Bricio-Moreno Laura, Ebruke Chinelo, Chaguza Chrispin, Cornick Jennifer, Kwambana-Adams Brenda, Yang Marie, Mackenzie Grant, Wren Brendan W, Everett Dean, Antonio Martin, Kadioglu Aras
Department of Clinical Immunology, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool.
Faculty of Infectious and Tropical Diseases, London School of Hygiene & Tropical Medicine.
J Infect Dis. 2017 Dec 5;216(10):1318-1327. doi: 10.1093/infdis/jix472.
Streptococcus pneumoniae serotype 1 is one of the leading causes of invasive pneumococcal disease (IPD) in West Africa, with ST618 being the dominant cause of IPD in The Gambia. Recently however, a rare example of clonal replacement was observed, where the ST3081 clone of serotype 1 replaced the predominant ST618 clone as the main cause of IPD. In the current study, we sought to find the reasons for this unusual replacement event. Using whole-genome sequence analysis and clinically relevant models of in vivo infection, we identified distinct genetic and phenotypic characteristics of the emerging ST3081 clone. We show that ST3081 is significantly more virulent than ST618 in models of invasive pneumonia, and is carried at higher densities than ST618 during nasopharyngeal carriage. We also observe sequence type-specific accessory genes and a unique sequence type-specific fixed mutation in the pneumococcal toxin pneumolysin, which is associated with increased hemolytic activity in ST3081 and may contribute to increased virulence in this clone. Our study provides evidence that, within the same serotype 1 clonal complex, biological properties differ significantly from one clone to another in terms of virulence and host invasiveness, and that these differences may be the result of key genetic differences within the genome.
肺炎链球菌1型是西非侵袭性肺炎球菌病(IPD)的主要病因之一,其中ST618是冈比亚IPD的主要病因。然而,最近观察到一个罕见的克隆替代例子,即1型的ST3081克隆取代了占主导地位的ST618克隆,成为IPD的主要病因。在本研究中,我们试图找出这一异常替代事件的原因。通过全基因组序列分析和体内感染的临床相关模型,我们确定了新兴的ST3081克隆的独特遗传和表型特征。我们表明,在侵袭性肺炎模型中,ST3081的毒力明显高于ST618,并且在鼻咽部携带期间,其携带密度高于ST618。我们还观察到序列类型特异性辅助基因以及肺炎球菌毒素肺炎溶血素中独特的序列类型特异性固定突变,这与ST3081中溶血活性增加有关,可能导致该克隆的毒力增加。我们的研究提供了证据,即在同一1型克隆复合体中,不同克隆在毒力和宿主侵袭性方面的生物学特性存在显著差异,而这些差异可能是基因组内关键遗传差异的结果。