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At least 19 recordsLinked to original sources
PubMed2026

Molecular epidemiology of levofloxacin-resistant Klebsiella pneumoniae and the association of plasmid-mediated quinolone resistance genes with key biological phenotypes.

UNLABELLED: Klebsiella pneumoniae is a major opportunistic pathogen in China, yet the molecular epidemiology of quinolone resistance remains poorly characterized. This study analyzed 2,433 clinical isolates from 37 Chinese hospitals (2018-2022). The overall levofloxacin-non-susceptible (NS) rate was 53.60%, with urinary tract isolates showing higher resistance. Whole-genome sequencing identified 12 plasmid-mediated quinolone resistance (PMQR) genes. Among 1,304 NS strains, 74.54% carried at least one PMQR gene (mainly qnrS, qnrB, and aac(6')-Ib-cr), and 60.20% also had quinolone resistance-determining region (QRDR) mutations. Functional studies revealed diverse phenotypic impacts. Most PMQR genes conferred low-level resistance (minimum inhibitory concentration [MIC] = 1 mg/L), while qnrB52 and qnrB91 caused high-level resistance (MIC = 8-16 mg/L). Notably, qnrB91 reduced biofilm formation, indicating a trade-off between resistance and colonization. Growth assays showed that qnrB52, qnrB91, and qnrS1 inhibited normal growth, whereas qepA1 and qnrS1 enhanced growth under ethanol stress. Most PMQR genes (except qnrB6) attenuated bacterial adhesion. qepA1 promoted intracellular survival in macrophages, suggesting a role in chronic infection. Animal models confirmed that qnrB6, qnrB7, qnrVC6, and aac(6')-Ib-cr significantly enhanced virulence. This study is the first in China to report qnrVC6 and novel gyrA mutations (Ser83Ala/Val, Asp87Phe/His) in K. pneumoniae. It systematically reveals how PMQR genes influence infection by modulating resistance, immune evasion, and pathogenicity. These findings highlight that PMQR genes contribute not only to antibiotic resistance but also to virulence, suggesting that treatment strategies should consider specific PMQR genotypes. This research provides the largest-scale molecular epidemiological data and a theoretical basis for controlling quinolone-resistant K. pneumoniae in China. IMPORTANCE: Quinolone-resistant Klebsiella pneumoniae poses a serious threat to public health, yet the role of plasmid-mediated quinolone resistance (PMQR) genes beyond antibiotic resistance remains underexplored. In this largest-scale multicenter study in China, we analyzed 2,433 clinical isolates and discovered that PMQR genes do more than just confer drug resistance-they also influence bacterial growth, stress survival, biofilm formation, and the ability to evade or persist within host immune cells. Some PMQR genes even enhance virulence in an animal model. These findings challenge the traditional view of resistance genes as mere contributors to drug failure, revealing that they can also shape infection outcomes by altering bacterial behavior. Understanding these dual roles may guide more precise treatment strategies targeting specific PMQR genotypes.

Klebsiella pneumoniae↗
PubMed1975

Studies of the mitochondria from Eimeria tenella and inhibition of the electron transport by quinolone coccidiostats.

Intact but fragile mitochondria were isolated from unsporulated oocysts of Eimeria tenella. The mitochondria respired in response to succinate, malate plus pyruvate, and L-ascorbate at rates of 1.00, 0.40, and 0.25 mu1 O2/min/mg protein, respectively. Spectrophotometric analyses of the cytochromes in mitochondria and whole oocysts revealed b-type and o-type cytochromes, at roughly similar levels, but no cytochrome c could be detected. The mitochondrial respiration was inhibited by cyanide, azide, carbon monoxide, antimycin A, and 2-heptyl-4-hydroxyquinoline-N-oxide, but was relatively resistant to rotenone and amytal. The quinolone coccidiostats buquinolate, amquinate, methyl benzoquate, and decoquinate were identified as very powerful inhibitiors of succinate and malate plus pyruvate supported respiration in E. tenella mitochondria. None of these four drugs exhibited any inhibitory effect on chicken liver mitochondria. Only 3 pmol of the quinolones per mg mitochondrial protein was needed to achieve 50% inhibition. The inhibition could not be reversed by coenzymes Q6 or Q10. Since the quinolones did not affect L-ascorbate-supported respiration or the activities of submitochondrial succinate dehydrogenase and NADH dehydrogenase, the site of action of the quinolone coccidiostats was tentatively identified as probably near cytochrome b in E. tenella mitochondria. Mitochondria isolated from an E. tenella amquinate-resistant mutant were much less susceptible to quinolone coccidiostats; 50% inhibition was attained by 300 pmol of the drugs/mg mitochondrial protein. The results suggest that the mechanisms of action of quinolone coccidiostats is by inhibiting the cytochrome-mediated electron transport in the mitochondria of coccidia. 2-Hydroxynaphthoquinone coccidiostats were identified as inhibitors of mitochondrial respiration of both E. tenella and chicken liver. They inhibited submitochondrial succinate dehydrogenase and NADH dehydrogenase of E. tenella, and remained equally active against the mitochondrial function of E. tenella amquinolate-resistant mutant.

