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Journal articles on the topic 'Mycobacterium smegmatis - Moxifloxacin'

Author: Grafiati
Published: 6 September 2023
Last updated: 31 July 2025

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1

Maurer, Florian P., Vera L. Bruderer, Claudia Ritter, Claudio Castelberg, Guido V. Bloemberg, and Erik C. Böttger. "Lack of Antimicrobial Bactericidal Activity in Mycobacterium abscessus." Antimicrobial Agents and Chemotherapy 58, no. 7 (2014): 3828–36. http://dx.doi.org/10.1128/aac.02448-14.

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ABSTRACTAntibiotic therapy of infections caused by the emerging pathogenMycobacterium abscessusis challenging due to the organism's natural resistance toward most clinically available antimicrobials. We investigated the bactericidal activity of antibiotics commonly administered inM. abscessusinfections in order to better understand the poor therapeutic outcome. Time-kill curves were generated for clinicalM. abscessusisolates,Mycobacterium smegmatis, andEscherichia coliby using antibiotics commonly categorized as bactericidal (amikacin and moxifloxacin) or bacteriostatic (tigecycline and linezo
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2

Pasca, Maria Rosalia, Paola Guglierame, Fabio Arcesi, Marco Bellinzoni, Edda De Rossi, and Giovanna Riccardi. "Rv2686c-Rv2687c-Rv2688c, an ABC Fluoroquinolone Efflux Pump in Mycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 48, no. 8 (2004): 3175–78. http://dx.doi.org/10.1128/aac.48.8.3175-3178.2004.

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ABSTRACT The Mycobacterium tuberculosis Rv2686c-Rv2687c-Rv2688c operon, encoding an ABC transporter, conferred resistance to ciprofloxacin and, to a lesser extent, norfloxacin, moxifloxacin, and sparfloxacin to Mycobacterium smegmatis. The resistance level decreased in the presence of the efflux pump inhibitors reserpine, carbonyl cyanide m-chlorophenylhydrazone, and verapamil. Energy-dependent efflux of ciprofloxacin from M. smegmatis cells containing the Rv2686c-Rv2687c-Rv2688c operon was observed.
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3

Malik, Muhammad, Tao Lu, Xilin Zhao, et al. "Lethality of Quinolones against Mycobacterium smegmatis in the Presence or Absence of Chloramphenicol." Antimicrobial Agents and Chemotherapy 49, no. 5 (2005): 2008–14. http://dx.doi.org/10.1128/aac.49.5.2008-2014.2005.

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ABSTRACT Quinolones were examined for rapid lethal activity against Mycobacterium smegmatis in the presence and absence of chloramphenicol, an inhibitor of protein synthesis. C-8 methoxy, C-6 fluorine, and particular C-7 ring substituents enhanced rapid killing. With the surprising exception of moxifloxacin, higher quinolone concentrations were required for lethal activity in the presence of chloramphenicol than in its absence. Moxifloxacin was also unusual in lacking the time lag characteristic of fluoroquinolone lethality. Several fluoroquinolone dimers, which represent quinolones with large
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4

Long, Quanxin, Qinglin Du, Tiwei Fu, Karl Drlica, Xilin Zhao, and Jianping Xie. "Involvement of Holliday Junction Resolvase in Fluoroquinolone-Mediated Killing of Mycobacterium smegmatis." Antimicrobial Agents and Chemotherapy 59, no. 3 (2014): 1782–85. http://dx.doi.org/10.1128/aac.04434-14.

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ABSTRACTThe absence of the Holliday-junction Ruv resolvase ofMycobacterium smegmatisincreased the bacteriostatic and bactericidal activities of the fluoroquinolone moxifloxacin, an important antituberculosis agent. The treatment ofruvAB-deficient cells with thiourea and 2,2′-bipyridyl lowered moxifloxacin lethality to wild-type levels, indicating that the absence ofruvABstimulates a lethal pathway involving reactive oxygen species. A hexapeptide that traps the Holliday junction substrate of RuvAB potentiated moxifloxacin-mediated lethality, supporting the development of small-molecule enhancer
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5

Danilchanka, Olga, Mikhail Pavlenok, and Michael Niederweis. "Role of Porins for Uptake of Antibiotics by Mycobacterium smegmatis." Antimicrobial Agents and Chemotherapy 52, no. 9 (2008): 3127–34. http://dx.doi.org/10.1128/aac.00239-08.

