TABLE 1.

The targets and modes of action of the main classes of bactericidal antibiotics

Bactericidal antibiotics	Targets and modes of action
β-Lactams	Disrupt cell wall synthesis: penicillins, cephalosporins, monobactams, and carbapenems. Bind covalently to the enzymes that synthesize and reorganize the bacterial cell wall: peptidoglycan synthetases and hydrolases (penicillin binding proteins [PBPs]). Induce bacterial lysis and abnormal cell shape (234).
Quinolones	Clinically important drugs are fluoroquinolones, e.g., ciprofloxacin, levofloxacin, ofloxacin, and gatifloxacin. Bind to the complexes of type II topoisomerases and DNA at the stage where both cleaved DNA strands are covalently attached to the topoisomerase subunits. Induce DNA brakes, SOS response, and mutagenesis in targeted bacteria (230).
Aminoglycosides	Target protein synthesis, bind to the decoding center of the small (30S) ribosomal subunit. Bactericidal action is caused by erroneous translation, particularly mistranslation of membrane protein leading to membrane damage (6, 231, 232).
Peptide antibiotics	Nonribosomally synthesized peptides: glycopeptides (e.g., vancomycin), polymyxins (e.g., colistin), gramicidins, and bacitracins. Target cell wall synthesis and cell membranes; clinical use is restricted due to their toxicity and a narrow spectrum of action (233).
Other classes	Diverse mechanisms of action: macrolides (e.g., erythromycin), chloramphenicol, and rifampin are bactericidal against some bacterial phyla/strains and bacteriostatic against others. The antituberculosis (pro)drug isoniazid is bactericidal against fast-growing and bacteriostatic against slow-growing mycobacteria. When activated by KatG, it inhibits synthesis of mycolic acids and the mycobacterial cell wall. An antituberculosis drug, bedaquiline of the diarylquinoline class, blocks the mycobacterial ATP synthesis.