FIGURE 1.

Categorization and mode of actions of antibiotics. According to their barrier structure, bacteria can be divided into gram positive (gr +) and gram negative (gr–). Antibiotics differ in terms of their mechanisms. Some antibiotics target the bacterial cell wall. Beta-lactam antibiotics directly inhibit the enzyme D-alanine-transpeptidase, which impedes cross-linking of building blocks in bacterial murein synthesis. Glycopeptides such as vancomycin, which only attack gram positive bacteria, inhibit bacterial cell wall synthesis by complex formation with murein components. Diaminopyrimidines, e.g., trimethoprim, inhibiting the enzyme dihydrofolate reductase, and sulfonamides, which target the diydropteroatsynthase, inhibit bacterial tetraydrofolate (THF) synthesis and, hence, DNA synthesis. Fluoroquinolones negatively regulate the bacterial enzymes topoisomerase II (gyrase) and topoisomerase IV, which impairs DNA replication. Actinomycin has cytostatic capabilities by intercalating into DNA and thus inhibiting RNA elongation. Moreover, certain antibiotics impede bacterial protein synthesis through binding to 70S ribosomes. In this context, macrolides, phenicols and oxazolidiones inhibit the large 50S subunit, whereas tetracyclins, aminoglycosides and glycylcylins are potent 30S inhibitors. In addition, drugs like puromycin interfere with tRNA function and thus represent another mechanism of protein synthesis inhibition. Metronidazol induces DNA strand breaks. The figure was created with BioRender.com.