Relevant bibliographies by topics / Mycobacterium smegmatis - Moxifloxacin

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Mycobacterium smegmatis - Moxifloxacin'

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

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Journal articles on the topic "Mycobacterium smegmatis - Moxifloxacin"

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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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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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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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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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Dissertations / Theses on the topic "Mycobacterium smegmatis - Moxifloxacin"

1

Sharmada, S. "Cellular and Molecular Features of the Response of Mycobacterium smegmatis to Rifampicin and Moxifloxacin Upon Prolonged Exposure." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4168.

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Bacterial persisters are a subpopulation of bacteria that can tolerate lethal concentrations of antibiotics. These are phenotypic variants that can give rise to drug‐susceptible population upon withdrawal of the antibiotic. Persistent bacteria play a crucial role in prolonging antibiotic treatment and are responsible for the recalcitrance of many chronic bacterial diseases, including tuberculosis. Several mechanisms have been proposed for the formation of persisters, which include expression of toxin‐antitoxin systems, generation of reactive oxygen species (ROS), and stochastic changes in gene
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Journal articles
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