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ABSTRACT The outer membrane of mycobacteria presents an effective permeability barrier for many antibiotics. Transport pathways across this membrane are unknown for most drugs. Here, we examined which antibiotics utilize the porin pathway across the outer membrane of the model organism Mycobacterium smegmatis. Deletion of the porins MspA and MspC drastically increased the resistance of M. smegmatis ML10 to β-lactam antibiotics, while its β-lactamase activity remained unchanged. These results are consistent with the ninefold-reduced outer membrane permeability of the M. smegmatis porin mutants
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6

Zhou, Qin, Na Pu, Ge Xu, et al. "Rifampicin and isoniazid resistance not promote fluoroquinolone resistance in Mycobacterium smegmatis." PLOS ONE 20, no. 1 (2025): e0315512. https://doi.org/10.1371/journal.pone.0315512.

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Background The emergence of drug-resistant Tuberculosis (TB) has made treatment challenging. Although fluoroquinolones (FQs) are used as key drugs in the treatment of multidrug-resistant tuberculosis (MDR-TB), the problem of FQs resistance is becoming increasingly serious. Rifampicin (RIF) resistance is considered a risk factor for FQs resistance. The objective of this study was to investigate the impact of RIF and isoniazid (INH) resistance on the FQs resistance in vitro experiment. Methods FQs resistant strains were selected in vitro from RIF and/or INH resistant Mycobacterium smegmatis (M.s
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7

Luo, Tao, Jinning Yuan, Xuan Peng, et al. "Double mutation in DNA gyrase confers moxifloxacin resistance and decreased fitness of Mycobacterium smegmatis." Journal of Antimicrobial Chemotherapy 72, no. 7 (2017): 1893–900. http://dx.doi.org/10.1093/jac/dkx110.

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8

Swaminath, Sharmada, Avraneel Paul, Atul Pradhan, Jees Sebastian, Rashmi Ravindran Nair, and Parthasarathi Ajitkumar. "Mycobacterium smegmatis moxifloxacin persister cells produce high levels of hydroxyl radical, generating genetic resisters selectable not only with moxifloxacin, but also with ethambutol and isoniazid." Microbiology 166, no. 2 (2020): 180–98. http://dx.doi.org/10.1099/mic.0.000874.

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9

Lu, T. "Effect of chloramphenicol, erythromycin, moxifloxacin, penicillin and tetracycline concentration on the recovery of resistant mutants of Mycobacterium smegmatis and Staphylococcus aureus." Journal of Antimicrobial Chemotherapy 52, no. 1 (2003): 61–64. http://dx.doi.org/10.1093/jac/dkg268.

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10

Ajitkumar, Parthasarathi, Avraneel Paul, RashmiRavindran Nair, and Kishor Jakkala. "Mycobacterium smegmatis strains genetically resistant to moxifloxacin emerge de novo from the moxifloxacin-surviving population containing high levels of superoxide, H2O2, hydroxyl radical, and Fe (II)." International Journal of Mycobacteriology 11, no. 2 (2022): 150. http://dx.doi.org/10.4103/ijmy.ijmy_58_22.

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11

Malik, Muhammad, Kalyan Chavda, Xilin Zhao, et al. "Induction of Mycobacterial Resistance to Quinolone Class Antimicrobials." Antimicrobial Agents and Chemotherapy 56, no. 7 (2012): 3879–87. http://dx.doi.org/10.1128/aac.00474-12.

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ABSTRACTAn agar plate assay was developed for detecting the induction of drug-resistant mycobacterial mutants during exposure to inhibitors of DNA gyrase. WhenMycobacterium smegmatison drug-containing agar, resistant colonies arose over a period of 2 weeks. ArecAdeficiency reduced mutant recovery, consistent with involvement of the SOS response in mutant induction. The C-8-methoxy compounds gatifloxacin and moxifloxacin allowed the recovery of fewer resistant mutants than either ciprofloxacin or levofloxacin when present at the same multiple of the MIC; a quinolone-like 8-methoxy-quinazoline-2
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12

Rai, Deepika, and Sarika Mehra. "The mycobacterial efflux pump EfpA can induce high drug tolerance to many anti-tuberculosis drugs, including moxifloxacin, in Mycobacterium smegmatis." Antimicrobial Agents and Chemotherapy, August 23, 2021. http://dx.doi.org/10.1128/aac.00262-21.

