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Procession to pediatric bacteremia and sepsis: covert operations and failures in diplomacy.

机译:进行小儿菌血症和败血症的游行:秘密行动和外交失败。

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摘要

Despite advances in diagnosis and treatment, bacterial sepsis remains a major cause of pediatric morbidity and mortality, particularly among neonates, the critically ill, and the growing immunocompromised patient population. Sepsis is the end point of a complex and dynamic series of events in which both host and microbial factors drive high morbidity and potentially lethal physiologic alterations. In this article we provide a succinct overview of the events that lead to pediatric bloodstream infections (BSIs) and sepsis, with a focus on the molecular mechanisms used by bacteria to subvert host barriers and local immunity to gain access to and persist within the systemic circulation. In the events preceding and during BSI and sepsis, Gram-positive and Gram-negative pathogens use a battery of factors for translocation, inhibition of immunity, molecular mimicry, intracellular survival, and nutrient scavenging. Gaps in understanding the molecular pathogenesis of bacterial BSIs and sepsis are highlighted as opportunities to identify and develop new therapeutics.
机译:尽管在诊断和治疗方面取得了进步,细菌性败血症仍然是儿童发病率和死亡率的主要原因,尤其是在新生儿,重症患者和免疫功能低下的人群中。脓毒症是一系列复杂而动态的事件的终点,在该事件中,宿主和微生物因素均导致高发病率和潜在的致命生理变化。在本文中,我们简要概述了导致小儿血流感染(BSI)和败血症的事件,并着重介绍了细菌用来破坏宿主屏障和局部免疫力的分子机制,以进入和维持全身循环。在BSI和败血症发生之前和期间,革兰氏阳性和革兰氏阴性病原体使用一系列因素进行易位,免疫抑制,分子模拟,细胞内存活和营养清除。认识细菌BSI和脓毒症的分子发病机理的空白被突出为发现和开发新疗法的机会。

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