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Some years ago the Staphylococcus aureus DNA topoiso-merase IV genes were cloned and named grlA and grlB ([2][1]). Alterations in the GrlA subunit have been associated with fluoroquinolone resistance in clinical isolates ([2][1]). Further work with laboratory mutants supported data which indicated

Analysis of grlA Mutations in Clinical Isolates of Staphylococcus aureus with Different Levels of Quinolone Resistance