Tanaka M, Fukuda H, Hirai K, Hosaka M, Matsumoto T, Kumazawa J
Department of Urology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Genitourin Med. 1994 Aug;70(4):253-5. doi: 10.1136/sti.70.4.253.
To investigate the alteration of cell permeability toward fluoroquinolones in Neisseria gonorrhoeae, which is a major quinolone-resistance mechanism along with the alteration of DNA gyrase in gram-negative bacteria. The prevalence of fluoroquinolone-resistant N gonorrhoeae strains is rapidly increasing in Japan.
The uptake and accumulation of norfloxacin by gonococcal cells, including six clinical and five World Health Organization (WHO) reference strains, were measured. Of the six clinical strains, two were highly resistant to norfloxacin (MIC 8.0 and 4.0 micrograms/ml), two were moderately resistant (MIC 1.0 and 0.5 microgram/ml), and two were sensitive (MIC 0.063 and 0.004 microgram/ml). All five WHO reference strains were sensitive to norfloxacin (MIC < or = 0.001 to 0.063 microgram/ml).
Mean initial norfloxacin uptake in the four resistant strains (104 ng/mg of dry cells) was significantly lower than that in the seven sensitive strains (158 ng/mg of dry cells) (p < 0.05). The mean uptake after 20 minutes was also significantly lower in the four resistant strains (130 ng/mg of dry cells) than in the seven sensitive strains (194 ng/mg of dry cells) (p < 0.05). However, there was no significant difference in mean norfloxacin accumulation after 20 minutes between the four resistant strains (26 ng/mg of dry cells) and the seven sensitive strains (36 ng/mg of dry cells). The accumulation of norfloxacin after 20 minutes was almost zero in two of the four resistant strains, while the remaining two strains accumulated norfloxacin as well as the sensitive strains.
These findings suggest that alteration of bacterial cell permeability is a quinolone-resistance mechanism in N gonorrhoeae isolated in Japan, and that this bacteria may exhibit other mechanisms such as alteration of DNA gyrase.
研究淋病奈瑟菌对氟喹诺酮类药物的细胞通透性改变情况，这是革兰氏阴性菌中与DNA旋转酶改变并存的主要喹诺酮耐药机制。在日本，耐氟喹诺酮淋病奈瑟菌菌株的流行率正在迅速上升。
测定了包括6株临床菌株和5株世界卫生组织（WHO）参考菌株在内的淋球菌细胞对诺氟沙星的摄取和积累情况。6株临床菌株中，2株对诺氟沙星高度耐药（MIC为8.0和4.0微克/毫升），2株中度耐药（MIC为1.0和0.5微克/毫升），2株敏感（MIC为0.063和0.004微克/毫升）。所有5株WHO参考菌株对诺氟沙星敏感（MIC≤0.001至0.063微克/毫升）。
4株耐药菌株的诺氟沙星平均初始摄取量（104纳克/毫克干细胞）显著低于7株敏感菌株（158纳克/毫克干细胞）（p<0.05）。4株耐药菌株在20分钟后的平均摄取量（130纳克/毫克干细胞）也显著低于7株敏感菌株（194纳克/毫克干细胞）（p<0.05）。然而，4株耐药菌株（26纳克/毫克干细胞）与7株敏感菌株（36纳克/毫克干细胞）在20分钟后的诺氟沙星平均积累量无显著差异。4株耐药菌株中有2株在20分钟后的诺氟沙星积累量几乎为零，而其余2株与敏感菌株一样积累了诺氟沙星。
这些发现表明，细菌细胞通透性改变是日本分离出的淋病奈瑟菌的一种喹诺酮耐药机制，并且这种细菌可能还表现出其他机制，如DNA旋转酶改变。
