Amino acid substitutions of quinolone resistance determining regions in GyrA and ParC associated with quinolone resistance in Acinetobacter baumannii and Acinetobacter genomic species 13TU

Liu, Yen-Hung; Kuo, Shu‐Chen; Lee, Yi-Tzu; Chang, Ian C; Yang, Shung‐Haur; Chen, Te‐Li; Fung, Chang-Phoné

doi:10.1016/j.jmii.2011.09.001

Cited by 24 publications

(22 citation statements)

References 30 publications

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“…[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. Because AdeABC and AdeIJK efflux transporters were highly specific to Acinetobacter baumannii , AdeDE and AdeXYZ were predominant in Acinetobacter genomospecies 3.…”

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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“…Moreover, a significantly increased positive rate was observed in the β-lactamase gene in strains subjected to drug induction, particularly OXA-23 (64.9%) and AmpC (91.9%). To our knowledge, OXA-23-producing A. baumannii was resistant to IPM (29)(30)(31)(32)(33)(34)(35)(36). AmpC enzyme was encoded by chromogene, and it's over expression could induce drug resistance towards penicillin and the third generation broad-spectrum cephalosporins, through hydrolysis.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, gyrA and parC were isolated in all strains, and gene mutations of these genes may be associated with the formation of drug resistance (29,32). As the efflux pump, which is located in the outer membrane, has been suggested to have an important role in multidrug resistance capacity in bacteria (31)(32)(33), the expression of the active efflux gene adeB was determined. The resistance-nodulation-cell-division-type multidrug efflux pump, adeb, was associated with aminoglycoside resistance and has previously been implicated in mediating the level of susceptibility towards other drugs, such as tetracyclines, chloramphenicol, erythromycin, trimethoprim, and ethidium bromide (34).…”

Section: Discussionmentioning

confidence: 99%

Active efflux pump adeB is involved in multidrug resistance of Acinetobacter baumannii induced by antibacterial agents

Zhang

Wang

Xie

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the resistance of Acinetobacter baumannii, which was induced by cefepime (FEP), cefoperazone-sulbactam (SCF), tazobactam (TZP), levofloxacin (LEV), amikacin (AK), imipenem (IPM), and ciprofloxacin (CIP), in vitro. Multi-step drug resistance selection of 16 A. baumannii strains was performed using seven antibacterial agents (FEP, TZP, CIP, AK, IPM, SCF, and LEV). The minimum inhibitory concentration (MIC) was determined using the agar dilution method. Random amplified polymorphic DNA polymerase chain reaction was performed to analyze the genotypes and the carrying rates of aac (3) (8-to 128-fold) were noted in the MIC and different genotypes were showed in RAPD of the strains before and after performing the drug resistant test. PCR data revealed significant differences (P<0.05) between the carrying rates of resistant genes before and after drug induction, with the exception of rmtA, OXA-24, TEM-1, and IMP. Significant increases were demonstrated in the comparative adeB grayscale in strains that underwent drug induction when compared with the sensitive strains (55.69±43.11% vs. 10.08±26.35%; P=0.001). Findings of the present study suggest that the active efflux pump, adeB, has an important role in multidrug resistance of the A. baumannii induced by antibacterial agents in vitro. IntroductionAlthough carbapenems antibiotics remain the backbone therapy for severe suspected bacterial infections, resistance to this antimicrobial treatment has been increasingly reported (1). Thus, therapeutic options have become limited. Multidrug-resistance to antibiotics currently available, in particular in Gram-negative bacteria, has created a critical global medical challenge (2). Acinetobacter baumannii is frequently observed as a nosocomial infection, which causes high mortality, morbidity and hospitalization cost (3). Crude mortality rate and attributable mortality of the infection were reported to be 52 and 10-35%, respectively (4). Multidrug-resistant A. baumannii is considered as a leading cause of nosocomial infection, particularly in critically ill patients (5). A. baumannii has been reported to be resistant to a broad range of antimicrobial agents, and the tendency for its epidemic spread has subsequently extended (6). An increasing drug resistance of A. baumannii to carbapenems has been demonstrated by the SENTRY Antimicrobial Surveillance Program, whose objective was to report antimicrobial susceptibility and pathogen occurrence data for >40,000 episodes of BSI in 72 medical centers representing 22 nations since January 1997 (7). The emergence of multidrug and pandrug-resistant A. baumannii has caused major threats to the infection control and treatment plans in clinical practices (8). According to our knowledge, drug resistance of A. baumannii is closely related with the application of antibacterial agents. However, few studies have been performed to investigate whether a single antibacterial agent was able to induce pandrug resistance of A. baumannii. In the...

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“…Antimicrobial susceptibility to quinolones (levo oxacin, cipro oxacin) and aminoglycosides (tobramycin, amikacin) was assessed by broth microdilution technique, according to 2018 Clinical and Laboratory Standards Institute (CLSI) guidelines (28), and as described by Gholami et al (23), except nalidixic acid whose resistance values were assessed according to Clinical and Laboratory Standards Institute (CLSI) guidelines (29). MIC concentrations tested ranged from 0.25 µg/mL up to 256 µg/mL in a 96-well microtiter plate with 100 µL of the antibiotic dilution and Müller-Hinton broth.…”

Section: Antimicrobial Susceptibility Testingmentioning

confidence: 99%

Efflux pump expression in MDR Acinetobacter baumannii strains from a tertiary care hospital in Lima, Peru

Plasencia-Rebata¹,

Levy-Blitchtein²,

Peña-Tuesta³

et al. 2020

Preprint

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Objetive: To analyze the contribution of the active efflux system to quinolones and aminoglycosides resistance in selected outbreak A. baumannii clinical isolates using the efflux pump inhibitor PAβN.Results: A total of nineteen Acinetobacter baumannii strains were included in the study. All were positive for the blaOXA-51 gene by PCR and had clinical information associated. The samples were non-duplicate and collected from different sources. Non-susceptibility rates were as following: tobramycin 31.6% (6), ciprofloxacin 31.6% (6), levofloxacin 21.1% (4), nalidixic acid 26.3% (5) and amikacin 15.8% (3). A total of eight strains (42,1%) demonstrated an increase in the susceptibility rates and sixteen (84,2%) expressed efflux pumps.

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Amino acid substitutions of quinolone resistance determining regions in GyrA and ParC associated with quinolone resistance in Acinetobacter baumannii and Acinetobacter genomic species 13TU

Cited by 24 publications

References 30 publications

TheAcinetobacter baumanniigroup:a systemic review

TheAcinetobacter baumanniigroup:a systemic review

Active efflux pump adeB is involved in multidrug resistance of Acinetobacter baumannii induced by antibacterial agents

Efflux pump expression in MDR Acinetobacter baumannii strains from a tertiary care hospital in Lima, Peru

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