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Active efflux of drugs across the membrane is a major survival strategy of bacteria against many drugs. In this work, we characterize an efflux pump EfpA, from the major facilitator superfamily, that is highly conserved among both slow growing and fast-growing mycobacterium species and has been found to be upregulated in many clinical isolates of Mycobacterium tuberculosis . The gene encoding EfpA from Mycobacterium smegmatis was over-expressed under both constitutive and an inducible promoter. Expression of efpA gene under both the promoters resulted in greater than 32-fold increased drug tol
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13

Paul, Avraneel, Rashmi Ravindran Nair, Kishor Jakkala, Atul Pradhan, and Parthasarathi Ajitkumar. "Elevated Levels of Three Reactive Oxygen Species and Fe(II) in the Antibiotic-Surviving Population of Mycobacteria Facilitate De Novo Emergence of Genetic Resisters to Antibiotics." Antimicrobial Agents and Chemotherapy, April 18, 2022. http://dx.doi.org/10.1128/aac.02285-21.

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We had earlier reported the de novo emergence of genetic resisters of Mycobacterium tuberculosis and Mycobacterium smegmatis to rifampicin and moxifloxacin from the antibiotic-surviving population containing elevated levels of the non-DNA-specific mutagenic reactive oxygen species (ROS) hydroxyl radical. Since hydroxyl radical is generated by Fenton reaction between Fe(II) and H 2 O 2 , which is produced by superoxide dismutation, we here report significantly elevated levels of these three ROS and Fe(II) in the M. smegmatis rifampicin-surviving population.
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14

Cvetnić, Luka, Miroslav Benić, Željko Cvetnić, et al. "Bovine mastitis caused by rapid-growth environmental mycobacteria." Veterinarska stanica 53, no. 5 (2022). http://dx.doi.org/10.46419/vs.53.5.11.

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Rapid-growth mycobacteria were isolated from two cases of cow mastitis with similar clinical appearance and within a narrow time frame. Mycobacteria were isolated on blood esculine agar. The isolated mycobacteria were Gram stained, Ziehl-Nielsen stained and tested for growth at 25°C, 37°C and 42°C, iron uptake, growth on Löwenstein-Jensen (LJ) agar with and without 5% NaCl, arylsulphatase (3 days), tween 80 hydrolysis, tellurite reduction, nitrate reductase and niacin synthesis. Molecular identification was performed using the Mycobacteria GenoType CM and AS tests (Hain Diagnostika, Nehren, Ge
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15

Fang, Cuiting, Han Zhang, Jing He, et al. "GrcC1 mediates low-level resistance to multiple drugs in M. marinum , M. abscessus, and M. smegmatis." Microbiology Spectrum, February 26, 2025. https://doi.org/10.1128/spectrum.02289-24.

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ABSTRACT The escalating threat of mycobacterial infectious diseases, particularly those caused by nontuberculous mycobacteria (NTM), poses a serious challenge to public health. Linezolid (LZD), an oxazolidinone antimicrobial, exhibits potent activity against Mycobacterium tuberculosis and NTM. Generally, mutations in the rrl and rplC genes are widely associated with resistance to LZD. However, in this study, we screened Mycobacterium marinum strains lacking such mutations, indicating the presence of an alternative resistance mechanism. Notably, through whole-genome sequencing, we identified a
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16

Pradhan, Atul, Sharmada Swaminath, Kishor Jakkala, and Parthasarathi Ajitkumar. "A method for the enrichment, isolation and validation of Mycobacterium smegmatis population surviving in the presence of bactericidal concentrations of rifampicin and moxifloxacin." FEMS Microbiology Letters 368, no. 14 (2021). http://dx.doi.org/10.1093/femsle/fnab090.

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ABSTRACT The bacterial populations surviving in the presence of antibiotics contain cells that have gained genetic resistance, phenotypic resistance and tolerance to antibiotics. Isolation of live bacterial population, surviving against antibiotics, from the milieu of high proportions of dead/damaged cells will facilitate the study of the cellular/molecular processes used by them for survival. Here we present a Percoll gradient centrifugation based method for the isolation of enriched population of Mycobacterium smegmatis surviving in the presence of bactericidal concentrations of rifampicin a
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17

Jakkala, Kishor, Avraneel Paul, Atul Pradhan, et al. "Unique Mode of Cell Division by the Mycobacterial Genetic Resister Clones Emerging De Novo from the Antibiotic-Surviving Population." mSphere 5, no. 6 (2020). http://dx.doi.org/10.1128/msphere.00994-20.

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ABSTRACT The emergence of antibiotic genetic resisters of pathogenic bacteria poses a major public health challenge. The mechanism by which bacterial antibiotic genetic resister clones formed de novo multiply and establish a resister population remained unknown. Here, we delineated the unique mode of cell division of the antibiotic genetic resisters of Mycobacterium smegmatis and Mycobacterium tuberculosis formed de novo from the population surviving in the presence of bactericidal concentrations of rifampicin or moxifloxacin. The cells in the rifampicin/moxifloxacin-surviving population gener
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