Fig 1.
Bactericidal drugs may be static in vivo.
In the absence of stress, when bacterial cells are undergoing replication, the bactericidal antibiotic fluoroquinolone binds to its target (DNA gyrase and topoisomerase IV) and prevents the religation step during DNA synthesis. This leads to double-strand breaks and cell death. Macrophage-produced stresses (such as ROS/RNS or acid stress) may down-regulate cellular processes targeted by antibiotics. In the absence of replication, the fluoroquinolone may bind to its target but does not cause double-strand breaks or cell death. This leads to antibiotic tolerance. Figure created using BioRender. ROS/RNS, reactive oxygen and nitrogen species.