TABLE 2.

Mechanisms of antibacterial resistance

OriginMechanismExamples of affected drug classes
ExogenousClass-specific effluxTetracycline, macrolides
Class-specific degradation/modificationβ-Lactams, aminoglycosides, chloramphenicol, streptogramin A, metronidazole (for anaerobes), fosfomycin
Target protection/modificationTetracycline, macrolides, lincosamides, oxazolidinones, streptogramin B
Replacement with reduced-affinity targetβ-Lactams, vancomycin, trimethoprim, mupirocin, sulfonamides
Sequestration of targetFluoroquinolones, fusidic acid
EndogenousSingle mutations reducing target affinityRifamycin, streptomycin, trimethoprim (for Gram-positive organisms), fusidic acid
Multistep mutations reducing affinity or remodeling of targetFluoroquinolones, oxazolidinones, daptomycin, vancomycin, polymyxin, β-lactams (for transformable species)
General efflux mechanismsMost classes for Pseudomonas; many classes for other species
Reduced uptake (porin or permease loss)Carbapenems, fosfomycin
Loss of activationMetronidazole (for H. pylori)
Upregulation of targetFosfomycin