猪链球菌(SS),猪的重要病原体,不仅被认为是人类的人畜共患病原体,但也被认为是抗生素耐药性的主要储库,有助于耐药基因向其他致病性链球菌传播。除了血清型2(SS2),血清型9(SS9)是从患病猪分离的另一种流行血清型。尽管已经对许多SS菌株进行了测序,迄今为止,尚未获得非SS2毒力菌株的完整基因组。这里,我们报告了从脑膜炎猪中分离出的SS9强毒株GZ0565的完整基因组。比较基因组分析揭示了菌株GZ0565中的五个新的推定毒力或抗菌素抗性相关基因,但在SS2毒力菌株中没有。这五个基因编码推定的三酰甘油脂肪酶,TipAS抗生素识别域蛋白,一个推定的TetR家族转录抑制因子,含有LPXTG结构域和G5结构域的蛋白质,和VII型分泌系统(T7SS)推定底物(EsxA),分别。Westernblot分析表明,菌株GZ0565可以分泌EsxA。我们产生了一个esxA缺失突变体,并显示EsxA有助于小鼠感染模型中的SS毒力。此外,鉴定了抗生素抗性基因vanZSS,vanZSS的表达赋予无乳链球菌对替考拉宁和达巴万星的抗性。我们认为这是T7SS推定底物EsxA的存在及其对SS中细菌毒力的贡献的第一个实验证明。一起,我们的研究结果有助于进一步了解SS的毒力和耐药性特征.
Streptococcus suis (SS), an important pathogen for pigs, is not only considered as a zoonotic agent for humans, but is also recognized as a major reservoir of antimicrobial resistance contributing to the spread of resistance genes to other pathogenic Streptococcus species. In addition to serotype 2 (SS2), serotype 9 (SS9) is another prevalent serotype isolated from diseased pigs. Although many SS strains have been sequenced, the complete genome of a non-SS2 virulent strain has been unavailable to date. Here, we report the complete genome of GZ0565, a virulent strain of SS9, isolated from a pig with meningitis. Comparative genomic analysis revealed five new putative virulence or antimicrobial resistance-associated genes in strain GZ0565 but not in SS2 virulent strains. These five genes encode a putative triacylglycerol lipase, a TipAS antibiotic-recognition domain protein, a putative TetR family transcriptional repressor, a protein containing a LPXTG domain and a G5 domain, and a type VII secretion system (T7SS) putative substrate (EsxA), respectively. Western blot analysis showed that strain GZ0565 can secrete EsxA. We generated an esxA deletion mutant and showed that EsxA contributes to SS virulence in a mouse infection model. Additionally, the antibiotic resistance gene vanZSS was identified and expression of vanZSS conferred resistance to teicoplanin and dalbavancin in Streptococcus agalactiae. We believe this is the first experimental demonstration of the existence of the T7SS putative substrate EsxA and its contribution to bacterial virulence in SS. Together, our results contribute to further understanding of the virulence and antimicrobial resistance characteristics of SS.