Mechanisms of antimicrobial resistance in Gram-negative bacilli

Annals of Intensive Care

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-lactamases^a	MGE acquisition	Penicillins, 3GC
Metallo-beta-lactamases^b (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 enzymes^d	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′).