A prominent feature of severe streptococcal infections is the profound inflammatory response that contributes to systemic toxicity. In sepsis the dysregulated host response involves both immunological and nonimmunological pathways. Here, we report a fatal case of an immunocompetent healthy female presenting with toxic shock and purpura fulminans caused by group B streptococcus (GBS; serotype III, CC19). The strain (LUMC16) was pigmented and hyperhemolytic. Stimulation of human primary cells with hyperhemolytic LUMC16 and STSS/NF-HH strains and pigment toxin resulted in a release of proinflammatory mediators, including tumor necrosis factor, interleukin (IL)-1β, and IL-6. In addition, LUMC16 induced blood clotting and showed factor XII activity on its surface, which was linked to the presence of the pigment. The expression of pigment was not linked to a mutation within the CovR/S region. In conclusion, our study shows that the hemolytic lipid toxin contributes to the ability of GBS to cause systemic hyperinflammation and interferes with the coagulation system.

中文翻译：

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β-溶血性 B 组链球菌色素的促血栓形成和促炎活性。

严重链球菌感染的一个突出特征是导致全身毒性的深刻炎症反应。在脓毒症中，失调的宿主反应涉及免疫和非免疫途径。在这里，我们报告了一例免疫功能正常的健康女性，出现由 B 组链球菌（GBS；血清型 III，CC19）引起的中毒性休克和暴发性紫癜的致命病例。该菌株 (LUMC16) 有色素和高溶血性。用高溶血性 LUMC16 和 STSS/NF-HH 菌株和色素毒素刺激人类原代细胞导致促炎介质的释放，包括肿瘤坏死因子、白细胞介素 (IL)-1β 和 IL-6。此外，LUMC16 诱导血液凝固并在其表面显示出因子 XII 活性，这与色素的存在有关。色素的表达与 CovR/S 区域内的突变无关。总之，我们的研究表明，溶血性脂质毒素有助于 GBS 引起全身性过度炎症并干扰凝血系统。