Apparent involvement of a multidrug transporter in the fluoroquinolone resistance of Streptococcus pneumoniae.

AUTOR(ES)

Baranova, N N

RESUMO

A Streptococcus pneumoniae strain selected for resistance to ethidium bromide demonstrated enhanced energy-dependent efflux of this toxic dye. Both the ethidium resistance and the ethidium efflux could be inhibited by the plant alkaloid reserpine. The ethidium-selected cells demonstrated cross-resistance to the fluoroquinolones norfloxacin and ciprofloxacin; this resistance could also be completely reversed by reserpine. Furthermore, reserpine potentiated the susceptibility of wild-type S. pneumoniae to fluoroquinolones and ethidium. The most plausible explanation for these results is that S. pneumoniae, like some other gram-positive bacteria, expresses a reserpine-sensitive multidrug transporter, which may play an important role in both intrinsic and acquired resistances of this pathogen to fluoroquinolone therapy.

Documentos Relacionados

• Characterization of a mutation in the parE gene that confers fluoroquinolone resistance in Streptococcus pneumoniae.
• Trovafloxacin, a new fluoroquinolone with potent activity against Streptococcus pneumoniae.
• Detection of tetracycline resistance in Streptococcus pneumoniae.
• Fluoroquinolone resistance protein NorA of Staphylococcus aureus is a multidrug efflux transporter.
• Identification of the tetracycline resistance gene, tet(O), in Streptococcus pneumoniae.