The distinction is functional, not taxonomic Bactericidal drugs kill; bacteriostatic drugs stop growth. The same drug can behave differently depending on concentration, organism, and growth phase, so the label describes the drug-target interaction under defined conditions rather than a permanent property of the molecule. Target disruption and its downstream consequence Bactericidal Beta-lactams and glycopeptides: wall cross-linking stops, osmotic pressure ruptures the cell. Aminoglycosides: mistranslation produces toxic misfolded proteins. Fluoroquinolones: trapped gyrase-DNA complexes generate lethal double-strand breaks. Polymyxins: outer membrane barrier is disrupted, permeability is lost. Bacteriostatic Tetracyclines: A-site block stops translation without producing toxic products. Macrolides: exit-tunnel block stops translation without producing toxic products. Sulfonamides and trimethoprim: folate synthesis is cut, starving the cell of thymidine and purines. Polymyxins act on the membrane, not the wall Polymyxins bind lipopolysaccharide in the Gram-negative outer membrane and displace the divalent cations that stabilize it. The membrane barrier fails and the cell dies, which is why polymyxins are bactericidal despite not touching peptidoglycan synthesis.
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Killing Versus Stalling: What the Target Tells You
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So what actually separates a drug that kills from one that only stalls growth? Start with the four we just watched. Fluoroquinolone leaves gyrase frozen on broken DNA, and rifamycin seals the RNA exit channel, so both leave the cell unable to function and it dies. Sulfonamide and trimethoprim merely starve the folate supply, so the cell stops growing but stays alive. Now widen the frame to every class we have covered, because the same split runs through all of them.
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