Amobarbital↗
PubMed1975

Eimeria tenella in chickens: development of resistance to quinolone anticoccidial drugs.

The development of drug resistance by the present Houghton strain of Eimeria tenella to the quinolones, methyl benzoquate and buquinolate, was found to take place after a single experimental passage. The development of resistance was independent of drug selection pressure and showed cross resistance to other quinolones, but not to amprolium and robenidine. When the Weybridge, Beltsville and Elberfeld strains of E. tenella were compared under similar laboratory conditions, the Weybridge and Elberfeld strains developed resistance to methyl benzoquate after 6 passages and the Beltsville after 5. Studies on the response of the Houghton strain to methyl benzoquate and buquinolate revealed that the drugs did not completely control the infection as measured by weight gain and that oocyst production was not suppressed. These observations indicate that the strain had already acquired some resistance to these drugs. This was confirmed by examining the resistance to methyl benzoquate of a culture of the Houghton strain of E. tenella which had been stored frozen in liquid nitrogen since 1969. This showed full sensitivity to the drug and developed resistance after 8 passages. This suggests that drug tolerance has been acquired by the Houghton strain since 1969. Oocyst lines were established from the Houghton strain by infecting single birds with approximately 10 oocysts. Eleven of these lines were found to be sensitive to methyl benzoquate, and nine to give rise to resistant parasites. It is concluded that the Houghton strain is contaminated by a small number of resistant oocysts which can be eliminated from a culture by dilution of the challenge inoculum. One of these Houghton oocyst lines, sensitive to methyl benzoquate, developed resistance after 8 serial passages.

Animals↗
PubMed1975

In vitro evaluation of a new quinolone antibacterial.

The activity of R-802, a quinolone antibacterial agent, was studied in vitro and found to be active against Enterobacteriaceae; less than 4 mug of drug per ml was required to inhibit most isolates. The majority of Pseudomonas aeruginosa grew in a concentration of 256 mug of R-802 per ml when studied in broth against an inoculum of 10(8) organisms per ml.

Anti-Bacterial Agents↗
PubMed1979

Quinolone antimicrobial agents. 2. Methylenedioxy positional isomers of oxolinic acid.

The synthesis and antimicrobial activity of the methylenedioxy positional isomers, 1-ethyl-1,4-dihydro-5,6-methylenedioxy-4-oxo-3-quinolinecarboxylic acid (9) and 1-ethyl-1,4-dihydro-7,8-methylenedioxy-4-oxo-3-quinolinecarboxylic acid (17), of oxolinic acid (18) have been accomplished. Isomer 9 was prepared by the reaction of N-ethyl-6,7-methylenedioxyisatoic anhydride with sodioethyl formylacetate [L. A. Mitscher, H. E. Gracey, G. W. Clark III, and T. Suzuki, J. Med. Chem., 21, 485 (1978)], while isomer 17 was prepared by thermal cyclization of diethyl 2-[(2,3-methylenedioxyanilino)methylene]malonate [D. Kaminsky and R. I. Meltzer, J. Med. Chem., 11, 160 (1968)]. Both of the new isomers are less active in vitro when compared to oxolinic acid (18) itself.

Isomerism↗
PubMed1978

Quinolone antimicrobial agents. 1. Versatile new synthesis of 1-alkyl-1,4-dihydro-4-oxo-3-quinolinecarboxylic acids.

