五株 2013 年以前的大肠埃希菌序列类型 (ST)1193 菌株的完整基因组序列揭示了一种新出现的病原体。

Access microbiology Pub Date : 2024-10-18 eCollection Date: 2024-01-01 DOI:10.1099/acmi.0.000894.v3
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引用次数: 0

摘要

耐氟喹诺酮大肠埃希菌序列类型(ST)1193 是一种与全身、泌尿道和新生儿感染有关的严重的新兴菌系。人类、伴侣动物和环境是 ST1193 的贮藏地,它已在全球范围内传播。ST1193 于 2007 年被发现后,在澳大利亚的耐氟喹诺酮克隆中反复被发现。然而,尽管 ST1193 的重要性与日俱增,但文献中只发表了三个完整的基因组,其中没有一个来自澳大利亚。在此,我们利用牛津纳米孔技术公司(Oxford Nanopore Technologies)和 Illumina 测序了五株 ST1193 菌株的完整基因组,从而扩展了现有的 ST1193 资源。通过使用硅基因分型技术,我们发现所有菌株都具有多重耐药性,包括对氟喹诺酮类和头孢菌素类的耐药性。体外抗生素药敏试验大多与个体基因型相关。MS8320 是个例外,它对哌拉西林/他唑巴坦、氨苄西林/舒巴坦、头孢唑啉和多尼培南(碳青霉烯类)具有额外的体外耐药性。进一步调查发现,携带 bla TEM-1B β-内酰胺酶基因的 IS26 转座单元又多了 7 个拷贝,这表明这种串联扩增与扩展的耐药性表型有关。尿致病因子,包括三个独立的苷元编码基因座,在染色体和质粒区域都是保守的。利用所有完整的基因组,我们进一步阐明了围绕先前描述的 K5/K1 胶囊基因座切换的重组事件。澳大利亚 ST1193 株系中不同胶囊的表型确认,加上揭示了胶囊基因座下游插入物的遗传分析,强调了 K5 和 K1 胶囊编码株系之间的遗传差异。本研究提供了来自澳大利亚的五个新的 ST1193 参考基因组。其中包括有记录以来最早的完整 K5 胶囊 ST1193 基因组(2007 年收集),以及我们的参考基因组(MS10858),后者是 ST1193 扩增早期获得的临床分离株,是主要 K1 相关支系的代表。这些发现为进一步的基因组和分子分析奠定了基础,可能有助于了解 ST1193 在全球迅速扩展的根本原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The complete genome sequence of five pre-2013 Escherichia coli sequence type (ST)1193 strains reveals insights into an emerging pathogen.

Fluoroquinolone-resistant Escherichia coli sequence type (ST)1193 is a profound, emerging lineage associated with systemic, urinary tract and neonatal infections. Humans, companion animals and the environment are reservoirs for ST1193, which has been disseminated globally. Following its detection in 2007, ST1193 has been identified repeatedly amongst fluoroquinolone-resistant clones in Australia. However, despite the growing importance of ST1193, only three complete genomes are published in the literature, none of which are from Australia. Here we expand on the available ST1193 resources with the complete genomes of five ST1193 strains sequenced using Oxford Nanopore Technologies and Illumina. Using in silico genotyping, we found that all strains were multi-drug resistant, including resistances to fluoroquinolones and cephalosporins. In vitro antibiotic susceptibility testing mostly correlated with individual genotypes. The exception was MS8320, which had additional in vitro resistance to piperacillin/tazobactam, ampicillin/sulbactam, cefazolin and doripenem (carbapenem). Further investigation identified seven additional copies of an IS26 transposable unit carrying a bla TEM-1B beta-lactamase gene, suggesting this tandem amplification is associated with extended resistance phenotypes. Uropathogenicity factors, including three separate siderophore-encoding loci, were conserved in chromosomal and plasmid regions. Using all complete genomes, we further elucidated the recombination events surrounding the previously described K5/K1 capsular locus switch. Phenotypic confirmation of differing capsules in Australian ST1193 strains, coupled with genetic analysis revealing insertions downstream of the capsular locus, underscored the genetic distinctions between K5 and K1 capsule encoding strains. This study provides five new reference ST1193 genomes from Australia. These include the earliest complete K5-capsule ST1193 genomes on record (collected 2007), alongside our reference genome (MS10858), a clinical isolate obtained early during the ST1193 expansion and representative of the predominant K1-associated clade. These findings lay the foundations for further genomic and molecular analyses that may help understand the underlying reasons for the rapid global expansion of ST1193.

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