Topic overview

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Antibiotic resistance is not a single process: bacteria can inactivate or sequester a drug, reduce its entry, pump it out, or prevent it from acting on its target. Target changes include altered penicillin-binding proteins, modified peptidoglycan termini, methylated ribosomal RNA, and mutations affecting DNA gyrase or topoisomerase IV. Other strategies include target-protection proteins, ribosomal protection, metabolic bypass, and overproduction of a target. Biofilms can limit drug diffusion and contain dormant persisters, while lipid A modification can reduce colistin binding. Resistance genes may move together on integrons, transposons, and plasmids; chromosomal mutations and changes in gene expression also contribute. Recognizing how these mechanisms differ helps connect molecular changes with their effects on antibiotic activity.