Killing Kinetics of Four Quinolones against Gram-Positive Cocci

Cantón, Emilia; Ramon, M S; Jimenez, M T; Martinez, Josè

doi:10.1159/000238983

Cited by 20 publications

(8 citation statements)

References 16 publications

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“…Comparing these results with those reported in gram-positive bacteria, we observe that the extracellular and intraphagocytic killing rate are greater in gram-negative bacteria [12,[37][38][39].…”

Section: Discussionsupporting

confidence: 73%

Killing of Gram-Negative Bacteria by Ciprofloxacin within both Healthy Human Neutrophils and Neutrophils with Inactivated O<sub>2</sub>-Dependent Bactericidal Mechanisms

et al. 1999

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The intraphagocytic killing of Escherichia coli, Serratia marcescens, Pseudomonas aeruginosa, and Salmonella typhi by ciprofloxacin (0.1, 1 and 5 μg/ml) within human neutrophils with intact and impaired (by phenylbutazone treatment) O₂-dependent killing mechanisms was studied and compared with the extracellular killing in the same medium of the intraphagocytic killing, but omitting neutrophils. The MIC/MBC of ciprofloxacin in vitro (assays performed according to NCCLS specifications) were: 0.015/0.06 for E. coli, 0.12/32 for S. marcescens, 1/16 for P. aeruginosa, and 0.007/0.06 for S. typhi. Ciprofloxacin showed bactericidal activity both extracellular and within phenylbutazone-treated and untreated neutrophils. The minimum concentration of ciprofloxacin to kill 90% of phagocytosed bacteria within neutrophils with normal O₂-dependent killing power after 30 min was: 0.1 μg/ml for E. coli, and S. typhi, 1 μg/ml for P. aeruginosa, and 5 μg/ml for S. marcescens. In contrast, exposure for 60 min was required to reach this percentage within phenylbutazone treated neutrophils. The minimum concentration to kill 90% of extracellular bacteria after 30 min was: 0.1 μg/ml for E. coli, P. aeruginosa and S. typhi, and 5 μg/ml, for S. marcescens. A positive interaction between ciprofloxacin and the O₂-dependent mechanisms of phagocytes was found. The reactive oxygen metabolites produced in the respiratory burst did not affect the intraphagocytic activity of ciprofloxacin. Phenylbutazone treatment of phagocytes would be a good experimental model to study the intraphagocytic killing of drugs in situations such as AIDS and chronic granulomatous disease where inefficient oxidative mechanisms of neutrophils exist.

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Section: Discussionsupporting

confidence: 73%

Killing of Gram-Negative Bacteria by Ciprofloxacin within both Healthy Human Neutrophils and Neutrophils with Inactivated O<sub>2</sub>-Dependent Bactericidal Mechanisms

et al. 1999

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“…A decrease in the number of bacteria killed at high drug concentrations was observed for the parent quinolone ligands and com- pound 7. The diminution in the number of bacteria killed at high drug concentration is known as ''the paradoxical effect'' and has been described and related to the mechanism of action of quinolones by several authors [57][58][59][60][61]. The fact that compounds 2, 3, and 6 do not present a paradoxical effect suggests different mechanisms of bactericidal action.…”

Section: Antimicrobial Testsmentioning

confidence: 99%

Antibacterial studies, DNA oxidative cleavage, and crystal structures of Cu(II) and Co(II) complexes with two quinolone family members, ciprofloxacin and enoxacin

Jiménez-Garrido

Perelló

Ortiz

et al. 2005

Journal of Inorganic Biochemistry

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140

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“…Some quinolones, such as sparfloxacin and trovafloxacin with a high bactericidal activity against Staphylococci, have been reported to exert mechanism B against these microorganisms [11,22], but a systematic study to relate a higher activity to specific mechanisms has never been carried out. The aim of this study is to extend previous experimental findings [27,28] concerning the mechanism of action of fluoroquinolones against Staphylococcus species and to investigate whether there is a correlation between the possession of an additional mechanism of action and a higher bactericidal activity. For this purpose, we have studied the activity of six fluoroquinolones against 4 Staphylococcus strains.…”

Section: Introductionmentioning

confidence: 89%

“…The killing activity of the quinolones alone and with 30 Ìg/ml of chloramphenicol (MIC; minimum concentration that produces bacteriostatic effect) was tested in MHB at the previously determined optimal bactericidal concentration (OBC) [27,28]. The activity in PBS was measured by exposing the bacteria to drug concentrations ranging from 0.5 to 1,024 Ìg/ml using serial 2-fold dilutions.…”

Section: Time-killing Studiesmentioning

confidence: 99%

Mechanisms of Action of Quinolones against Staphylococci and Relationship with Their in vitro Bactericidal Activity

Ramon¹,

Cantón²,

Pemán³

et al. 1999

Chemotherapy

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Ciprofloxacin and norfloxacin exhibited mechanism A (requires cell division as well as bacterial protein and RNA synthesis to kill bacteria) and C (active against nondividing bacteria but requires protein and RNA synthesis) against the reference strain Staphylococcus aureus ATCC 25923, yet only mechanism A was exhibited by these fluoroquinolones when tested against three clinical isolates: S. aureus Sa-215, Staphylococcus epidermidis Se-81 and Staphylococcus haemolyticus Sx-1. On the contrary, fleroxacin exerted mechanism A and C against the three clinical isolates but only mechanism A against the reference strain. Ofloxacin displayed mechanism A against S. epidermidis Se-81, mechanism A and C against S. haemolyticus and mechanism A and B (active against nondividing bacteria and does not require protein and RNA synthesis) against the two S. aureus tested. Sparfloxacin showed mechanism A and C against the four Staphylococcus species studied, and temafloxacin was the only fluoroquinolone tested that exhibited mechanism A and B against the four bacterial strains assayed. No correlation was found between the in vitro bactericidal activity (expressed as minimum inhibitory concentration and optimal bactericidal concentration) and the mechanisms of action exhibited by these fluoroquinolones.

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Killing Kinetics of Four Quinolones against Gram-Positive Cocci

Cited by 20 publications

References 16 publications

Killing of Gram-Negative Bacteria by Ciprofloxacin within both Healthy Human Neutrophils and Neutrophils with Inactivated O<sub>2</sub>-Dependent Bactericidal Mechanisms

Killing of Gram-Negative Bacteria by Ciprofloxacin within both Healthy Human Neutrophils and Neutrophils with Inactivated O<sub>2</sub>-Dependent Bactericidal Mechanisms

Antibacterial studies, DNA oxidative cleavage, and crystal structures of Cu(II) and Co(II) complexes with two quinolone family members, ciprofloxacin and enoxacin

Mechanisms of Action of Quinolones against Staphylococci and Relationship with Their in vitro Bactericidal Activity

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