Mechanisms of resistance to fluoroquinolones.
Article
in English
| IMSEAR
| ID: sea-118474
ABSTRACT
Fluoroquinolones have some of the properties of an 'ideal' anti-microbial agent. Because of their potent broad spectrum activity and absence of transferable mechanism of resistance or inactivating enzymes, it was hoped that clinical resistance to this useful group of drugs would not occur. However, over the years, due to intense selective pressure and relative lack of potency of the available quinolones against some strains, bacteria have evolved at least two mechanisms of resistance (i) alteration of molecular targets, and (ii) reduction of drug accumulation. DNA gyrase and topoisomerase IV are the two molecular targets of fluoroquinolones. Mutations in specified regions (quinolone resistance-determining region) in genes coding for the gyrase and/or topoisomerase leads to clinical resistance. An efflux pump effective in pumping out hydrophilic quinolones has been described. Newer fluoroquinolones which recognize both molecular targets and have improved pharmacokinetic properties offer hope of higher potency, thereby reducing the probability of development of resistance.
Full text:
Available
Index:
IMSEAR (South-East Asia)
Main subject:
Staphylococcus aureus
/
Humans
/
DNA, Bacterial
/
Drug Resistance, Microbial
/
Cell Membrane Permeability
/
DNA Topoisomerases, Type I
/
Fluoroquinolones
/
Escherichia coli
/
Anti-Infective Agents
/
Mutation
Language:
English
Year:
1999
Type:
Article
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