ReviewDrugs1999
Mechanisms of fluoroquinolone resistance: an update 1994-1998.
Review in Drugs, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 307 citations in OpenAlex.
- Plasmid-mediated quinolone resistance in Enterobacteriaceae: a systematic review with a focus on Mediterranean countries.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2017Pooled it
- Methicillin-ResistantInternational journal of molecular sciences · 2026Review
- The molecular mechanisms of quinolone resistance in Salmonella: a review.Archives of microbiology · 2025Review
- An alternative approach to combat multidrug-resistant bacteria: new insights into traditional Chinese medicine monomers combined with antibiotics.Advanced biotechnology · 2025Review
- Genomic and phenotypic characterisation ofFrontiers in microbiology · 2025Article
- Genomic characteristics of quinolone resistance in colistin-resistantJAC-antimicrobial resistance · 2024Article
- Isolation, Characterization, and Complete Genome Sequence of Escherichia Phage KIT06 Which Infects Nalidixic Acid-ResistantAntibiotics (Basel, Switzerland) · 2024Article
- Survey of Bacterial Isolates and Their Antimicrobial Susceptibility Patterns from Dogs with Infective Endocarditis.Pathogens (Basel, Switzerland) · 2023Article
- Antimicrobial and antibiofilm effects of essential fatty acids against clinically isolated vancomycin-resistantFrontiers in cellular and infection microbiology · 2023Article
- Investigation of In Vitro Susceptibility and Resistance Mechanisms in Skin Pathogens: Perspectives for Fluoroquinolone Therapy in Canine Pyoderma.Antibiotics (Basel, Switzerland) · 2022Article
- Prevalence and Antimicrobial Susceptibility of BovineBiology · 2022Article
- Alternative Pathways to Ciprofloxacin Resistance in Neisseria gonorrhoeae: An In Vitro Study of the WHO-P and WHO-F Reference StrainsAntibiotics (Basel, Switzerland) · 2022Article
- Enrofloxacin-The Ruthless Killer of Eukaryotic Cells or the Last Hope in the Fight against Bacterial Infections?International journal of molecular sciences · 2022Review
- Horizontal Gene Transfer of Fluoroquinolone Resistance-Conferring Genes From CommensalFrontiers in microbiology · 2022Article
- Study on the drug resistance and pathogenicity ofFrontiers in microbiology · 2022Article
- Mechanisms of antibiotic action shape the fitness landscapes of resistance mutations.Computational and structural biotechnology journal · 2022Article
- Mutational Diversity in the Quinolone Resistance-Determining Regions of Type-II Topoisomerases ofAntibiotics (Basel, Switzerland) · 2021Review
- The role of potentiating mutations in the evolution of pandemic Escherichia coli clones.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021Review
- Cracking the Challenge of Antimicrobial Drug Resistance with CRISPR/Cas9, Nanotechnology and Other Strategies in ESKAPE Pathogens.Microorganisms · 2021Review
- Distribution of Virulence Factors and Resistance Determinants in Three Genotypes ofPathogens (Basel, Switzerland) · 2021Article
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fluoroquinolone resistance is mediated by target changes (DNA gyrase and/or topoisomerase IV) and/or decreased intracellular accumulation. The genes (gyrA/gyrB/parC/parE) and proteins of DNA topoisomerase IV show great similarity, both at the nucleotide and amino acid sequence level to those of DNA gyrase. It has been shown that there are hotspots, called the quinolone resistance determining region (QRDR), for mutations within gyrA and parC. Based on the Escherichia coli co-ordinates, the hotspots most favoured for giving rise to decreased susceptibility and/or full resistance to quinolones are at serine 83 and aspartate 87 of gyrA, and at serine 79 and aspartate 83 for parC. Few mutations in gyrB or parE/grlB of any bacteria have been described. Efflux of fluoroquinolones is the major cause of decreased accumulation of these agents; for Staphylococcus aureus, the efflux pump involved in norfloxacin resistance is NorA, and for Streptococcus pneumoniae, PmrA. By analysis of minimum inhibitory concentration (MIC) data derived in the presence and absence of the efflux inhibitor reserpine, it has been shown that up to 50% of ciprofloxacin-resistant clinical isolates of S. pneumoniae may possess enhanced efflux. This suggests that efflux may be an important mechanism of clinical resistance in this species. In Pseudomonas aeruginosa, several efflux operons have been demonstrated genetically and biochemically. These operons are encoded by mex (Multiple EffluX) genes: mexAmexB-oprM, mexCD-OprJ system and mexEF-oprN system. The E. coli efflux pump is the acrAB-tolC system. Both the mar operon and the sox operon can give rise to multiple antibiotic resistance. It has been shown that mutations giving rise to increased expression of the transcriptional activators marA and soxS affect the expression of a variety of different genes, including ompF and acrAB. The net result is that expression of OmpF is reduced and much less drug is able to enter the cell; expression of acrAB is increased, enhancing efflux from the cell.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.