## 1 Introduction  
With the advent of modern medicine, many implantable medical devices such as breast, dental, and gluteal implants; orthopedic devices; heart valves; stents; pacemakers; hernia mesh; and a host of others have been introduced with either cosmetic or curative intent. Although these implants are successful in treating several diseases, as well as enhancing cosmetic appearance, they are prone to bacterial colonization and infection, which are often treated with antibiotics [1, 2, 3]; however, chronic recurrence often leads to hospitalization with surgical removal or debridement [4, 5]. Various bacteria are known to colonize these implants, while the type of bacteria infecting certain types of implants seems to be specific [6, 7, 8] and treatment response may be organism-specific. The results for hernia repair treatments have been improved with the insertion of surgical mesh [9]. Infections in approximately 1% of the groin or up to 8% of ventral hernia mesh repairs are seen [10] Although different individual bacteria can invade these implants, sometimes two or three different strains of the same genus may exist in a colony [11; 12], with subsequent treatment failure owing to susceptibility differences to bactericides [13]. Further, treatment can be difficult because the invading bacterial colony exudes a slimy secretion (biofilm) over the implanted mesh [14]. The biofilm is a complex material that provides residence for the bacteria, as well as protection against the external environment and bactericides. Although there are some differences in the compositions of biofilms secreted by various bacteria [15], they are similar in their basic architecture and composition. A biofilm is composed of a hydrophobic outer layer of complex carbohydrate with an interior backbone (rigid structure) composed of protein [16]. Whilst the main component of the biofilm is the polysaccharide, a hexosamine comprising mainly N-acetyl-D-glucosamine residues with \(\beta\) (1,6)-linkages, the secreted protein within the matrix with amyloid-type behavior forms protein fibrils that inter-link themselves to form the rigid backbone of most biofilms [17]. The extracellular polymeric substances (EPS) secreted by the bacteria contain micro-channels for the inflow of water and nutrients, whilst at the same time providing a barrier from the external environment [18; 19]. Additionally, other vital protein molecules that provide adhesion of bacteria to the biofilm and the host tissue, known as cell wall adhesins (CWA) [20], provide an immunomodulatory function for evasion from the host's innate immune system [21; 22]. Overall, the biofilm provides a safe residence for the colonizing bacteria. Hence, the prevention of the formation of biofilms will prevent the colonization of these pathogens whilst improving the safety of implants. Treatment of bacterial infection is often difficult, since several mechanisms exist to preserve or protect bacterial colonies in biofilms. Indeed, the surface charges on the EPS may either repel or attract antibiotics with subsequent repulsion or penetration through the biofilm, resulting in the observed differential antibacterial action [23; 24]. Differential antibacterial action amongst antibiotics may also be related to their mode of action, whilst at the same time residual exposure may increase resistance owing to the development of endogenous mechanisms within the bacteria against antibiotics [25]. Bacteria can also enter a resting state or sporulate with the development of very high resistance to current antibiotic therapy [26]. Further, the size of the micro-channels may regulate the passage of antibiotics [27]. Therefore, resistance to antibiotics may be due to exogenous or endogenous mechanisms. Hence, in light of the current information on the structure of biofilms, agents that disintegrate biofilms may act as an effective therapy to destroy the matrix within which bacteria reside, thereby exposing them to the innate immune system [28], with further full exposure to bactericides.