PharmacologyTier 1Medical Sciences concept

Antibiotic classification by mechanism of action and bactericidal/bacteriostatic activity

Core concept

Antibiotics classified by target structure/pathway -- mechanism determines both spectrum and whether the drug is bactericidal or bacteriostatic
Bactericidal (kills): beta-lactams (penicillins, cephalosporins, carbapenems), aminoglycosides, fluoroquinolones, vancomycin, metronidazole
Bacteriostatic (inhibits growth, relies on host immunity to clear): macrolides, tetracyclines, clindamycin, trimethoprim-sulfamethoxazole, linezolid (though bactericidal against some organisms)

Target	Class	Example	Cidal/static
Cell wall (peptidoglycan)	Beta-lactams	Flucloxacillin, ceftriaxone, meropenem	Cidal
Cell wall (glycopeptide)	Glycopeptides	Vancomycin	Cidal
30S ribosome	Aminoglycosides	Gentamicin	Cidal
30S ribosome	Tetracyclines	Doxycycline	Static
50S ribosome	Macrolides	Azithromycin	Static
50S ribosome	Clindamycin, linezolid	--	Static (some cidal activity)
DNA gyrase/topoisomerase	Fluoroquinolones	Ciprofloxacin	Cidal
Folate synthesis	Sulfonamides/trimethoprim	Cotrimoxazole	Static (cidal in combination)
DNA strand breakage (anaerobic)	Nitroimidazoles	Metronidazole	Cidal
RNA polymerase	Rifamycins	Rifampicin	Cidal

Cidal/static distinction matters most in immunocompromised or high-inoculum infections (endocarditis, meningitis, neutropenic sepsis) -- bactericidal agents preferred as host immune clearance cannot be relied upon
Combining a static + cidal agent acting on the same growth-dependent pathway can antagonise (e.g. classically taught: a static protein synthesis inhibitor can theoretically blunt the cidal action of a cell-wall agent that requires active growth) -- rationale for care in empirical combination choices, though clinical significance varies by pairing
Gram-positive vs Gram-negative cell wall structure (thick peptidoglycan + no outer membrane vs thin peptidoglycan + outer membrane/porins) underlies why some agents (e.g. vancomycin) cannot penetrate Gram-negative organisms

Cell-wall agents (beta-lactams) require actively dividing bacteria to be effective -- relevant to why they act more slowly/less effectively against dormant or stationary-phase organisms
Mechanism also predicts key resistance strategies: beta-lactamase enzymes (cell wall agents), efflux pumps and ribosomal target mutation (protein synthesis inhibitors), gyrase mutation (fluoroquinolones)
This classification underlies rational empirical antibiotic selection by presumed organism and site, before culture results return

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