A flexible reaction sequence has been developed which starts with readily available anthranilic acids or isatoic anhydrides and leads regiospecifically to 1-alkyl-1,4-dihydro-4-oxo-3-quinolinecarboxylic acids after reaction with 1,3-dicarbonyl compounds. The sequence is superior to earlier published methods by allowing electron-releasing and -withdrawing groups in any position on the aro;atic ring, by allowing convenient substitution at C2, and better overall yield. A number of new and known antimicrobial agents were prepared and tested in vitro, demonstrating, inter alia, that substitution of the H at C2 abolished antibacterial activity.

Anti-Infective Agents↗
PubMed2026

Global Diffusion of IncC Plasmid Harboring blaNDM-1in the High-Risk Escherichia coli ST131 Clone.

AIMS: The global expansion of quinolone-resistant Escherichia coli (QR-EC) is increasingly associated with β-lactam resistance and mobile genetic elements that facilitate resistance dissemination. This study investigated the molecular mechanisms underlying fluoroquinolone and β-lactam resistance in clinical QR-EC isolates and explored the plasmid type associated. METHODS AND RESULTS: A total of 123 non-duplicate QR-EC clinical isolates responsible mainly for gastrointestinal colonization were collected between 2019 and 2021. Plasmid-mediated quinolone resistance (PMQR), extended-spectrum β-lactamase (ESBL), and carbapenemase genes were screened by PCR. Mutations in the quinolone resistance-determining regions (QRDR) of gyrA and parC were analyzed using sequencing and mismatch amplification mutation assay PCR (MAMA-PCR). Selected isolates underwent multilocus sequence typing (MLST). Whole-genome sequencing (WGS) of a representative extensively drug-resistant strain carrying multiple quinolone resistance determinants, ESBL genes, and carbapenemase genes, was performed. PMQR genes were prevalent among QR-EC, dominated by aac(6')-Ib-cr (60.9% of isolates). ESBL genes were identified in 93.5% of isolates, predominantly blaCTX-M (95.7%). Among ertapenem-resistant isolates (QCR-EC) (n=18), blaNDM-1 and blaOXA-48 were detected in 13 and 11 isolates, respectively. QRDR mutations were highly frequent, particularly gyrA83 (98.4%) and parC80 (30.9%). Major QCR-EC genotypes belonged to sequence types ST167 (n=2), ST1196, ST469, and ST410. High-risk E. coli ST131 clone harboring IncC plasmid encoding blaNDM-1 was described for the first time in Africa, following its emergence, in two continents, Asia and America. Despite the very rare description of these strains worldwide, their description in three continents sign their global diffusion. CONCLUSIONS: This finding highlights the ongoing spread of carbapenem resistance and underscores the urgent need for strengthened genomic surveillance.

Escherichia coli↗
PubMed1978

Synthesis of pyrimido[5,4-c]quinolines and related quinolines as potential antimalarials.

3-Ethylaminomethyl-2-methyl-4(1H)-quinolone (1a) and its 6-CH3, 6-OCH3, and 7-Cl derivatives were prepared by means of the Mannich reaction. Conversion to the 4-chloro derivatives and condensation with 3-chloroaniline gave the corresponding 4-(3-chloroanilino) derivatives. Cyclization of 4-(3-chloroanilino)-2,6-dimethyl-3-ethyl-aminomethylquinoline (3a) and its 6-OCH3 derivative with paraformaldehyde gave 1-(3-chlorophenyl)-3,9-dimethyl-3-ethyltetrahydropyrimido[5,4-c]quinoline (4a) and the 9-OCH3 derivative 4b. Treatment of 4b with benzaldehyde gave 1-(3-chlorophenyl)-3-ethyl-9-methoxy-5-styryltetrahydropyrimido[5,4-c]quinoline (5). 3-Benzylaminomethyl-6-methoxy-2-methyl-4(1H)-quinolone (1e) and 3,3'-(1,3-benzyliminodimethylene)di[2-methyl-4(1H)-quinolone] (6b) were also synthesized. The compounds were inactive as antimalarials.

Animals↗
PubMed2026

Genomic determinants of fluoroquinolone resistance in Escherichia coli in Nigeria: dominance of QRDR mutations and limited contribution of PMQR in a cross-sectional study.

