ArticleActa pharmaceutica Sinica. B2014
Genetic basis of high level aminoglycoside resistance in Acinetobacter baumannii from Beijing, China.
Article in Acta pharmaceutica Sinica. B, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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28 citing papers in PubMed, 59 citations in OpenAlex.
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- Molecular Typing of Multidrug-Resistant Acinetobacter baumannii Isolates from Clinical Specimens by ERIC-PCR and MLVA.Current microbiology · 2023Article
- Phylogenetic analyses of antimicrobial resistant Corynebacterium striatum strains isolated from a nosocomial outbreak in a tertiary hospital in China.Antonie van Leeuwenhoek · 2023Article
- Exploring Synergistic Combinations in Extended and Pan-Drug Resistant (XDR and PDR) Whole Genome SequencedMicroorganisms · 2023Article
- Mobile genetic elements carrying aminoglycoside resistance genes inFrontiers in microbiology · 2023Article
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- Evasion of Antimicrobial Activity inInternational journal of molecular sciences · 2022Review
- Whole-genome analysis of carbapenem-resistantComputational and structural biotechnology journal · 2022Article
- Whole genome sequence of pan drug-resistant clinical isolate of Acinetobacter baumannii ST1890.PloS one · 2022Article
- High-Level Aminoglycoside Resistance in Human ClinicalFrontiers in microbiology · 2021Article
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12 authors at 1 institution in 1 country.
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Abstract
The objective of this study was to investigate the genetic basis of high level aminoglycoside resistance in Acinetobacter baumannii clinical isolates from Beijing, China. 173 A. baumannii clinical isolates from hospitals in Beijing from 2006 to 2009 were first subjected to high level aminoglycoside resistance (HLAR, MIC to gentamicin and amikacin>512 µg/mL) phenotype selection by broth microdilution method. The strains were then subjected to genetic basis analysis by PCR detection of the aminoglycoside modifying enzyme genes (aac(3)-I, aac(3)-IIc, aac(6')-Ib, aac(6')-II, aph(4)-Ia, aph(3')-I, aph(3')-IIb, aph(3')-IIIa, aph(3')-VIa, aph(2″)-Ib, aph(2″)-Ic, aph(2″)-Id, ant(2″)-Ia, ant(3″)-I and ant(4')-Ia) and the 16S rRNA methylase genes (armA, rmtB and rmtC). Correlation analysis between the presence of aminoglycoside resistance gene and HLAR phenotype were performed by SPSS. Totally 102 (58.96%) HLAR isolates were selected. The HLAR rates for year 2006, 2007, 2008 and 2009 were 52.63%, 65.22%, 51.11% and 70.83%, respectively. Five modifying enzyme genes (aac(3)-I, detection rate of 65.69%; aac(6')-Ib, detection rate of 45.10%; aph(3')-I, detection rate of 47.06%; aph(3')-IIb, detection rate of 0.98%; ant(3″)-I, detection rate of 95.10%) and one methylase gene (armA, detection rate of 98.04%) were detected in the 102 A. baumannii with aac(3)-I+aac(6')-Ib+ant(3″)-I+armA (detection rate of 25.49%), aac(3)-I+aph(3')-I+ant(3″)-I+armA (detection rate of 21.57%) and ant(3″)-I+armA (detection rate of 12.75%) being the most prevalent gene profiles. The values of chi-square tests showed correlation of armA, ant(3″)-I, aac(3)-I, aph(3')-I and aac(6')-Ib with HLAR. armA had significant correlation (contingency coefficient 0.685) and good contingency with HLAR (kappa 0.940). The high rates of HLAR may cause a serious problem for combination therapy of aminoglycoside with β-lactams against A. baumannii infections. As armA was reported to be able to cause high level aminoglycoside resistance to most of the clinical important aminoglycosides (gentamicin, amikacin, tobramycin, etc), the function of aminoglycoside modifying enzyme gene(s) in A. baumannii carrying armA deserves further investigation.
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