[Phil J Microbiol Infect Dis 199634;25(1):S25-S34] ANTIMICROBIAL ACTION

In general, all antibiotics exert their effect on the bacteria by binding to some target site and interrupting a cell function that is essential to the organism. As expected, the specific mechanism by which antibiotics cause cell death is different for each of the antimicrobial classes. For the fluoroquinolones, this mechanism involves the DNA gyrase; for the beta-lactams, the penicillin-binding proteins of the cell wall; and for the aminoglycosides, the ribosomes.1,2,3 Because drug must first reach the outside of the bacterial cell wall before its penetration via passive diffusion to the target site, the influence of the human body on the disposition or pharmacokinetics of the antimicrobial is of paramount importance if the agent is to eradicate the organism because it is the pharmacokinetics in the host body that governs the presentation of drugs to the bacteria. The inherent presence of the antimicrobial at the site of infection, however, is not sufficient to ensure cell death. The antimicrobial must be capable of not only penetrating the cell wall in high enough concentrations, but also must have ample affinity for the binding sites such that a critical number are occupied, and the normal physiologic function of the cell is interrupted resulting in cell death.4 This process is analogous to what is commonly termed the microbiologi