ArticleAntimicrobial agents and chemotherapy2016
Dynamics of Mutations during Development of Resistance by Pseudomonas aeruginosa against Five Antibiotics.
Article in Antimicrobial agents and chemotherapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- Phenotypic convergence and collateral susceptibility development in Pseudomonas aeruginosa under antibiotic exposure in ICU patients.npj antimicrobials and resistance · 2026Article
- In vitro exposure to non-antipseudomonal antibiotics (NAPA) induces Pseudomonas aeruginosa resistance to antipseudomonal antibiotics (APA).The Journal of antimicrobial chemotherapy · 2026Article
- Collateral sensitivity and cross-resistance in six species of bacteria exposed to six classes of antibiotics.Microbiology spectrum · 2025Article
- Differences in antimicrobial resistance between exoU and exoS isolates of Pseudomonas aeruginosa.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Unlocking Enhanced Efficacy of Aminoglycoside Antibiotics Against Pseudomonas aeruginosa.Microbial biotechnology · 2025Review
- Article
- Keeping up with the pathogens: improved antimicrobial resistance detection and prediction from Pseudomonas aeruginosa genomes.Genome medicine · 2024Article
- The Pseudomonas aeruginosa Resistome: Permanent and Transient Antibiotic Resistance, an Overview.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Age of Antibiotic Resistance in MDR/XDR Clinical Pathogen ofPharmaceuticals (Basel, Switzerland) · 2023Review
- The Art of War withAntibiotics (Basel, Switzerland) · 2023Review
- Collateral Sensitivity to Fosfomycin of Tobramycin-Resistant Mutants ofInternational journal of molecular sciences · 2023Article
- Virulence regulation of ZnFrontiers in veterinary science · 2023Article
- Rapid Decline of Ceftazidime Resistance in Antibiotic-Free and Sublethal Environments Is Contingent on Genetic Background.Molecular biology and evolution · 2022Article
- Convergent phenotypic evolution towards fosfomycin collateral sensitivity of Pseudomonas aeruginosa antibiotic-resistant mutants.Microbial biotechnology · 2022Article
- The predictive potential of different molecular markers linked to amikacin susceptibility phenotypes in Pseudomonas aeruginosa.PloS one · 2022Article
- The resistance mechanisms of bacteria against ciprofloxacin and new approaches for enhancing the efficacy of this antibiotic.Frontiers in public health · 2022Review
- Effect of Ferredoxin Receptor FusA on the Virulence Mechanism ofFrontiers in cellular and infection microbiology · 2022Article
- Antibiotic-resistant organisms establish reservoirs in new hospital built environments and are related to patient blood infection isolates.Communications medicine · 2022Article
- β-lactam Resistance inPathogens (Basel, Switzerland) · 2021Review
- Review of Ceftazidime-Avibactam for the Treatment of Infections Caused byAntibiotics (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa is an opportunistic pathogen that causes considerable morbidity and mortality, specifically during intensive care. Antibiotic-resistant variants of this organism are more difficult to treat and cause substantial extra costs compared to susceptible strains. In the laboratory, P. aeruginosa rapidly developed resistance to five medically relevant antibiotics upon exposure to stepwise increasing concentrations. At several time points during the acquisition of resistance, samples were taken for whole-genome sequencing. The increase in the MIC of ciprofloxacin was linked to specific mutations in gyrA, parC, and gyrB, appearing sequentially. In the case of tobramycin, mutations in fusA, HP02880, rplB, and capD were induced. The MICs of the beta-lactam compounds meropenem and ceftazidime and the combination of piperacillin and tazobactam correlated linearly with beta-lactamase activity but not always with individual mutations. The genes that were mutated during the development of beta-lactam resistance differed for each antibiotic. A quantitative relationship between the frequency of mutations and the increase in resistance could not be established for any of the antibiotics. When the adapted strains are grown in the absence of the antibiotic, some mutations remained and others were reversed, but this reversal did not necessarily lower the MIC. The increased MIC came at the cost of moderately reduced cellular functions or a somewhat lower growth rate. In all cases except ciprofloxacin, the increase in resistance seems to be the result of complex interactions among several cellular systems rather than individual mutations.
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