Ferry T, Thomas D, Perpoint T, Lina G, Monneret G, Mohammedi I, Chidiac C, Peyramond D, Vandenesch F, Etienne J
INSERM U851, Université Lyon 1, Centre National de Référence des Staphylocoques, Faculté de Médecine Laennec, Lyon, France.
Clin Microbiol Infect. 2008 Jun;14(6):546-54. doi: 10.1111/j.1469-0691.2008.01975.x. Epub 2008 Mar 27.
Most clinical isolates of Staphylococcus aureus harbour genes encoding superantigenic toxins that bind the Vbeta domain of T-cells, but little information is available concerning superantigenic toxin production during staphylococcal toxic shock syndrome (TSS) and septic shock. This prospective study investigated 14 patients with staphylococcal TSS or septic shock; the toxin gene profile of each isolate was determined and flow-cytometry was used to identify the discriminant Vbeta signature (DVbetaS) of each superantigenic toxin in vitro. Attempts were also made to identify in-vivo production of superantigenic toxin DVbetaS in patients' blood. The DVbetaS identified in vitro were: toxic shock syndrome toxin (TSST)-1, Vbeta 2; staphylococcal enterotoxin (SE), Vbeta 9, Vbeta 22; SEB, Vbeta 3, Vbeta 14, Vbeta 17; SED, Vbeta 1, Vbeta 8; egc, Vbeta 5.3, Vbeta 7.1, Vbeta 9, Vbeta 23; and SElK, Vbeta 5.1. The DVbetaS of TSST-1 and SEB were detected in patients with menstrual and non-menstrual TSS, respectively, whereas no Vbeta signature was detected during septic shock. All patients with septic shock (but only one patient with TSS) had lymphopenia and/or impaired cellular immunity. Detection of a superantigenic toxin DVbetaS may help to show which toxin is produced during staphylococcal TSS, thus confirming the diagnosis and hastening the administration of anti-toxin therapy. In contrast, this approach failed to demonstrate superantigenic toxin involvement in cases of septic shock. In this latter condition, a superantigenic toxin may not be produced by S. aureus, or its production may occur without expansion of targeted T-cells because of T-cell apoptosis and/or anergy.
大多数金黄色葡萄球菌临床分离株都携带编码能结合T细胞Vβ结构域的超抗原毒素的基因,但关于葡萄球菌中毒性休克综合征(TSS)和感染性休克期间超抗原毒素的产生情况,目前所知甚少。这项前瞻性研究调查了14例葡萄球菌性TSS或感染性休克患者;确定了每个分离株的毒素基因谱,并使用流式细胞术在体外鉴定每种超抗原毒素的鉴别性Vβ特征(DVβS)。还尝试鉴定患者血液中超抗原毒素DVβS的体内产生情况。在体外鉴定出的DVβS如下:中毒性休克综合征毒素(TSST)-1,Vβ2;葡萄球菌肠毒素(SE),Vβ9、Vβ22;SEB,Vβ3、Vβ14、Vβ17;SED,Vβ1、Vβ8;egc,Vβ5.3、Vβ7.1、Vβ9、Vβ23;以及SElK,Vβ5.1。分别在月经期和非月经期TSS患者中检测到TSST-1和SEB的DVβS,而在感染性休克期间未检测到Vβ特征。所有感染性休克患者(但只有1例TSS患者)有淋巴细胞减少和/或细胞免疫受损。检测超抗原毒素DVβS可能有助于显示葡萄球菌性TSS期间产生了哪种毒素,从而确诊并加快抗毒素治疗的给药。相比之下,这种方法未能证明超抗原毒素与感染性休克病例有关。在后一种情况下,金黄色葡萄球菌可能不产生超抗原毒素,或者由于T细胞凋亡和/或无反应性,其产生可能在没有靶向T细胞扩增的情况下发生。