Manoharan Harish, Lalitha Aishwarya K V, Mariappan Shanthi, Sekar Uma, Venkataramana Geetha P
Department of Microbiology, Sri Ramachandra Institute for Higher Education and Research, Chennai, Tamil Nadu, India.
J Lab Physicians. 2022 Feb 23;14(3):290-294. doi: 10.1055/s-0042-1742423. eCollection 2022 Sep.
are nosocomial pathogen. They can develop high-level resistance to aminoglycoside by producing aminoglycoside modifying enzymes (AMEs). In enterococci, high level resistance to aminoglycosides is mediated by acquisition of plasmid mediated genes encoding for aminoglycoside modifying enzymes (AMEs). High level gentamicin resistance (MIC ≥ 500μg /mL) is predominantly mediated by aac(6')-Ie-aph(2″)-Ia, encoding the bifunctional aminoglycoside modifying enzyme AAC(6')-APH(2″). This enzyme eliminates the synergistic activity of gentamicin when combined with a cell wall active agent. Other AME genes such as aph(2″)-Ib, aph(2″)-Ic, aph(2″)-Id and ant(4')-1a have also been detected in enterococci. This study was carried out to determine the diverse prevalence of AME and their pattern of occurrence in the clinical isolates of . A total number of 150 clinical isolates were included in this study. Susceptibility to various antibiotics was determined by disc diffusion. Minimum Inhibitory Concentration (MIC) was ascertained by agar dilution method. Polymerase chain reaction was done to screen the following AMEs and . 51.3% of the study isolates exhibited high level gentamicin resistance. Polymerase chain reaction revealed that is the most prevalent AME, followed by . The combination of both the genes were detected in 44.1% of the study isolates. The rest of the AMEs and their combinations were not encountered in this study. 8.6% of the study isolates did not harbour any AME genes screened for, but was phenotypically resistant to gentamicin. In contrast 31.3% anchored the AME genes but phenotypically appeared susceptible to gentamicin. This study indicates the high- level aminoglycoside resistance disseminated among in our geographical region. It also emphasizes the detection of AMEs by PCR is mandatory because strains that appear susceptible by disc diffusion and/or MIC method may harbour one or more AMEs genes leading to therapeutic failure.
是医院病原体。它们可通过产生氨基糖苷修饰酶（AMEs）对氨基糖苷类产生高水平耐药性。在肠球菌中，对氨基糖苷类的高水平耐药性是由获得编码氨基糖苷修饰酶（AMEs）的质粒介导基因介导的。高水平庆大霉素耐药性（MIC≥500μg/mL）主要由aac(6')-Ie-aph(2″)-Ia介导，该基因编码双功能氨基糖苷修饰酶AAC(6')-APH(2″)。当与细胞壁活性剂联合使用时，这种酶会消除庆大霉素的协同活性。在肠球菌中也检测到了其他AME基因，如aph(2″)-Ib、aph(2″)-Ic、aph(2″)-Id和ant(4')-1a。 本研究旨在确定AMEs在 临床分离株中的不同流行率及其出现模式。 本研究共纳入150株临床分离株。通过纸片扩散法测定对各种抗生素的敏感性。通过琼脂稀释法确定最低抑菌浓度（MIC）。进行聚合酶链反应以筛选以下AMEs 和 。 51.3%的研究分离株表现出高水平庆大霉素耐药性。聚合酶链反应显示 是最常见的AME，其次是 。44.1%的研究分离株中检测到这两种基因的组合。本研究未遇到其他AMEs及其组合。8.6%的研究分离株未携带任何筛选的AME基因，但对庆大霉素表现出表型耐药。相比之下，31.3%的分离株携带AME基因，但表型上对庆大霉素敏感。 本研究表明，在我们的地理区域内， 中广泛存在高水平氨基糖苷类耐药性。它还强调通过PCR检测AMEs是必不可少的，因为通过纸片扩散法和/或MIC法看似敏感的菌株可能携带一个或多个AME基因，导致治疗失败。
