FLUOROQUINOLONE ANTIBIOTIC AGAINST BLOOD CUUTURE ISOLATE

对4年来从骨髓移植(BMT)患者血培养中分离的37株绿色链球菌和39株非BMT患者分离的绿色链球菌进行了氟喹诺酮类药物敏感性试验。在5株对左氧氟沙星、曲瓦沙星和/或格列帕沙星耐药的骨髓移植患者分离株中，有1株(NIH-(R02))对多重氟喹诺酮类药物高度耐药。DNA旋转酶A是喹诺酮类抗生素的主要靶点之一。测定了NIH-(R02)旋转酶A的喹诺酮耐药决定区(QRDR)内的氨基酸序列。与10株敏感菌株相比，NIH-(R02)在gyrA基因的QRDR(丝氨酸到亮氨酸替换)的“GKYHPHGDS”框中存在单点突变。因此，这种米氏链球菌对氟喹诺酮类药物的耐药机制可能与先前报道的肺炎链球菌的耐药机制类似。我们将对NIH-(R02)株和10株敏感株的拓扑异构酶IV(ParC基因)的ParC亚单位的QRDR进行测序，以寻找可能导致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.