School of Life and Environmental Sciences, The University of Sydney, NSW 2006, Australia.
The ithree institute, University of Technology Sydney, NSW, 2007, Australia.
J Antimicrob Chemother. 2021 Mar 12;76(4):893-900. doi: 10.1093/jac/dkaa553.
To understand the acquisition of resistance genes by a non-GC1, non-GC2 Acinetobacter baumannii strain responsible for a 4 year outbreak at a Sydney hospital.
Representative isolates were screened for resistance to antibiotics. Three were subjected to WGS using Illumina HiSeq. One genome was completed with MinION long reads. Resistance regions were compared with known sequences using bioinformatics.
Isolates were resistant to third-generation cephalosporins, gentamicin and tobramycin, sulfamethoxazole and erythromycin. Sequenced isolates were ST49 (Institut Pasteur scheme) and ST128 (Oxford scheme) and carried KL11 at the capsule locus and OCL8 at the lipooligosaccharide outer core locus. The complete genome of isolate J9 revealed that the resistance genes were all in plasmids; pRAY* contained aadB, and a large plasmid, pJ9-3, contained sul2 and floR genes and a dif module containing the mph(E)-msr(E) macrolide resistance genes. Transposon Tn6168, consisting of a second copy of the chromosomal ampC gene region flanked by ISAba1s, confers resistance to third-generation cephalosporins. Tn6168 is located inside the mph(E)-msr(E) dif module. pJ9-3 includes a set of four dif modules and the orientation of the pdif sites, XerC-XerD or XerD-XerC, alternates. A large transposon, Tn6175, containing tniCABDE transposition genes and genes annotated as being involved in heavy metal metabolism, uptake or export was found in the comM gene. Other ST49:ST128:KL11:OCL8 genomes found in the GenBank WGS database carried Tn6175 but neither of the plasmids carrying the resistance genes.
An early carbapenem-susceptible A. baumannii outbreak recorded in Australia was caused by an unusual clone that had acquired plasmids carrying antibiotic resistance genes.
了解导致悉尼一家医院 4 年爆发的非 GC1、非 GC2 鲍曼不动杆菌菌株获得耐药基因的情况。
对代表性分离株进行抗生素耐药性筛选。其中 3 株进行 Illumina HiSeq WGS 测序。用 MinION 长读长完成 1 个基因组。使用生物信息学比较耐药区与已知序列。
分离株对第三代头孢菌素、庆大霉素和妥布霉素、磺胺甲恶唑和红霉素耐药。测序分离株为 ST49(巴斯德研究所方案)和 ST128(牛津方案),在荚膜基因座携带 KL11,在外核心脂质寡糖基因座携带 OCL8。分离株 J9 的全基因组显示,耐药基因均位于质粒上;pRAY* 携带 aadB,大质粒 pJ9-3 携带 sul2 和 floR 基因以及含有 mph(E)-msr(E) 大环内酯类耐药基因的 dif 模块。由染色体 ampC 基因区域的第二个拷贝侧翼的 ISAba1s 组成的转座子 Tn6168 赋予对第三代头孢菌素的耐药性。Tn6168 位于 mph(E)-msr(E) dif 模块内。pJ9-3 包括一组四个 dif 模块,pdif 位点的 XerC-XerD 或 XerD-XerC 方向交替。在 comM 基因中发现了一个大型转座子 Tn6175,包含 tniCABDE 转座基因和注释为参与重金属代谢、摄取或外排的基因。在 GenBank WGS 数据库中发现的其他 ST49:ST128:KL11:OCL8 基因组携带 Tn6175,但不携带耐药基因的质粒。
澳大利亚记录的早期碳青霉烯敏感型鲍曼不动杆菌爆发是由携带抗生素耐药基因的不寻常克隆引起的。