Matrat Stéphanie, Veziris Nicolas, Mayer Claudine, Jarlier Vincent, Truffot-Pernot Chantal, Camuset Juliette, Bouvet Elisabeth, Cambau Emmanuelle, Aubry Alexandra
Laboratoire de Bactériologie, Centre National de Référence des Mycobactéries et de la Résistance des Mycobactéries aux Antituberculeux, site Pitié-Salpêtrière, Université Paris 6, Assistance Publique-Hôpitaux de Paris, Paris, France.
Antimicrob Agents Chemother. 2006 Dec;50(12):4170-3. doi: 10.1128/AAC.00944-06. Epub 2006 Oct 2.
We investigated the enzymatic efficiency and inhibition by quinolones of Mycobacterium tuberculosis DNA gyrases carrying the previously described GyrA G88C mutation and the novel GyrA G88A mutation harbored by two multidrug-resistant clinical strains and reproduced by site-directed mutagenesis. Fluoroquinolone MICs and 50% inhibitory concentrations for both mutants were 2- to 43-fold higher than for the wild type, demonstrating that these mutations confer fluoroquinolone resistance in M. tuberculosis.
我们研究了携带先前描述的GyrA G88C突变以及两种耐多药临床菌株所具有并通过定点诱变重现的新型GyrA G88A突变的结核分枝杆菌DNA促旋酶的酶促效率及喹诺酮类药物对其的抑制作用。两种突变体的氟喹诺酮最低抑菌浓度(MIC)和50%抑制浓度比野生型高2至43倍,表明这些突变赋予结核分枝杆菌对氟喹诺酮类药物的耐药性。