Medical implants serve as a polymer surface to which bacteria can attach to via hydrophobic or electrostatic attraction [2, 18]. Binding of bacteria to the hydrophobic surfaces of implants is energetically favorable and is a critical first step in biofilm formation [2]. Biofilm development occurs in a stepwise manner, beginning with adherence of bacteria to the implant surface, followed by their proliferation and differentiation, and culminating with their dispersion (Figure 1) [16, 18]. Adhesion occurs via surface adhesins such as polysaccharides and components of bacterial membranes such as teichoic acids in gram-positive bacteria [18]. Common to many bacteria is the adhesin poly-GlcNAc (Pga) and its biosynthesizing proteins PgaA and PgaD [4]. Pga production regulation depends on the bacterial nucleotide second messengers guanosine-bis 3', 5'(diphosphate) (ppGpp) and c-di-GMP [4, 21]. Nucleotide second messengers are universal signal transduction molecules that regulate transition between motile and sessile states in many bacteria by altering adhesin expression [5, 20]. For example, ribosomal stress caused by sub-inhibitory concentrations of ribosome-targeting antibiotics triggers biofilm formation via the nucleotide second messengers C-di-GMP and ppGpp upregulating PgaA and PgaD synthesis, leading to Pga adhesin biosynthesis and consequent attachment of the bacteria (Figure 2) [4].