BACKGROUND: Fluoroquinolone-resistant Escherichia coli is a major global clinical threat, particularly in low- and middle-income countries like Nigeria. However, the full genomic landscape, including the relative contributions of chromosomal mutations, plasmid-mediated resistance, and the role of high-risk clones, remains poorly characterized in this setting. This study aimed to define the genomic mechanisms, clonal distribution, and genotype-phenotype relationships of fluoroquinolone resistance in clinical E. coli isolates from Nigeria. METHODS: A cross-sectional study of 107 clinical E. coli isolates was conducted. Phenotypic susceptibility to ciprofloxacin and nalidixic acid was determined using VITEK 2 and broth microdilution. Whole-genome sequencing was performed, and analysis included detection of quinolone resistance determining region (QRDR) mutations (gyrA, parC, parE) and plasmid-mediated quinolone resistance (PMQR) genes, multilocus sequence typing (MLST), and phylogenetic analysis. Statistical associations were evaluated using chi-squared tests or Fisher's exact tests. RESULTS: Ciprofloxacin non-susceptibility was high at 86.0%. Resistance was primarily driven by a conserved chromosomal mutation profile; the combination of gyrA S83L, gyrA D87N, and parC S80I was present in 85 isolates and was associated with ciprofloxacin non-susceptibility in all affected isolates in this cohort. Isolates with only gyrA mutations were resistant to nalidixic acid but susceptible to ciprofloxacin, consistent with a stepwise resistance pathway. In this cohort, the triple QRDR signature (gyrA S83L + gyrA D87N/Y + parC S80I) was a perfect positive predictor of ciprofloxacin non-susceptibility (85/85; 100%). The ST131 lineage dominated, accounting for 21.5% of isolates and universally carrying the complete triple QRDR profile; notably, no ST131 isolate carried a PMQR determinant. Plasmid-mediated quinolone resistance (PMQR) genes were detected in 15.0% of isolates but were not independently associated with ciprofloxacin non-susceptibility in this cohort in the absence of concomitant QRDR mutations. Efflux pump genes were ubiquitous and non-predictive. Notably, six isolates, all from urine, were non-susceptible (R/I) despite lacking all known QRDR and PMQR determinants, pointing to uncharacterized mechanisms. In a multivariable logistic regression model that included ST131 status, PMQR carriage, and parE mutation status, ST131 was associated with ciprofloxacin non-susceptibility (adjusted OR 5.96, 95% CI 1.21-29.4, p = 0.028), whereas PMQR carriage was not (adjusted OR 0.94, 95% CI 0.18-4.85, p = 0.94). The triple QRDR signature was not included in this model because it perfectly predicted ciprofloxacin non-susceptibility in this cohort. Resistance patterns varied by clinical source, with the highest burden in bloodstream and wound infections. This stepwise hierarchy from first-step gyrA mutations to the classic triple QRDR profile is summarised in the graphical abstract, Fig. 1. CONCLUSIONS: Fluoroquinolone resistance in Nigerian clinical E. coli is predominantly driven by chromosomal QRDR mutations within successful clones like ST131. PMQR genes and efflux pumps appeared to play a supplementary role rather than being independent drivers of ciprofloxacin resistance in this cohort. These data support prioritising key QRDR mutations in genomic reporting and local stewardship decisions, while the QRDR-negative resistant urine isolates require further investigation.

Escherichia coli↗
PubMed1979

Studies of the biliary excretion and metabolites of the antioxidant ethoxyquin, 6-ethoxy-2,2,4-trimethyl-1,2-dihydroquinoline in the rat.

1. Biliary excretion and metabolites of ethoxyquin, and gastro-intestinal absorption of ethoxyquin were studied in rat. 2. An average of 28 and 36% of the dose of 14C following intragastric administration of [14C]ethoxyquin was recovered in the bile of bile-duct cannulated rats in 12 and 24 h, respectively. 3. By g.l.c.-mass spectrometry, 75 to 85% of the 14C excreted in the 12 h bile was identified as unchanged ethoxyquin, and the following metabolites were isolated and identified: 8-hydroxy-ethoxyquin, hydroxylated 8-hydroxy-ethoxyquin, 6-ethoxy-2,2,4-trimethyl-8-quinolone, hydroxylated 6-ethoxy-2,2,4-trimethyl-8-quinolone, 6-ethoxy-2,4-dimethylquinoline and 2,2,4-trimethyl-6-quinolone. 4. Three groups of rats were used in the biliary excretion experiments, and the effect of standardization of experimental conditions was demonstrated. Infusion of sodium taurocholate following bile-duct cannulation did not affect the biliary excretion kinetics of ethoxyquin. 5. Only about 3% of the radioactivity administered was absorbed from the gastrointestinal tract via the lymphatic pathway in thoracic-duct connulated rats within 24 h. It was concluded that ethoxyquin was absorbed primarily by the portal route.

