Bill Costerton
Direct observations have revealed that the bacteria that cause device-related and other chronic diseases grow in matrix-enclosed biofilms, adherent to the surfaces of biomaterials and tissues. In this biofilm mode-of-growth, the organisms are virtually impervious to antibiotics, and to the antibodies and phagocytes that constitute the defense systems of virtually all mammals. Within the biofilm community the cells communicate by means of chemical and (possibly) electrical signals, so that these sessile communities can coordinate their responses to host countermeasures, and persist for months or even for years. Biofilm communities can withstand the attacks of antibacterial agents (e.g. antibiotics) that would readily kill planktonic cells of the same strain, and many medical specialties surgically remove the biofilms and their living or inert substrata, as their rational basis of anti-biofilm therapy. In general, biofilms cause damage to the affected tissues by their persistence. When host defenses and antibiotic therapy fail to resolve chronic infections, the inflammation that they stimulate becomes the predominant factor in damage to affected tissues.
Because of recent advances in Biofilm Microbiology, the clinical pendulum is swinging away form frontal attacks with antibiotics, towards the use of immune modulation to minimize the effects of inflammation on the host tissues. These same data have stimulated interest in the use of signals to minimize biofilm formation, and even to stimulate the dissolution of existing biofilms by promoting detachment. The notion of using physical forces (e.g. DC fields, and ultrasonic waves) to disrupt the internal communications within biofilms is also gaining traction, and a more complete understanding of the structure and function of whole microbial communities will engender new and practical technologies for biofilm control.
