With the initial discovery of penicillin and the ensuing mass production of antibiotics in the 1940s, infectious bacteria quickly adapted and developed resistance to the deleterious molecules. In fact, a report published in 1947 found that of 100 staphylococcus infections tested, 38 were classified as highly resistant to penicillin (1). The initial resistance was primarily associated with individual enzymes inactivating specific antibiotics, such as β-lactamases on penicillin. As novel antibiotics were implemented to combat resistant pathogens, selective pressure led to fundamentally new methods of drug resistance. Currently, there are roughly three major mechanisms utilized by bacteria to evade the toxic effects of biocidal agents. These mechanisms include enzymes that modify the drug, alteration of the antibacterial target, and reduced drug uptake due to the presence of efflux pumps or a decrease in porin expression.