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. 2015 Aug 12;5:21. doi: 10.1186/s13613-015-0061-0

Table 5.

Main mechanisms of acquired antimicrobial resistance in Acinetobacter baumannii

Mechanism Genetic event Antimicrobials
High-level expressed AmpC cephalosporinase Chromosomal mutation Penicillins (with or without beta-lactamase inhibitors), 3GC
High-level expressed OXA-51-like beta-lactamase Chromosomal mutation (insertion of ISAba1 upstream of bla OXA-51) Carbapenems
Other beta-lactamases
 Extended-spectrum beta-lactamasesa MGE acquisition Penicillins, 3GC
 Metallo-beta-lactamasesb (carbapenemases) Penicillins, 3GC, carbapenems
 Oxacillinase-type carbapenemases3 Penicillins, carbapenems
Functional loss of porins (impermeability) Chromosomal mutation Variable
Altered penicillin-binding proteins Chromosomal mutation Variable
Active efflux pumps
 AdeABC Chromosomal mutation Beta-lactams (variable), aminoglycosides, fluoroquinolones, tigecycline
 AdeM Aminoglycosides, fluoroquinolones
 AdeIJK Tigecycline
Aminoglycoside-modifying enzymesd MGE acquisition Aminoglycosides
16S rRNA methylases MGE acquisition Aminoglycosides
Topoisomerases modifications Chromosomal mutation Fluoroquinolones
Lipid A (LPS) modifications Chromosomal mutation Polymyxins

MGE mobile genetic element (plasmid or transposon), 3GC third-generation cephalosporins.

Most common enzyme types: aPER, VEB and GES (TEM, SHV and CTX-M are rare in A. baumannii); bVIM, SIM, IMP and NDM; cOXA-23-, OXA-40-, OXA-58-, OXA-143 and OXA-235-like; dAAC(3), AAC(6′) and APH(3′).