Table 3. Antimicrobial resistance mechanisms.

Drug	Drug Uptake Limitation	Drug Target Modification	Drug Inactivation	Efflux Pumps
β-Lactams	Decreased numbers of porins, no outer cell wall	Gram pos—alterations in PBPs	Gram pos, gram neg—β-lactamases	RND
Carbapenems	Changed selectivity of porin
Cephalosporins	Changed selectivity of porin
Monobactams
Penicillins
Glycopeptides	Thickened cell wall, no outer cell wall	Modified peptidoglycan
Lipopeptides		Modified net cell surface charge
Aminoglycosides	Cell wall polarity	Ribosomal mutation, methylation	Aminoglycoside modifying enzymes, acetylation, phosphorylation, adenylation	RND
Tetracyclines	Decreased numbers of porins	Ribosomal protection	Antibiotic modification, oxidation	MFS, RND
Chloramphenicol		Ribosomal methylation	Acetylation of drug	MFS, RND
Lincosamides		Gram pos—ribosomal methylation		ABC, RND
Macrolides		Ribosomal mutation, methylation		ABC, MFS, RND
Oxazolidinones		Ribosomal methylation		RND
Streptogramins				ABC
Fluoroquinolones		Gram neg—DNA gyrase modification	Acetylation of drug	MATE, MFS, RND
		Gram pos—topoisomerase IV
Sulfonamides		DHPS reduced binding, overproduction of resistant DHPS		RND
Trimethoprim		DHFR reduced binding, overproduction of DHFR		RND

ABC—ATP binding cassette family, DHFR—dihydrofolate reductase, DHPS—dihydropteroate synthase, MATE—multidrug and toxic compound extrusion family, MFS—major facilitator superfamily, PBP—penicillin-binding protein, RND—resistance-nodulation-cell division family.