Antibiotics

One-Sentence Definition

Antibiotics are antimicrobial agents that kill or inhibit bacteria by attacking structures or pathways that bacteria have and human cells do not.

Simple Explanation

Selective toxicity: hit something the bacterium needs and we don’t have.

Detailed Scientific Explanation

By target

TargetClassesNotes
Cell wall synthesisβ-lactams (penicillins, cephalosporins, carbapenems, monobactams), glycopeptides (vancomycin)Bactericidal; need actively dividing cells
Protein synthesis (50S)Macrolides, lincosamides, oxazolidinones, chloramphenicolMostly bacteriostatic
Protein synthesis (30S)Aminoglycosides, tetracyclinesAminoglycosides bactericidal, concentration-dependent
DNA replicationFluoroquinolones (gyrase/topoisomerase IV)Broad, but collateral damage and toxicity
RNA polymeraseRifamycinsRapid resistance if used alone
Folate pathwaySulfonamides, trimethoprimSynergistic in combination
MembranePolymyxins (colistin), daptomycinLast-line; nephrotoxicity

Pharmacodynamics

  • Time-dependent (β-lactams): efficacy tracks time above MIC → frequent dosing or extended infusion
  • Concentration-dependent (aminoglycosides, fluoroquinolones): peak/MIC ratio → once-daily high dose
  • AUC/MIC (vancomycin, linezolid)

Spectrum and stewardship — narrow-spectrum when the organism is known; broad only while it is not. See Antimicrobial Stewardship.

Mechanism

Selective toxicity depends on targets absent or sufficiently different in humans: peptidoglycan, 70S ribosome, bacterial gyrase, bacterial folate synthesis.

Clinical Importance

  • Choice depends on site (CSF/bone/urine penetration), host (renal/hepatic function, allergy, pregnancy), and local resistance patterns

Research Importance

Diagnostic Relevance

AMR Relevance

Every use selects for resistance — see Antimicrobial Resistance and Mechanisms of Antibiotic Resistance.

Active Recall Questions

  1. What does “selective toxicity” mean and give two examples of exploited targets.
  2. Time-dependent vs concentration-dependent killing — how does each change dosing?
  3. Why is rifampicin rarely used as monotherapy?

Connections