Activity of Levofloxacin and Ciprofloxacin in Combination with Cefepime, Ceftazidime, Imipenem, Piperacillin-Tazobactam and Amikacin against Different &lt;i&gt;Pseudomonas aeruginosa&lt;/i&gt; Phenotypes and &lt;i&gt;Acinetobacter&lt;/i&gt; spp.

Drago, Lorenzo; Vecchi, Elena De; Nicola, L.; Colombo, Alberto; Guerra, Anna; Gismondo, Maria Rita

doi:10.1159/000081033

Cited by 28 publications

(20 citation statements)

References 27 publications

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“…Treatment of P. aeruginosa clinical isolates with ciprofloxacin in combination with amikacin or gentamicin showed either synergistic, additive, or indifferent effects (31)(32)(33). Our results with the PAO1 strain are consistent with these previous observations since we observed no antagonistic effect of the ciprofloxacin-amikacin combination.…”

supporting

confidence: 92%

Ciprofloxacin-Mediated Mutagenesis Is Suppressed by Subinhibitory Concentrations of Amikacin in Pseudomonas aeruginosa

Valencia

Esposito

Spira

et al. 2017

Antimicrob Agents Chemother

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Resistance to antibiotics is a global health problem. Activation of the SOS response, and the subsequent elevation in mutagenesis, contributes to the appearance of resistance mutations. Among currently used drugs, quinolones are the most potent inducers of the SOS response. In the present study, we show that amikacin inhibits ciprofloxacin-mediated SOS induction and mutagenesis in Pseudomonas aeruginosa.KEYWORDS Pseudomonas aeruginosa, SOS response, ciprofloxacin, recA A ntibiotics may cause genetic changes involving different pathways, and one of them is the induction of error-prone polymerases mediated by SOS response (1, 2). Ciprofloxacin (CIP), one of the antimicrobials of choice for the treatment of Pseudomonas aeruginosa, induces the SOS response (3-5) by interfering with gyrase or topoisomerase activity (6, 7). The SOS regulon controls 15 genes, including imuABC and dinB (4, 5), which encode error-prone polymerases (8,9). By inducing the SOS response, ciprofloxacin increases mutagenesis (e.g., see references 10 and 11), facilitating the appearance of drug resistance.We investigated the effect of antibiotic combinations on the SOS response and mutagenesis induced by ciprofloxacin in P. aeruginosa PAO1. recA is among the SOS-regulated genes in this organism (4,5). To analyze the induction of the SOS response, we constructed a chromosomal PrecA-lux reporter. The regulatory region upstream from recA (Ϫ501 bp relative to the start codon) was cloned into the pUC18T-mini-Tn7T-lux-Gm plasmid (12) and transferred to P. aeruginosa for integration at attTn7, resulting in strain attTn7::PrecA-lux. The effect of antibiotics on the expression of the reporter was evaluated in solid medium using disk-based qualitative assays. The PrecA-lux strain was diluted to an optical density at 260 nm (OD 600 ) of 0.1. Fifty microliters of this dilution was seeded on Mueller-Hinton (MH) agar, and test antibiotic disks and CIP (5 g) disks (Sensifar-Cefar, Brazil) were placed close to one another to observe the effect of the antibiotic interaction on recA expression. Luciferase activity was detected in the ChemiDoc MP system (Bio-Rad, USA).Amikacin (AMI), imipenem, meropenem, polymyxin B, ceftazidime, cefepime, and aztreonam were tested, representing different drug classes. We found that amikacin is not an inducer of the SOS response but is in fact a strong inhibitor of recA induction by sub-MICs of ciprofloxacin (Fig. 1A). Amikacin is an aminoglycoside derived from kanamycin (13). Aminoglycosides bind, with high affinity, to the A-site on the 16S rRNA of the 30S ribosome (14) and can cause mRNA decoding errors, block mRNA and tRNA translocation, and inhibit ribosome recycling (15).

