Institute of Clinical Medicine, School of Medicine, National Yang-Ming University, and Department of Medicine, Taipei Veterans General Hospital, No. 201, Section 2, Shih-Pai Road, Taipei, 11217, Taiwan.
Antimicrob Agents Chemother. 2010 Aug;54(8):3107-12. doi: 10.1128/AAC.00128-10. Epub 2010 Jun 1.
The contribution of the blaOXA-58 gene and its promoter to beta-lactam resistance has not been validated in Acinetobacter spp. other than Acinetobacter baumannii. We identified a multidrug-resistant (including carbapenem resistance) Acinetobacter genomic species 13TU in which blaOXA-58 was the only detected carbapenemase gene. The blaOXA-58 gene was plasmid located, flanked by ISAba3 (downstream) and an ISAba3-like element (upstream). An IS1006 element was inserted into ISAba3-like (IS1006-DeltaISAba3-like) to generate a hybrid promoter for blaOXA-58, with a -35 promoter located in IS1006 and a -10 promoter in ISAba3-like. The reference strain of Acinetobacter genomic species 13TU, ATCC 17903, revealed higher MICs of amoxicillin, ticarcillin, and piperacillin and heteroresistance to imipenem and meropenem when it was transformed with a shuttle vector containing a fragment encompassing DeltaISAba3-like-blaOXA-58, compared to the same host containing only blaOXA-58. When the fragment was changed from DeltaISAba3-like-blaOXA-58 to IS1006-DeltaISAba3-like-blaOXA-58, the ATCC 17903 transformant revealed a markedly higher level of blaOXA-58 transcription (12-fold), increased cefuroxime and piperacillin-tazobactam MICs, and homoresistance to imipenem and meropenem. Different roles of the insertion elements preceding the blaOXA-58 gene in Acinetobacter genomic species 13TU are demonstrated. The ISAba3-like--blaOXA-58 construct can mediate resistance to penicillin derivatives but only heteroresistance to carbapenems. The insertion of IS1006 into ISAba3-like, generating a hybrid promoter, could further enhance the transcription of blaOXA-58 and mediate homoresistance to carbapenems and also enhanced resistance to piperacillin-tazobactam.
blaOXA-58 基因及其启动子对除鲍曼不动杆菌以外的其他不动杆菌属细菌产生的β-内酰胺类耐药性的作用尚未得到证实。我们在一株多药耐药(包括碳青霉烯类耐药)的基因组种 13TU 型不动杆菌中鉴定出 blaOXA-58 为唯一检出的碳青霉烯酶基因。blaOXA-58 基因位于质粒上,下游为 ISAba3,上游为 ISAba3 样元件。IS1006 元件插入 ISAba3 样元件(IS1006-DeltaISAba3-like)中,为 blaOXA-58 生成一个杂合启动子,-35 启动子位于 IS1006 中,-10 启动子位于 ISAba3 样元件中。参考菌株基因组种 13TU 型不动杆菌 ATCC 17903 与仅含有 blaOXA-58 的相同宿主相比,当含有包含 DeltaISAba3-like-blaOXA-58 片段的穿梭载体转化时,其阿莫西林、替卡西林和哌拉西林 MIC 值更高,对亚胺培南和美罗培南的异质性耐药性更强。当片段由 DeltaISAba3-like-blaOXA-58 变为 IS1006-DeltaISAba3-like-blaOXA-58 时,ATCC 17903 转化株的 blaOXA-58 转录水平显著升高(12 倍),头孢呋辛和美罗培南/哌拉西林他唑巴坦 MIC 值升高,对亚胺培南和美罗培南的同源耐药性增强。该研究展示了 blaOXA-58 基因前插入元件在基因组种 13TU 型不动杆菌中的不同作用。ISAba3 样- blaOXA-58 构建体可介导对青霉素衍生物的耐药性,但仅对碳青霉烯类产生异质性耐药性。IS1006 插入 ISAba3 样元件,生成杂合启动子,可进一步增强 blaOXA-58 的转录,并介导对碳青霉烯类的同源耐药性,同时增强对哌拉西林-他唑巴坦的耐药性。