TY - JOUR
T1 - Genetic mechanisms of antimicrobial resistance of Acinetobacter baumannii
AU - Esterly, John S.
AU - Richardson, Chad L.
AU - Eltoukhy, Noha S.
AU - Qi, Chao
AU - Scheetz, Marc H.
PY - 2011/2
Y1 - 2011/2
N2 - OBJECTIVE: To summarize published data identifying known genetic mechanisms of antibiotic resistance in Acinetobacter baumanniiand the correlating phenotypic expression of antibiotic resistance. DATA SOURCES: MEDLINE databases (1966-July 15, 2010) were searched to identify original reports of genetic mechanisms of antibiotic resistance in A. baumannii. DATA SYNTHESIS: Numerous genetic mechanisms of resistance to multiple classes of antibiotics are known to exist in A. baumannii, a gram-negative bacterium increasingly implicated in nosocomial infections. Mechanisms may be constitutive or acquired via plasmids, integrons, and transposons. Methods of resistance include enzymatic modification of antibiotic molecules, modification of antibiotic target sites, expression of efflux pumps, and downregulation of cell membrane porin channel expression. Resistance to b-lactams appears to be primarily caused by b-lactamase production, including extended spectrum β-lactamases ( blaTEM, blaSHV, blaCTX-M, blaKPC), metallo- β-lactamases ( blaIMP, blaVIM, blaSIM), and most commonly, oxacillinases ( blaOXA). Antibiotic target site alterations confer resistance to fluoroquinolones ( gyrA, parC) and aminoglycosides ( arm, rmt), and to a much lesser extent, β-lactams. Efflux pumps ( tet, ade, abe) contribute to resistance against b-lactams, tetracyclines, fluoroquinolones, and aminoglycosides. Finally, porin channel deletion ( carO, oprD) appears to contribute to β-lactam resistance and may contribute to rarely seen polymyxin resistance. Of note, efflux pumps and porin deletions as solitary mechanisms may not render clinical resistance to A. baumannii. CONCLUSIONS: A. baumanniipossesses copious genetic resistance mechanisms. Knowledge of local genotypes and expressed phenotypes for A. baumanniimay aid clinicians more than phenotypic susceptibilities reported in large epidemiologic studies.
AB - OBJECTIVE: To summarize published data identifying known genetic mechanisms of antibiotic resistance in Acinetobacter baumanniiand the correlating phenotypic expression of antibiotic resistance. DATA SOURCES: MEDLINE databases (1966-July 15, 2010) were searched to identify original reports of genetic mechanisms of antibiotic resistance in A. baumannii. DATA SYNTHESIS: Numerous genetic mechanisms of resistance to multiple classes of antibiotics are known to exist in A. baumannii, a gram-negative bacterium increasingly implicated in nosocomial infections. Mechanisms may be constitutive or acquired via plasmids, integrons, and transposons. Methods of resistance include enzymatic modification of antibiotic molecules, modification of antibiotic target sites, expression of efflux pumps, and downregulation of cell membrane porin channel expression. Resistance to b-lactams appears to be primarily caused by b-lactamase production, including extended spectrum β-lactamases ( blaTEM, blaSHV, blaCTX-M, blaKPC), metallo- β-lactamases ( blaIMP, blaVIM, blaSIM), and most commonly, oxacillinases ( blaOXA). Antibiotic target site alterations confer resistance to fluoroquinolones ( gyrA, parC) and aminoglycosides ( arm, rmt), and to a much lesser extent, β-lactams. Efflux pumps ( tet, ade, abe) contribute to resistance against b-lactams, tetracyclines, fluoroquinolones, and aminoglycosides. Finally, porin channel deletion ( carO, oprD) appears to contribute to β-lactam resistance and may contribute to rarely seen polymyxin resistance. Of note, efflux pumps and porin deletions as solitary mechanisms may not render clinical resistance to A. baumannii. CONCLUSIONS: A. baumanniipossesses copious genetic resistance mechanisms. Knowledge of local genotypes and expressed phenotypes for A. baumanniimay aid clinicians more than phenotypic susceptibilities reported in large epidemiologic studies.
KW - Acinetobacter baumannii
KW - Antibiotics
KW - Genetic mechanisms
KW - Resistance
KW - β-lactamases
UR - http://www.scopus.com/inward/record.url?scp=79951906190&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79951906190&partnerID=8YFLogxK
U2 - 10.1345/aph.1P084
DO - 10.1345/aph.1P084
M3 - Review article
C2 - 21304033
AN - SCOPUS:79951906190
SN - 1060-0280
VL - 45
SP - 218
EP - 228
JO - Annals of Pharmacotherapy
JF - Annals of Pharmacotherapy
IS - 2
ER -