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supporting

confidence: 92%

Ciprofloxacin-Mediated Mutagenesis Is Suppressed by Subinhibitory Concentrations of Amikacin in Pseudomonas aeruginosa

Valencia

Esposito

Spira

et al. 2017

Antimicrob Agents Chemother

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“…There are many reports in the literature on synergism with several rates observed with quinolone and beta-lactam antibiotics 26-30. In our study, synergy was not demonstrated in resistant strains with imipenem-ciprofloxacin combination while synergy was observed in 8% of the susceptible strains.…”

Section: Discussioncontrasting

confidence: 58%

In-Vitro Efficacy of Synergistic Antibiotic Combinations in Multidrug Resistant Pseudomonas Aeruginosa Strains

Dündar

Otkun

2010

Yonsei Med J

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PurposeCombination antibiotic treatment is preferred in nosocomial infections caused by Pseudomonas aeruginosa (P. aeruginosa). In vitro synergism tests were used to choose the combinations which might be used in clinic. The aim of this study was to investigate the synergistic efficacy of synergistic antibiotic combinations in multidrug resistant P. aeruginosa strains.Materials and MethodsSynergistic efficacies of ceftazidime-tobramycin, piperacillin/tazobactam-tobramycin, imipenem-tobramycin, imipenem-isepamycin, imipenem-ciprofloxacin and ciprofloxacin-tobramycin combinations were investigated by checkerboard technique in 12 multiple-resistant and 13 susceptible P. aeruginosa strains.ResultsThe ratios of synergy were observed in ceftazidime-tobramycin and piperacillin/tazobactam-tobramycin combinations as 67%, and 50%, respectively, in resistant strains, whereas synergy was not detected in other combinations. The ratios of synergy were observed in ceftazidime-tobramycin, piperacillin/tazobactam-tobramycin, imipenem-tobramycin, imipenem-ciprofloxacin and imipenem-isepamycin combinations as 31%, 46%, 15%, 8%, 8%, and respectively, in susceptible strains, whereas synergy was not detected in ciprofloxacin-tobramycin combination. Antagonism was not observed in any of the combinations.ConclusionAlthough the synergistic ratios were high in combinations with ceftazidime or piperacillin/tazobactam and tobramycin, the concentrations in these combinations could not usually reach clinically available levels. Thus, the solution of the problems caused by multiple resistant P. aeruginosa should be based on the prevention of the development of resistance and spread of the causative agent between patients.

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“…The studies involving combination therapy with either sulbactam or the polymyxins that are described above form the major and most promising group. Other combinations have also been studied using in vitro techniques and animal models, including various combinations of quinolones, ␤-lactams, and/or amikacin (45,80,139,280,467). The results for quinolone combination therapy are varied, with reduced efficacy being described when ciprofloxacin was used for ciprofloxacin-resistant A. baumannii (151), as well as a lack of enhanced activity with levofloxacin combined with imipenem or amikacin in a mouse pneumonia model (273).…”

Section: Other Combination Therapymentioning

confidence: 99%

Acinetobacter baumannii : Emergence of a Successful Pathogen

2008

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SUMMARY Acinetobacter baumannii has emerged as a highly troublesome pathogen for many institutions globally. As a consequence of its immense ability to acquire or upregulate antibiotic drug resistance determinants, it has justifiably been propelled to the forefront of scientific attention. Apart from its predilection for the seriously ill within intensive care units, A. baumannii has more recently caused a range of infectious syndromes in military personnel injured in the Iraq and Afghanistan conflicts. This review details the significant advances that have been made in our understanding of this remarkable organism over the last 10 years, including current taxonomy and species identification, issues with susceptibility testing, mechanisms of antibiotic resistance, global epidemiology, clinical impact of infection, host-pathogen interactions, and infection control and therapeutic considerations.

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Activity of Levofloxacin and Ciprofloxacin in Combination with Cefepime, Ceftazidime, Imipenem, Piperacillin-Tazobactam and Amikacin against Different <i>Pseudomonas aeruginosa</i> Phenotypes and <i>Acinetobacter</i> spp.

Cited by 28 publications

References 27 publications

Ciprofloxacin-Mediated Mutagenesis Is Suppressed by Subinhibitory Concentrations of Amikacin in Pseudomonas aeruginosa

Ciprofloxacin-Mediated Mutagenesis Is Suppressed by Subinhibitory Concentrations of Amikacin in Pseudomonas aeruginosa

In-Vitro Efficacy of Synergistic Antibiotic Combinations in Multidrug Resistant Pseudomonas Aeruginosa Strains

Acinetobacter baumannii : Emergence of a Successful Pathogen

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