Table 2.
Overview of antibiotic classes: mechanisms, resistance mechanisms, and therapeutic implications.
| Antibiotic class | Examples | Mechanism of action | Spectrum | Resistance mechanisms | Key clinical notes | References |
|---|---|---|---|---|---|---|
| β-Lactams | Penicillin G, Amoxicillin, Cefazolin, Meropenem | Inhibit cell wall synthesis via PBPs, blocking peptidoglycan cross-linking | Broad (Gram+/Gram–) | β-lactamases, altered PBPs, porin loss | Carbapenems active vs ESBLs; resistance rising | (8, 14) |
| Glycopeptides | Vancomycin, Teicoplanin | Bind D-Ala-D-Ala, inhibit peptidoglycan transglycosylation | Gram-positive (MRSA, VRE) | Altered binding site (VanA/VanB genes) | Reserved for resistant Gram+; nephrotoxicity risk | (14) |
| Aminoglycosides | Gentamicin, Amikacin | Bind 30S ribosomal subunit, cause mRNA misreading | Aerobic Gram-negative | Enzymatic modification, efflux, ribosome methylation | Nephrotoxic, ototoxic; post-antibiotic effect | (17) |
| Tetracyclines | Doxycycline, Minocycline | Bind 30S, block aminoacyl-tRNA attachment | Broad (Gram+/Gram–, atypicals) | Efflux pumps, ribosome protection proteins | Avoid in pregnancy; dental discoloration | (18–20) |
| Macrolides | Erythromycin, Azithromycin | Bind 50S, inhibit translocation | Gram+ and atypicals | Methylation of 23S rRNA, efflux | Used in penicillin allergy; QT prolongation | (17) |
| Fluoroquinolones | Ciprofloxacin, Levofloxacin | Inhibit DNA gyrase and topoisomerase IV | Broad (Gram– > Gram+) | Target mutations, qnr genes, efflux | Risk of tendon rupture; increasing resistance | (13) |
| Sulfonamides + TMP | Sulfamethoxazole + Trimethoprim | Block folate synthesis at two steps | Broad (esp. UTIs, PJP) | Target alteration, plasmid-mediated resistance | Synergistic combo; used for PJP, UTIs | (18–20) |
| Lipopeptides | Daptomycin | Insert into membrane → depolarization and ion leakage | Gram-positive (MRSA, VRE) | Membrane charge alteration | Inactive in pneumonia (surfactant inhibition) | (16) |
| Nitroimidazoles | Metronidazole | Generate free radicals that damage DNA | Anaerobes, C. difficile | Decreased uptake, nitroreductase mutation | Avoid alcohol (disulfiram-like reaction) | (13) |
| Oxazolidinones | Linezolid, Tedizolid | Bind 50S, prevent initiation complex formation | Gram-positive (MRSA, VRE) | 23S rRNA mutations, L3 protein alterations | Monitor for myelosuppression; reserved for resistant cases | (18–20) |
| Polymyxins | Colistin, Polymyxin B | Disrupt outer membrane via LPS binding | Gram-negative (MDR) | MCR-1 gene (modifies lipid A), efflux | Last-resort agent; high nephrotoxicity | (13, 16) |
| Rifamycins | Rifampin, Rifabutin | Inhibit RNA polymerase → block transcription | Gram-positive, TB | rpoB gene mutations | Potent inducer of CYP450; orange discoloration | (17) |
| Lincosamides | Clindamycin | Bind 50S → inhibit peptide bond formation | Gram-positive, anaerobes | erm-mediated methylation | Risk of C. difficile colitis | (18–20) |
Overview of major antibiotic classes, their mechanisms of action, clinical spectrum, resistance mechanisms, and key therapeutic considerations. This table provides a rapid reference for both established and emerging resistance determinants across clinically important drug classes.
ESBL, extended-spectrum β-lactamase; MRSA, methicillin-resistant Staphylococcus aureus; VRE, vancomycin-resistant Enterococcus; PBPs, penicillin-binding proteins; PJP, Pneumocystis jirovecii pneumonia; MDR, multidrug-resistant; LPS, lipopolysaccharide; CYP450, cytochrome P450; TB, tuberculosis; UTIs, urinary tract infections; TMP, trimethoprim.
See text for further details.