Genetic basis of resistance to aminoglycosides in Acinetobacter spp. and spread of armA in Acinetobacter baumannii sequence group 1 in Korean hospitals

Cho, Yoo Jin; Moon, Dong Chan; Jin, Jong Sook; Choi, Chul Hee; Lee, Yoo Chul; Lee, Je Chul

doi:10.1016/j.diagmicrobio.2009.02.010

Cited by 76 publications

(50 citation statements)

References 20 publications

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“…[28] For genes encoding aminoglycoside-modifying enzymes, Acinetobacter baumannii carried armA and aph(3’)-Ia, whereas Acinetobacter genospecies 13TU possessed aph (3’)-VI. [29] Moreover, Acinetobacter baumannii resistant to fluoroquinolones all contained a Ser83Leu substitution in the gyrA gene, but most of Acinetobacter genomospecies 3 and 13TU were fluoroquinolones susceptible and contained a wild-type Ser83 in gyrA. [30,31] Furthermore, the presence of RND-type efflux systems was likely species-specific.…”

Section: Resultsmentioning

confidence: 99%

TheAcinetobacter baumanniigroup:a systemic review

Zhang

Qiao

2013

World Journal of Emergency Medicine

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BACKGROUND:The Acinetobacter baumannii group, including Acinetobacter baumannii, Acinetobacter genomospecies 3 and 13TU, is phenotypically indistinguishable and uniformly identified as Acinetobacter baumannii by laboratories of clinical microbiology. This review aimed to demonstrate the differences among them.METHODS:Literatures associated with the Acinetobacter baumannii group were identified and selected from PubMed databases and relevant journals.RESULTS:Acinetobacter genospecies 3 and 13TU possess a certain proportion in clinical isolates. There were considerable differences in epidemiologic features, clinical manifestations, antimicrobial resistances and therapeutic options among the Acinetobacter baumannii group. Compared with Acinetobacter genomospecies 3 and 13TU, Acinetobacter baumannii with a higher resistance to antimicrobial agents are easier to be treated inappropriately, and present a worse outcome in patients.CONCLUSION:The Acinetobacter baumannii group comprises three distinct clinical entities, and their clinical value are not equal.

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Section: Resultsmentioning

confidence: 99%

TheAcinetobacter baumanniigroup:a systemic review

Zhang

Qiao

2013

World Journal of Emergency Medicine

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“…A high overall incidence of APH(3Ј)-VI (46.2%) was reported. More recently, a South Korean study reported a different prevalence of AME genes in a polyclonal group of A. baumannii isolates: aac(3)-Ia in 14.8%, aac(6Ј)-Ib in 83.6%, ant(3Љ)-Ia in 85.2%, aph(3Ј)-Ia in 88.5%, and aph(3Ј)-VI in 1.6% (9). In contrast, we found AMEs that acetylate to be less common (42.6%) among our isolates.…”

Section: Discussionmentioning

confidence: 99%

Aminoglycoside Resistance and Susceptibility Testing Errors in Acinetobacter baumannii-calcoaceticus Complex

et al. 2010

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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.

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“…Aminoglycoside antibiotics are frequently ineffective against strains of A. baumannii, but are nevertheless used together with carbapenems to treat infected patients because the two agents have a synergistic effect [15]. The incidence of infection by A. baumannii with armA 16S rRNA methylase has increased, leading to reports of highlevel resistance to most aminoglycosides [29]. Moreover, North American [12], Chinese [30,31], and South Korean [32] reports have documented the co-production of blaOXA-23 and armA, which can pose therapeutic challenges.…”

Section: Discussionmentioning

confidence: 99%

Characterization ofAcinetobacter baumanniiCo-producing Carbapenemases OXA-23 and OXA-66, andarmA16S Ribosomal RNA Methylase at a University Hospital in South Korea

Jeong

Son

Shin

et al. 2011

Korean J Clin Microbiol

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Background:In the present study, the resistance mechanisms against carbapenems and aminoglycosides for 23 strains of multi-drug-resistant Acinetobacter baumannii isolated at a university hospital were investigated. Methods: The minimal inhibitory concentrations (MICs) were determined via broth microdilution or Etest. The genes encoding OXA-type carbapenemases and 16S rRNA methylase were identified using multiplex PCR, and the amplified products were sequenced. Conjugation experiments were conducted, and an epidemiologic study was performed using enterobacterial repetitive intergenic consensus (ERIC)-PCR. Results: In the isolates, the MICs of the tested aminoglycosides, including arbekacin, were ＞1024 μg/ mL; the MICs of aztreonam, cefepime, ceftazidime, and ciprofloxacin ranged from 64 to 128 μg/mL; and the MICs of carbapenem ranged from 32 to 64 μg/ mL, as determined through the broth microdilution test. According to the E-test, the MICs of ampicillin/ sulbactam and colistin were 8 and 0.25 to 0.38 μg/ mL, respectively. Sequence analysis confirmed that all of the isolates expressed carbapenemases OXA-23 and OXA-66, as well as armA 16S rRNA methylase. In addition, ISAba1 was identified upstream of the gene encoding OXA-23. OXA-23 and armA were not transferred to Escherichia coli J53 cells in the transconjugation experiments. ERIC-PCR molecular fingerprinting produced a single pattern in all cases. Conclusion:The co-production of OXA-23 and armA 16S rRNA methylase may be attributed to the multidrug resistance of the A. baumannii isolates in the present study. Stricter surveillance and more rapid detection are necessary to prevent the spread of this type of resistance in the future. (Korean J Clin Microbiol 2011;14:67-73)

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Genetic basis of resistance to aminoglycosides in Acinetobacter spp. and spread of armA in Acinetobacter baumannii sequence group 1 in Korean hospitals

Cited by 76 publications

References 20 publications

TheAcinetobacter baumanniigroup:a systemic review

TheAcinetobacter baumanniigroup:a systemic review

Aminoglycoside Resistance and Susceptibility Testing Errors in Acinetobacter baumannii-calcoaceticus Complex

Characterization ofAcinetobacter baumanniiCo-producing Carbapenemases OXA-23 and OXA-66, andarmA16S Ribosomal RNA Methylase at a University Hospital in South Korea

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