymes targeting the 1,4 linkages in the polymer backbone such as glycoside hydrolases (Cellulase and -amylase) and polymer specific enzymes such as DNase targeting the pel (pellicle) and eDNA complex in P. aeruginosa biofilms and dispersin B targeting the polysaccharide intercellular adhesion in S. aureus biofilms were compared for their efficiency to disrupt biofilms. Overall, precise prediction and characterization of the effect of biofilm disrupting agents will provide new insights towards the development of methods for treating interfacial biofilms.