Comparative genome analyses of Staphylococcus aureus from platelet concentrates reveal rearrangements involving loss of type VII secretion genes.

Access microbiology Pub Date : 2024-09-13 eCollection Date: 2024-01-01 DOI:10.1099/acmi.0.000820.v4
Sylvia Ighem Chi, Annika Flint, Kelly Weedmark, Franco Pagotto, Sandra Ramirez-Arcos
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Abstract

Staphylococcus aureus has been involved in transfusion-transmitted fatalities associated with platelet concentrates (PCs) due to its heightened pathogenicity enhanced by genome-encoded virulence and antibiotic resistance genes. This may be facilitated by mobile genetic elements (MGEs) that can cause rearrangements. Several factors contribute to S. aureus virulence, including the type VII secretion system (T7SS), composed of six core genes conserved across S. aureus strains. In this study, we conducted comparative genome analyses of five S. aureus isolates from PCs (CI/BAC/25/13 /W, PS/BAC/169/17 /W and PS/BAC/317/16 /W were detected during PCs screening with the BACT/ALERT automated culture system, and ATR-20003 and CBS2016-05 were missed during screening and caused septic transfusion reactions). Multiple alignments of the genomes revealed evidence of rearrangements involving phage Sa3int in PS/BAC/169/17 /W and PS/BAC/317/16 /W. While the former had undergone translocation of its immune evasion cluster (IEC), the latter had lost part of the phage, leaving behind the IEC. This observation highlights S. aureus genome plasticity. Unexpectedly, strain CBS2016-05 was found to encode a pseudo-type VII secretion system (T7SS) that had lost five of the conserved core genes (esxA, esaA, essA, esaB and essB) and contained a 5' truncated essC. Since these genes are essential for the function of the T7SS protein transport machinery, which plays a key role in S. aureus virulence, CBS2016-05 probably compensates by recruiting other export mechanisms and/or alternative virulence factors, such as neu-tralizing immunity proteins. This study unravels genome rearrangements in S. aureus isolated from PCs and reports the first S. aureus isolate lacking conserved T7SS core genes.

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来自血小板浓缩物的金黄色葡萄球菌的比较基因组分析揭示了涉及VII型分泌基因丢失的重排。
金黄色葡萄球菌参与了与血小板浓缩物(PCs)相关的输血传播死亡,因为它的致病性被基因组编码的毒力和抗生素耐药基因增强。这可能是由可引起重排的移动遗传元件(MGEs)促进的。几个因素有助于金黄色葡萄球菌的毒力,包括VII型分泌系统(T7SS),由6个核心基因组成,在金黄色葡萄球菌菌株中保守。本研究采用BACT/ALERT自动培养系统对pc进行筛选时,检测到CI/BAC/25/13 /W、PS/BAC/169/17 /W和PS/BAC/317/16 /W,筛选时漏检ATR-20003和CBS2016-05,导致败血症性输血反应。多个基因组比对显示,PS/BAC/169/17 /W和PS/BAC/317/16 /W中存在噬菌体Sa3int重排的证据。前者经历了其免疫逃避簇(IEC)的易位,后者失去了部分噬菌体,留下了IEC。这一观察结果突出了金黄色葡萄球菌基因组的可塑性。出乎意料的是,菌株CBS2016-05编码了一个伪VII型分泌系统(T7SS),该系统丢失了5个保守的核心基因(esxA, esaA, essA, esaB和essB),并含有一个5'截断的essC。由于这些基因对于在金黄色葡萄球菌毒力中起关键作用的T7SS蛋白转运机制的功能至关重要,CBS2016-05可能通过招募其他输出机制和/或替代毒力因子(如新激活免疫蛋白)来补偿。本研究揭示了从pc分离的金黄色葡萄球菌的基因组重排,并报道了第一个缺乏保守的T7SS核心基因的金黄色葡萄球菌分离物。
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