Fluoroquinolone Antibodies And Blood Culture Isolates

对4年来骨髓移植（BMT）患者血培养分离的37株绿绿链球菌和非BMT患者分离的39株绿绿链球菌进行了氟喹诺酮类药物的敏感性检测。在对左氧氟沙星、曲瓦沙星和/或格雷帕沙星耐药的5株BMT患者中，1株（NIH-(R02)）对多种氟喹诺酮类药物表现出高水平耐药。DNA旋切酶A是喹诺酮类抗生素的主要靶点之一。测定了NIH-(R02)旋切酶A喹诺酮类药物耐药区（QRDR）内的氨基酸序列。与10株S. mitis敏感菌株相比，NIH-(R02)在gyrA基因（丝氨酸到亮氨酸替代）QRDR内的“GKYHPHGDS”框中携带单点突变。因此，该分离株对氟喹诺酮类药物耐药的机制可能与先前报道的肺炎链球菌的机制相似。我们将对NIH-(R02)拓扑异构酶IV （parC基因）的parC亚基的QRDR和10个敏感菌株进行测序，以寻找可能赋予链球菌对喹诺酮类抗生素耐药的其他点突变。

Thirty-seven strains of viridans streptococci isolated from blood cultures on bone marrow transplant (BMT) recipients during the past 4 years and 39 strains of viridans streptococci isolated from non-BMT patients were tested for fluoroquinolone susceptibility. Of the five strains from BMT patients that were resistant to levofloxacin, trovafloxacin, and/or grepafloxacin, one isolate (NIH-(R02) demonstrated high-level resistance to multiple fluoroquinolones tested. DNA gyrase A is one of the major targets for quinolone antibiotics. The amino acid sequence within the quinolone resistance-determining region (QRDR) of the gyrase A of NIH-(R02) was determined. When compared with ten sensitive strains of S. mitis, NIH-(R02) carried a single point mutation in the "GKYHPHGDS" box within the QRDR of the gyrA gene (serine to leucine replacement). The mechanism of fluoroquinolone resistance in this isolate of S. mitis is thus likely similar to the previously reported mechanisms in S. pneumoniae. We will sequence the QRDR of the parC subunit of topoisomerase IV (parC gene) of NIH-(R02) and the ten sensitive strains to search for additional point mutations that may confer resistance to the quinolone antibiotics in the viridans group of streptococci.