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Bacterial adhesion and colonization on stainless steel (SSL) based surgical instruments, hospital equipment, orthopedic implants, water purification and food processing units are a major problem. Imparting rechargeable antibacterial properties to SSL offers the prospect of a reusable and clean surface. In this study, the SSL surface was functionalized with a hydantoin-based antibacterial polymer that prevents bacterial adhesion and colonization. A new hydantoin monomer with three halogen binding sites, (Z)-N-((4-(2,5-dioxoimidazolidin-4-ylidene)methyl)phenyl)methacrylamide (DMPM), was synthesized, characterized and copolymerized with a commercially available 3-(methacryloyloxy)propyltrimethoxysilane monomer to develop the antibacterial polymer. The SSL surface was treated with piranha solution and the copolymer was covalently immobilized on the surface. The modified surface was examined for its antibacterial and anti-biofilm activity. The modified surface exhibited total kill (6 log reduction) of bacteria such as S. aureus and E. coli in 10 and 12 min respectively. The anti-biofilm activity of the modified surface was evaluated using a combination of fluorescence-based metabolic activity and scanning electron microscopy imaging suggested the comprehensive damage of S. aureus and E. coli biofilm architecture.

Zinc-complexing ligands are prospective anti-biofilm agents because of the pivotal role of zinc in the formation of Staphylococcus aureus biofilm. Accordingly, the potential of a thiosemicarbazone (compound C1) and a benzothiazole-based ligand (compound C4) in the prevention of S. aureus biofilm formation was assessed. Compound C1 displayed a bimodal activity, hindering biofilm formation only at low concentrations and promoting biofilm growth at higher concentrations. In the case of C4, a dose-dependent inhibition of S. aureus biofilm growth was observed. Atomic force microscopy analysis suggested that at higher concentrations C1 formed globular aggregates, which perhaps formed a substratum that favored adhesion of cells and biofilm formation. In the case of C4, zinc supplementation experiments validated zinc complexation as a plausible mechanism of inhibition of S. aureus biofilm. Interestingly, C4 was nontoxic to cultured HeLa cells and thus has promise as a therapeutic anti-biofilm agent. The essential understanding of the structure-driven implications of zinc-complexing ligands acquired in this study might assist future screening regimes for identification of potent anti-biofilm agents.