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Titolo:
Mechanisms and frequency of resistance to gatifloxacin in comparison to AM-1121 and ciprofloxacin in Staphylococcus aureus
Autore:
Ince, D; Hooper, DC;
Indirizzi:
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, Boston, MA 02114 USA Harvard Univ Boston MA USA 02114 ed, Div Infect Dis, Boston, MA 02114 USA Harvard Univ, Massachusetts Gen Hosp, Sch Med, Med Serv, Boston, MA 02114 USA Harvard Univ Boston MA USA 02114 Sch Med, Med Serv, Boston, MA 02114 USA
Titolo Testata:
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY
fascicolo: 10, volume: 45, anno: 2001,
pagine: 2755 - 2764
SICI:
0066-4804(200110)45:10<2755:MAFORT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA TOPOISOMERASE-IV; GYRASE-A-PROTEIN; STREPTOCOCCUS-PNEUMONIAE; QUINOLONE RESISTANCE; IN-VITRO; 6-FLUORO-8-METHOXY QUINOLONE; FLUOROQUINOLONE RESISTANCE; ANTIBACTERIAL ACTIVITY; ANTIMICROBIAL ACTIVITY; COUMARIN ACTIVITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
55
Recensione:
Indirizzi per estratti:
Indirizzo: Hooper, DC Harvard Univ, Massachusetts Gen Hosp, Sch Med, Div Infect Dis, 55 Fruit St, Boston, MA 02114 USA Harvard Univ 55 Fruit St Boston MA USA 02114 ston, MA 02114 USA
Citazione:
D. Ince e D.C. Hooper, "Mechanisms and frequency of resistance to gatifloxacin in comparison to AM-1121 and ciprofloxacin in Staphylococcus aureus", ANTIM AG CH, 45(10), 2001, pp. 2755-2764

Abstract

Gatifloxacin, an 8-methoxyfluoroquinolone, was found to be two- to fourfold more active against wild-type Staphylococcus aureus ISP794 than its desmethoxy derivative, AM-1121, and ciprofloxacin, another desmethoxy fluoroquinolone. Single grlBA mutations caused two- to fourfold increases in the MIC of gatifloxacin, and a single gyrase mutation was silent. Double mutations in gyrA and grl4 or grlB caused a 32-fold increase in the MIC of gatifloxacin, in contrast to a 128-fold increase for ciprofloxacin and AM-1121. Overexpression of the NorA efflux pump had minimal effect on the MIC of gatifloxacin. The bactericidal activity of the three quinolones at four times the MIC differed only for a double mutant, with gatifloxacin exhibiting a killing pattern similar to that for ISP794, whereas ciprofloxacin and AM-1121 failed to show any killing. With gatifloxacin, selection of resistant mutants at twice the MIC was 100- to 1,000-fold less frequent than with the comparison quinolones, and mutants could rarely be selected at four times the MIC. The limit resistance in ISP74 was 512 times the MIC of gatifloxacin and 1,024 times the MICs of ciprofloxacin and AM-1121. Novel mutations in topoisomerase IV were selected in five of the six single-step mutants, three of which were shown to cause quinolone resistance by genetic studies. In conclusion, topoisomerase IV is the primary target of gatifloxacin. In contrast tocomparison quinolones, mutations in both topoisomerase IV and gyrase are required for resistance to gatifloxacin by clinical breakpoints; and do not abolish bactericidal effect, further supporting the benefit of the 8-methoxy substituent in gatifloxacin.

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Documento generato il 04/04/20 alle ore 02:50:10