Bacteria on the plate grow and divide; the chosen antibiotic adds a concentration-dependent kill rate on top of growth, following a Hill/Emax pharmacodynamic model. Cells whose kill rate exceeds their growth rate die faster than they reproduce and the colony shrinks; resistant mutants — which need a much higher concentration to feel the same effect — keep dividing and take over.
Kill rate: E(C) = Emax · C^h / (MIC_eff^h + C^h)
Net growth: dN/dt ∝ k_growth − E(C)
Resistant MIC: MIC_eff = MIC_base × resistance factor
β-lactam × 32 (β-lactamase hydrolyses the drug)
macrolide × 16 (efflux pumps / ribosomal methylation)
fluoroquinolone × 8 (gyrase/topoisomerase point mutation)
- β-Lactam (penicillins, cephalosporins) — binds penicillin-binding proteins, blocking peptidoglycan cross-linking; the wall fails and osmotic pressure bursts the cell (lysis).
- Macrolide (e.g. azithromycin) — binds the 50S ribosomal subunit and blocks translocation, stalling protein synthesis; mostly bacteriostatic, cells shrink and stop dividing rather than burst.
- Fluoroquinolone (e.g. ciprofloxacin) — inhibits DNA gyrase / topoisomerase IV, trapping the enzyme on DNA and blocking replication; cells filament (keep growing without dividing) before fragmenting and dying.
- Mutation rate — probability that a dividing susceptible cell's daughter acquires a resistance mutation; resistance is then inherited by all its descendants.
This is exactly why finishing a prescribed antibiotic course matters: a sub-lethal concentration kills only the most susceptible cells and selectively breeds the resistant survivors — the same natural-selection dynamic you can trigger here by dialing concentration below the effective MIC.