TABLE 2.

Mechanisms of antibacterial resistance

Origin	Mechanism	Examples of affected drug classes
Exogenous	Class-specific efflux	Tetracycline, macrolides
	Class-specific degradation/modification	β-Lactams, aminoglycosides, chloramphenicol, streptogramin A, metronidazole (for anaerobes), fosfomycin
	Target protection/modification	Tetracycline, macrolides, lincosamides, oxazolidinones, streptogramin B
	Replacement with reduced-affinity target	β-Lactams, vancomycin, trimethoprim, mupirocin, sulfonamides
	Sequestration of target	Fluoroquinolones, fusidic acid
Endogenous	Single mutations reducing target affinity	Rifamycin, streptomycin, trimethoprim (for Gram-positive organisms), fusidic acid
	Multistep mutations reducing affinity or remodeling of target	Fluoroquinolones, oxazolidinones, daptomycin, vancomycin, polymyxin, β-lactams (for transformable species)
	General efflux mechanisms	Most classes for Pseudomonas; many classes for other species
	Reduced uptake (porin or permease loss)	Carbapenems, fosfomycin
	Loss of activation	Metronidazole (for H. pylori)
	Upregulation of target	Fosfomycin