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Procession to Pediatric Bacteremia and Sepsis: A Series of Covert Operations and Failures in Diplomacy

机译：小儿细菌血症和败血症的游行：一系列秘密行动和外交上的失败

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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 endpoint of a complex and dynamic series of events in which both host and microbial factors drive the high morbidity and potentially lethal physiological alterations. This article provides a succinct overview of the events that lead to pediatric bloodstream infections (BSI) and sepsis, with a focus on the molecular mechanisms employed 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 employ a battery of factors for translocation, inhibition of immunity, molecular mimicry, intracellular survival, and nutrient scavenging. Gaps in understanding the molecular pathogenesis of bacterial BSI 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。败血症是一系列复杂而动态的事件的终点，其中宿主和微生物因素共同驱动高发病率和潜在的致死性生理变化。本文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利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制的空白被突出为发现和开发新疗法的机会。

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