摘要
为了解临床分离金黄色葡萄球菌（金葡菌）对氟喹诺酮类药物的耐药机制。应用聚合酶链反应限制性片段长度多态性（ＰＣＲＲＦＬＰ）分析和ＰＣＲ单链构象多态分析（ＳＳＣＰ）技术及利血平逆转实验，分别检测３１株临床分离耐环丙沙星（ＭＩＣ≥４μｇ／ｍｌ）金葡菌株ｇｙｒＡ基因的突变及ｎｏｒＡ基因的表达。结果表明，３１株菌中有２２株检出ｇｙｒＡ基因８４位点突变，有２８株在利血平逆转实验中对环丙沙星和诺氟沙星的ＭＩＣ同时降低，表明存在ｎｏｒＡ耐药表型。同时涉及以上两种耐药机制的至少有２０株。结果提示：临床分离的耐药菌株耐氟喹诺酮机制大多同时涉及药物作用的靶位改变和细菌的膜耐药，即双重耐药机制共存。
To investigate the mechanism of resistance to fluoroquinolones in staphylococcus aureus, a total of 31 clinical isolates resistant to ciprofloxacin (MIC≥4μg/ml,collected from three hospitals in Tianjin during 1993 to 1995) were studied for the presence of point mutations in the gyrA gene by PCR-RFLP and PCR-SSCP method and for the expression of norA gene by reserpine reverse test, respectively. It was found that twenty-two strains (71%) had a mutation at codon 84, whereas MIC of twenty-eight strains (90%) decreased to cprofloxacin and norfloxacin in reserpine reverse test indicated the presence of norA resistance phenotype. At least twenty strains involved in the two mechanisms mentioned above. These results suggested that the resistance to fluoroquinolone in clinical isolates of S. aureus are mostly due to the mutation of the gyrA gene encoding the target enzyme of fluoroquinolones and cell membrane associated resistance.
出处
《中华传染病杂志》
CAS
CSCD
北大核心
1997年第3期130-133,共4页
Chinese Journal of Infectious Diseases
关键词
氟喹诺酮
金黄色葡萄球菌
耐药性
Fluoroquinolone Staphylococcus aureus gene,gyrA gene,norA
