Aminoglycoside resistance and susceptibility testing errors in Acinetobacter baumannii-calcoaceticus complex.
Antimicrobial resistance is depleting the pharmacopeia of agents clinically useful against Gram-negative bacilli. As the number of active agents diminishes, accurate susceptibility testing becomes critical. We studied the susceptibilities of 107 isolates of the Acinetobacter baumannii-calcoaceticus complex to amikacin, gentamicin, and tobramycin using disk diffusion, Etest, as well as the Phoenix, Vitek 2, and MicroScan automated systems, and compared the results to those obtained by broth microdilution. Genes encoding aminoglycoside-modifying enzymes (AMEs) were detected by multiplex PCR, and clonal relationships were determined by pulsed-field gel electrophoresis. Tobramycin was the most active aminoglycoside (27.1% of isolates were susceptible). Disk diffusion and Etest tended to be more accurate than the Vitek 2, Phoenix, and MicroScan automated systems; but errors were noted with all methods. The Vitek 2 instrument incorrectly reported that more than one-third of the isolates were susceptible to amikacin (a very major error). Isolates were polyclonal, with 26 distinct strains, and carried multiple AME genes unrelated to the strain type. The presence of the ant(2")-Ia gene was statistically associated with resistance to each aminoglycoside. The AME genotype accounted for the resistance profile observed in a minority of isolates, suggesting the involvement of multiple resistance mechanisms. Hospital pharmacy records indicated the preferential use of amikacin over other aminoglycosides in the burn intensive care unit, where aminoglycoside resistance is prevalent. The resistance in that unit did not correlate with a predominant strain, AME genotype, or total annual aminoglycoside consumption. Susceptibility to tobramycin increased, even though susceptible isolates carried AME genotypes predicting the inactivation of tobramycin. Determination of the relative contribution of multiple concurrent resistance mechanisms may improve our understanding of aminoglycoside resistance in the Acinetobacter baumannii-calcoaceticus complex.
Akers
Kevin S
KS
Infectious Disease Service, San Antonio Military Medical Center, 3851 Roger Brooke Drive, Fort Sam Houston, Texas 78234-6200, USA.
Chaney
Chris
C
Barsoumian
Alice
A
Beckius
Miriam
M
Zera
Wendy
W
Yu
Xin
X
Guymon
Charles
C
Keen
Edward F
EF
Robinson
Brian J
BJ
Mende
Katrin
K
Murray
Clinton K
CK
D040981:Acinetobacter baumannii / Q000145:classification / Q000187:drug effects* / Q000235:genetics; D016954:Acinetobacter calcoaceticus / Q000145:classification / Q000187:drug effects* / Q000235:genetics; D000328:Adult; D000617:Aminoglycosides / Q000494:pharmacology*; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D015373:Bacterial Typing Techniques; D003951:Diagnostic Errors / Q000706:statistics & numerical data*; D024881:Drug Resistance, Bacterial; D005798:Genes, Bacterial; D005838:Genotype; D006801:Humans; D008826:Microbial Sensitivity Tests; D055815:Young Adult
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents