Peterson M L, Rotschafer J C, Piddock L J V
University of Minnesota, Minneapolis, MN, USA.
J Antimicrob Chemother. 2003 Sep;52(3):481-4. doi: 10.1093/jac/dkg368. Epub 2003 Aug 13.
To identify whether mutations in gyrA and gyrB confer fluoroquinolone resistance in Bacteroides fragilis.
Eight fluoroquinolone-resistant (FQR) strains were complemented with plasmid-mediated B. fragilis wild-type gyrA (pMP1) and gyrB (pMP2), and MICs determined. Sequence analysis of the gyrA and gyrB quinolone resistance determining region (QRDR) was performed for all strains.
MICs of fluoroquinolones were two- to 32-fold higher than wild-type for all mutants. Five mutants had a substitution in GyrA (Ser-82-->Phe), one mutant had a substitution in GyrA (Asp-81-->Gly), one mutant had a substitution in GyrB (Glu-478-->Lys), and one resistant strain did not contain mutations in the QRDR of gyrA or gyrB. Following complementation with pMP1 or pMP2, the MICs of fluoroquinolones were reduced two- to 32-fold for the mutants.
These studies verify that substitutions in GyrA and GyrB confer resistance in B. fragilis. Other mechanisms are also responsible for resistance since not all resistant strains fully complemented to the wild-type phenotype.
确定脆弱拟杆菌中gyrA和gyrB的突变是否赋予对氟喹诺酮类药物的抗性。
用质粒介导的脆弱拟杆菌野生型gyrA（pMP1）和gyrB（pMP2）对8株耐氟喹诺酮（FQR）菌株进行互补，并测定最低抑菌浓度（MIC）。对所有菌株的gyrA和gyrB喹诺酮抗性决定区（QRDR）进行序列分析。
所有突变体的氟喹诺酮类药物MIC比野生型高2至32倍。5个突变体的GyrA发生替换（Ser-82→Phe），1个突变体的GyrA发生替换（Asp-81→Gly），1个突变体的GyrB发生替换（Glu-478→Lys），1株耐药菌株的gyrA或gyrB的QRDR未发生突变。用pMP1或pMP2互补后，突变体的氟喹诺酮类药物MIC降低了2至32倍。
这些研究证实GyrA和GyrB中的替换赋予脆弱拟杆菌抗性。由于并非所有耐药菌株都能完全互补为野生型表型，其他机制也与抗性有关。
