CIRI, Centre International de Recherche en Infectiologie, Inserm U1111, Université Claude Bernard Lyon 1, CNRS UMR5308, ENS de Lyon, Lyon, France.
Centre National de Référence des Staphylocoques, Hospices Civils de Lyon, Lyon, France.
Front Cell Infect Microbiol. 2018 Jun 8;8:187. doi: 10.3389/fcimb.2018.00187. eCollection 2018.
induces severe infective endocarditis (IE) where embolic complications are a major cause of death. Risk factors for embolism have been reported such as a younger age or larger IE vegetations, while methicillin resistance conferred by the gene appeared as a protective factor. It is unclear, however, whether embolism is influenced by other characteristics such as clonal complex (CC) or virulence pattern. We examined clinical and microbiological predictors of embolism in a prospective multicentric cohort of 98 French patients with monomicrobial IE. The genomic contents of causative isolates were characterized using DNA array. To preserve statistical power, genotypic predictors were restricted to CC, secreted virulence factors and virulence regulators. Multivariate regularized logistic regression identified three independent predictors of embolism. Patients at higher risk were younger than the cohort median age of 62.5 y (adjusted odds ratio [OR] 0.14; 95% confidence interval [CI] 0.05-0.36). characteristics predicting embolism were a CC30 genetic background (adjusted OR 9.734; 95% CI 1.53-192.8) and the absence of pIB485-like plasmid-borne enterotoxin-encoding genes , and (; adjusted OR 0.07; 95% CI 0.004-0.457). CC30 has been repeatedly reported to exhibit enhanced fitness in bloodstream infections, which might impact its ability to cause embolism. -encoded enterotoxins, whose superantigenic activity is unlikely to protect against embolism, possibly acted as a proxy to others genes of the pIB485-like plasmid found in genetically unrelated isolates from mostly embolism-free patients. did not independently predict embolism but was strongly associated with . This - association might have driven previous reports of a negative association of and embolism. Collectively, our results suggest that the influence of genotypic features on the risk of embolism may be stronger than previously suspected and independent of clinical risk factors.
导致严重感染性心内膜炎（IE），其中栓塞并发症是主要死亡原因。已经报道了栓塞的危险因素，例如年龄较小或 IE 赘生物较大，而 基因赋予的耐甲氧西林被认为是保护因素。然而，尚不清楚栓塞是否受其他 特征（如克隆复合体（CC）或毒力模式）的影响。我们检查了 98 例法国单微生物 IE 前瞻性多中心队列中临床和微生物学栓塞预测因子。使用 DNA 阵列对病原体分离株的基因组内容进行了特征描述。为了保持统计能力，基因型预测因子仅限于 CC、分泌性毒力因子和毒力调节剂。多变量正则化逻辑回归确定了栓塞的三个独立预测因子。风险较高的患者比队列的中位数年龄 62.5 岁年轻（校正优势比[OR]0.14；95%置信区间[CI]0.05-0.36）。 预测栓塞的特征是 CC30 遗传背景（调整后的 OR 9.734；95%CI 1.53-192.8）和不存在 pIB485 样质粒携带肠毒素编码基因 ，以及 （；调整后的 OR 0.07；95%CI 0.004-0.457）。CC30 已被反复报道在血流感染中表现出增强的适应性，这可能影响其引起栓塞的能力。编码肠毒素，其超抗原活性不太可能预防栓塞，可能作为在遗传上不相关的分离株中发现的 pIB485 样质粒上其他基因的替代物，这些分离株主要来自无栓塞患者。 本身并不能独立预测栓塞，但与 强烈相关。这种 - 关联可能导致了先前关于 和栓塞之间负相关的报道。总的来说，我们的研究结果表明， 基因型特征对栓塞风险的影响可能比以前怀疑的更强烈，并且独立于临床危险因素。
