Untangling the Diverse and Redundant Mechanisms of Staphylococcus aureus Biofilm Formation

A major challenge in the management of device-related infections (DRIs) involving microbial biofilms derives from the rapid coating of implanted biomaterials by host-derived glycoproteins and other macromolecules. The performance of modified biomaterial surfaces that limit bacterial colonisation under laboratory conditions is difficult to predict in this in vivo milieu. Biofilms formed by staphylococci have for many decades been recognised as the most frequent cause of biofilm-associated infections with Staphylococcus epidermidis and Staphylococcus aureus being the two main species of staphylococci associated with DRI. Advances in our understanding of staphylococcal biofilm mechanisms have made one fact clear: namely, that this important pathogen has adopted the mantra "to stick to surfaces at all costs" and employs a remarkable array of adherence mechanisms to achieve this goal. Here we will review these diverse biofilm mechanisms, raise questions about why such redundancy exists, and outline potential implications for the development of new biofilm-targeted therapeutics.