Barada Kazunari, Hanaki Hideaki, Ikeda Shinsuke, Yamaguchi Yoshio, Akama Hiroyuki, Nakae Taiji, Inamatsu Takashi, Sunakawa Keisuke
Laboratory of Infectious Diseases, Graduate School of Infection Control Sciences, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8642, Japan.
J Infect Chemother. 2007 Apr;13(2):74-8. doi: 10.1007/s10156-006-0497-0. Epub 2007 May 8.
It is generally accepted that methicillin-resistant Staphylococcus aureus (MRSA) is also resistant to aminoglycoside antibiotics. We investigated trends of gentamicin and arbekacin susceptibilities and the prevalence of the genes encoding aminoglycoside-modifying enzymes (AMEs) for a total of 218 strains of MRSA isolated from blood specimens obtained from 1978 through 2002 in one hospital. The minimum inhibitory concentrations of gentamicin at which 50% of the strains were inhibited (MIC(50)) were > or =128 and 32 microg/ml for isolates obtained from 1978 to 1984 and from 1985 to 1989, respectively, and 0.5 microg/ml for isolates obtained from 1990 to 2002. The MIC(90) of gentamicin was consistently > or =128 microg/ml. Investigation of the occurrence of AME revealed that the MIC(50) of gentamicin was highly correlated with the presence of aac(6')/aph(2'') encoding aminoglycoside acetyl/phosphotransferase. The MIC(50) of arbekacin was 2 microg/ml for strains isolated in 1978-1984 and </=0.5 microg/ml for strains isolated from 1985 to 2002. The MIC(90) of arbekacin was 8 microg/ml for the strains isolated in 1978-1989 and 1 to 2 microg/ml for strains isolated in 1990-2002. Though it has been established that AAC(6')/APH(2'') modifies arbekacin, the trend of arbekacin resistance was not necessarily consistent with the presence of this enzyme. However, the prevalence of both aac(6')/aph(2'') and aph(3')-III in the strains isolated from 1978 through 2002 was correlated with the MIC(90) values of arbekacin. Thus, it is most likely that APH(3')-III, in addition to AAC(6')/APH(2''), is somehow involved in arbekacin resistance in S. aureus. Our results imply that gentamicin- and arbekacin-resistant MRSAs have consistently decreased for the past 25 years and that this finding is, most likely, attributable to the declining prevalence of genes encoding for AMEs.
一般认为，耐甲氧西林金黄色葡萄球菌（MRSA）也对氨基糖苷类抗生素耐药。我们调查了1978年至2002年期间从一家医院采集的血液标本中分离出的总共218株MRSA对庆大霉素和阿贝卡星的敏感性趋势以及编码氨基糖苷类修饰酶（AMEs）的基因的流行情况。1978年至1984年分离出的菌株，庆大霉素抑制50%菌株的最低抑菌浓度（MIC(50)）≥128μg/ml，1985年至1989年分离出的菌株为32μg/ml，1990年至2002年分离出的菌株为0.5μg/ml。庆大霉素的MIC(90)始终≥128μg/ml。对AMEs出现情况的调查显示，庆大霉素的MIC(50)与编码氨基糖苷乙酰/磷酸转移酶的aac(6')/aph(2'')的存在高度相关。1978 - 1984年分离出的菌株阿贝卡星的MIC(50)为2μg/ml，1985年至2002年分离出的菌株≤0.5μg/ml。1978 - 1989年分离出的菌株阿贝卡星的MIC(90)为8μg/ml，1990 - 2002年分离出的菌株为1至2μg/ml。虽然已确定AAC(6')/APH(2'')会修饰阿贝卡星，但阿贝卡星耐药趋势不一定与该酶的存在一致。然而，1978年至2002年分离出的菌株中aac(6')/aph(2'')和aph(3') - III的流行情况与阿贝卡星的MIC(90)值相关。因此，除了AAC(6')/APH(2'')外，APH(3') - III很可能也以某种方式参与了金黄色葡萄球菌对阿贝卡星的耐药。我们的结果表明，在过去25年中，耐庆大霉素和耐阿贝卡星的MRSA一直呈下降趋势，这一发现很可能归因于编码AMEs的基因流行率的下降。