Adsorption↗
PubMed1977

Effect of temperature and relative humidity on nitrazepam stability in solid state.

The decomposition of a 1% dilution of nitrazepam in microcrystalline cellulose was established by quantitative determination of the two main breakdown products, 2-amino-5-nitrobenzophenone and 3-amino-6-nitro-4-phenyl-2(1H)-quinolone, using in situ diffuse reflectance measurements on thin-layer chromatograms. The decomposition and formation rate constant of nitrazepam and of the breakdown products, respectively, were determined at four temperatures and six relative humidities. By means of a three-parameter regression equation, it was possible to correlate quantitatively the decomposition constant of nitrazepam to both temperature and relative humidity.

Chromatography, Thin Layer↗
PubMed2026

Metagenomics Reveals Microbial Community Shifts Associated With Contrasting Anthropogenic Impacts in Freshwater Sources of A Coastal Protected Area in Southeastern Brazil.

This study aimed to characterize freshwater microbial communities, environmental drivers, and anthropogenic impact patterns across three sites on Marambaia Island (southeastern Brazil) using metagenomics. Samples collected from freshwater sources used for human consumption were processed through concentration, nucleic acid extraction, and sequencing on the Illumina NextSeq 2000 platform. A total of 67.2 million reads were assembled into 89,230 bacterial contigs, mostly attributed to Gammaproteobacteria, Alphaproteobacteria, and Betaproteobacteria. Sites under lower anthropogenic influence exhibited higher microbial diversity, whereas impacted sites showed enrichment of opportunistic and fecal-associated genera. A heterogeneous anthropogenic impact profile was observed across sites, corroborated by the proposed Anthropogenic Impact Index (AII). Fourteen antimicrobial resistance genes conferring resistance to beta-lactams, quinolones, sulfonamides, tetracyclines, and macrolides were detected predominantly in sewage-impacted areas, indicating potential diffuse contamination. Redundancy analysis revealed that environmental variables explained 88.1% of microbial community variation, with conductivity, salinity, and turbidity as key drivers. These findings demonstrate the applicability of metagenomics as a powerful tool for assessing microbial diversity, ecological dynamics, and contamination risks in vulnerable freshwater systems.

Brazil↗
PubMed2026

A Strain of Mycoplasma hominis Causing Pleuropneumonia Infection in an Immunocompetent Patient and Recent Epidemiological Trends: Implications for Clinical Management.

Mycoplasma hominis (M. hominis) is an opportunistic pathogen linked to urogenital and neonatal infections; however, limited genetic and epidemiological data are available. Extragenital infections in healthy adults are rare, and effective antibiotics are species-specific, complicating diagnosis and treatment. Hence, this study aimed to elucidate the clinical process, update the epidemiological characteristics, and investigate the genomic features of a fluoroquinolone-resistant M. hominis isolate from an immunocompetent patient with pleuropneumonia in China. The M. hominis isolate ZY_MH01 was recovered from pleural fluid and was identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and Whole Genome Sequencing (WGS). The completed genome was annotated using the NCBI Prokaryotic Genome Annotation Pipeline (PGAP). Snippy v4.4.5 was utilized to conduct a core genome single nucleotide polymorphism (cgSNP) analysis between ZY_MH01 and 144 M. hominis strains from the NCBI GenBank database. Subsequently, phylogenies were constructed using IQ-TREE v3.1.2 and visualized by iTOL. Antimicrobial resistance determinants were identified using strict criteria of Comprehensive Antibiotic Resistance Database (CARD) RGI 6.0.5 (Web portal) and broth microdilution test. Virulence genes were screened using Abricate v1.0.1 against the Virulence Factor Database (VFDB). A total of 42 strains (including ZY_MH01) from Genbank with an assembly level of Complete or Chromosome were re-annotated using Prokka v1.2.0 and pangenome analysis was performed using the Roary. The core genome constitutes only 17.1%, which may contribute to the unusually high level of polymorphism observed among M. hominis strains. No antibiotic resistance genes or virulence genes were detected in the genome of ZY_MH01. However, some resistance-associated mutations of gene parC and gyrA in the Quinolone Resistance Determining Region (QRDR) were identified. Phylogenetic analysis indicates that strains originating from the same geographic region typically exhibit reduced genetic distances; this trend is especially pronounced in regions with a higher number of publicly available strain sequences. In specific circumstances, when conventional broad-spectrum antibiotics are ineffective, even immunocompetent patients should consider the possibility of M. hominis infection. This study presents a detailed account of the diagnostic and therapeutic course of a pleuropneumonia infection caused by M. hominis in an immunocompetent patient, and performs an epidemiological analysis of all M. hominis sequences that have been recently made publicly available.

