Analysis of the mechanism that elaborate an alternative pathogenicity by loss of capsule in Streptococcus suis

猪链球菌是一种引起猪和人脑膜炎或心内膜炎的细菌病原体。衣壳是该细菌产生的一种表面成分，是抑制白细胞吞噬的重要毒力因子。本研究表明猪心内膜炎分离株中有时发现的猪链球菌无囊化细胞存在囊膜多糖合成(Cps)基因的自发突变，其中一些cps基因的突变似乎对细菌是致命的，而其他cps基因的突变则缓解了这些致死效应。此外，与包膜细胞相比，无囊细胞对猪和人血小板(感染性心内膜炎的主要致病决定因素)的粘附性增强，并且无囊细胞促进了包膜细胞与由无囊细胞形成的生物膜的结合。

Streptococcus suis is a bacterial pathogen that causes meningitis or endocarditis in pigs and humans. Capsule, a surface component produced by this bacterium, is an important virulence factor that inhibits phagocytosis of white blood cells. This study showed that acapsular cells of S. suis, which have sometimes been found in swine endocarditis isolates, have spontaneous mutations in capsular polysaccharide synthesis (cps) genes, and that mutations in some cps genes appeared lethal for the bacteria, whereas these lethal effects were relieved by mutations in the other cps genes. Moreover, acapsular cells showed elevated adherence to porcine and human platelets, a major virulence determinant for infective endocarditis, compared with capsular cells and the acapsular cells facilitated the incorporation of capsular cells to the biofilm formed by acapsular cells.