Inhibition of bacterial biofilm formation on polymer surfaces by a natural antimicrobial agent

In modern medicine, medical devices are used for different applications, including the repair or replacement of damaged parts of the body, the delivery of drugs and the monitoring of critically ill patients. However, artificial surfaces are often susceptible to colonization by bacteria and fungi. Once adhered, microrganisms grow forming biofilms and the associated local or systemic infections are highly resistant local or systemic infections. Strategies to prevent these infections include catheter’s coatings with antimicrobials that eluting from the device avoid microbial colonization. Current evidence suggests that (+)-usnic acid, a secondary lichen metabolite, possesses antimicrobial activity against a number of planktonic Gram positive bacteria, including Staphylococcus aureus, Enterococcus faecalis and E. faecium. We evaluated the possible inhibiting effect of usnic acid by loading polymers widely employed to produce several medical devices. As usnic acid exhibits acidic properties, the surface of a polyether urethane acid was specifically modified to introduce basic functional groups (amino groups) able to establish electrostatic interactions with the acidic groups displayed by usnic acid. These functionalised polymers were then incorporated in a flow cell designed for growing biofilms under a wide range of hydrodynamic conditions, and subsequently analysed using confocal microscopy. The capacity of usnic acid to control biofilm formation was assessed using Staphylococcus aureus and the Gram negative pathogen, Pseudomonas aeruginosa. Results: Usnic acid-loaded polymers have been shown to be resistant to biofilm formation by S. aureus and possibly other Gram positive organisms. In contrast, P. aeruginosa biofilm was formed on the surfaces of both the untreated and usnic acid-loaded polymer. However, usnic acid affected the morphology of the P. aeruginosa biofilm, possibly indicating that drug interfered with cell-cell communication by influencing signalling pathways. These promising results open new perspectives in the development of medical devices able to inhibit biofilm formation.