Humans↗
PubMed2026

Genomic Analysis of CTX-M-15-Producing E. coli Colonizing a Rescued Capuchin Monkey.

Illegal wild animal trade and possession represents a threat to One Health due to the pathogens exchange between wild animals and humans. We report the detection and genomic characterization of a multidrug-resistant (MDR) Escherichia coli strain (MP02) colonizing a capuchin monkey (Sapajus sp.) rescued from illegal possession. MP02 exhibited ExPEC-related genes, harbored an IncHI2-ST1 plasmid composed of quinolones, aminoglycosides, and sulfonamides resistance genes, besides the extended-spectrum β-lactamase (ESBL)-encoding gene blaCTX-M-15 located in a conserved Tn3-like transposon. To the author's knowledge, this is the first report and genomic analysis of a MDR bacterium isolated from an illegally traded non-human primate.

antibiotic resistance↗
PubMed2026

Phenotypic and phylogenomic characterization of Lactococcus garvieae isolates from rainbow trout (Oncorhynchus mykiss) in Türkiye.

Lactococcosis is an important bacterial disease of farmed fish and causes substantial economic losses in rainbow trout (Oncorhynchus mykiss) aquaculture. In this study, Lactococcus garvieae isolates recovered from rainbow trout farms in Türkiye were characterized using phenotypic, molecular, and phylogenomic methods. Among 32 presumptive Lactococcus isolates recovered from 127 dead rainbow trout, four were confirmed as L. garvieae and exhibited identical biochemical characteristics, Pulsed Field Gel Electrophoresis (PFGE) profiles, and broad growth tolerance across different pH, salinity, and temperature conditions. All isolates were presumptively classified as resistant to ciprofloxacin and florfenicol, while remaining susceptible to tetracycline and penicillin. Based on the AMR profiles, strain LG2, which exhibited the most susceptible antimicrobial profile among the isolates, was selected for whole-genome sequencing (WGS). WGS of the representative isolate LG2 generated a single 2,214,687-bp chromosomal contig with 38.5% GC content and 99.0% BUSCO completeness. In silico PCR assigned LG2 to serotype I, and the genome contained an intact capsule-associated cps/kps locus. The chromosomal lsa(D) determinant and an mdt(A)-like efflux-associated gene were detected, whereas no plasmid replicons or acquired quinolone or florfenicol resistance genes were identified, indicating discordance between the phenotypic and genomic AMR results. Taxonomic verification of 236 publicly available Lactococcus assemblies yielded 41 verified public L. garvieae genomes, which, together with LG2, formed a 42-genome within-species dataset. LG2 was most closely related to the Turkish isolate OS-37, sharing 99.96% ANI and differing by three core SNPs; both belonged to ST109, whereas the other Turkish isolates belonged to ST139. cgMLST identified a conserved genomic backbone, while pan-genome analysis identified 5,655 gene clusters and an open pan-genome characterized by a large cloud-gene fraction. These findings demonstrate the importance of species verification in Lactococcus population genomics and reveal substantial accessory-genome diversity within L. garvieae. The genomic features of LG2 provide a basis for future pathogenicity and immunogenicity studies, although experimental validation is required. Overall, these findings highlight the importance of local genomic surveillance for understanding L. garvieae population structure and provide a genomic framework for future region-specific vaccine research.

Animals↗