Delineating the Epidemiology-Host-Microbe Relationship for Methicillin-Resistant Staphylococcus aureus Infection.
Delineating the Epidemiology-Host-Microbe Relationship for Methicillin-Resistant Staphylococcus aureus Infection.
复制标题
描述耐甲氧西林金黄色葡萄球菌感染的流行病学-宿主-微生物关系。
DOI：
10.1093/infdis/jiu555
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Hayden,MaryK
中科院分区：
文献类型：
--
作者：
Popovich,KyleJ;Hayden,MaryK
耐甲氧西林金黄色葡萄球菌(MRSA)是医院感染的主要原因，并与延长住院时间、发病率和死亡率有关[1]。在过去15年中，耐甲氧西林金黄色葡萄球菌(MRSA)已成为医疗保健环境外感染的重要原因，现在社区环境中观察到由所谓的社区相关MRSA(CA-MRSA)引起的感染[2，3]。CA-MRSA引起的感染最初与传统的医院获得的MRSA菌株不同，因为它们甚至在年轻的、以前健康的人中也会引起疾病[2]。长期以来，MRSA菌株一直被认为表达各种毒素和毒力因子，这些毒素和毒力因子被认为是导致与MRSA感染相关的高发病率和死亡率的原因[4]。随着CA-MRSA的出现，出现了其他问题，即哪些微生物因素可能是导致严重疾病的最重要的因素[5]，特别是考虑到在疫情早期报告的暴发性表现[6-8]。通过脉冲场凝胶电泳法测定，美国最常见的CA-MRSA菌株是克隆复合体8(CC8)的成员USA300[9]。USA300通常携带SCCmecIV，并经常表达潘顿-瓦伦丁杀白素(PVL)，这是一种被一些人提议导致毒力增加的细胞毒素[10]。在医院环境中，属于克隆复合体5(CC5)的USA100传统上一直是最流行的MRSA菌株；感染USA100在很大程度上会影响有重大共病和既往医疗保健暴露的个人[11]。然而，随着CA-MRSA的出现，MRSA的流行病学发生了变化。除了来自社区的广泛报告[3]，USA300还被报告为美国医院感染的一个原因[12]。虽然USA300 MRSA最常见的临床表现是皮肤和软组织感染[13]，但也有严重感染，如坏死性肺炎[14]、坏死性筋膜炎[6]和压倒性败血症[7]。这些严重的USA300 MRSA感染通常发生在不同于传统医院获得的MRSA菌株影响的人群中，导致了对USA300 MRSA菌株是否增加了毒力因素的研究。虽然一项研究发现，由USA300菌株类型引起的侵袭性社区肺炎病例更有可能出现早期并发症[15]，但几项研究表明，与非USA300菌株相比，USA300菌株类型与更高的死亡率无关[16]。目前尚不清楚为什么某些人会因MRSA而发生压倒性感染，以及哪些宿主或微生物因素可能对此负责。Calderwood等人最近的一项研究[17]使用基因组测序来识别葡萄球菌因素，这些因素预测了在MRSA定植的个人中血液感染的发展。在分析中控制了各种宿主因素后，作者观察到MRSA在携带葡萄球菌肠毒素P(SEP)基因的菌株上定植与随后MRSA感染的发生显著相关。作者[17]和随附的一篇社论[18]指出了将宿主因素纳入毒力因素分析的重要性，并建议这一领域的未来工作应着眼于这些因素的综合影响，以优化谁将患上最严重疾病的预测模型。
(MRSA) is a major cause of nosocomial infections and is associated with prolonged length of hospitalization, morbidity, and mortality [1]. Over the past 15 years, MRSA has emerged as an important cause of infection outside of healthcare settings, with infections due to so-called community-associated MRSA (CA-MRSA) now observed in community settings [2, 3]. Infections due to CA-MRSA were initially distinct from those due to traditional hospital-acquired MRSA strains in that they were noted to cause disease even in young, previously healthy individuals [2]. MRSA strains have long been recognized to express a variety of toxins and virulence factors that are felt to contribute to the high morbidity and mortality associated with MRSA infection [4]. With the emergence of CA-MRSA, additional questions have arisen as to which microbial factors may be most important for causing severe disease [5], especially given the fulminant manifestations that were reported early in the epidemic [6–8]. The most common CA-MRSA strain in the United States, as determined by pulsed-field gel electrophoresis, is USA300 [9], a member of clonal complex 8 (CC8). USA300 typically carries SCCmecIV and often expresses Panton-Valentine leukocidin (PVL), a cytotoxin that has been proposed by some to lead to increased virulence [10]. In hospital settings, USA100, which belongs to clonal complex 5 (CC5), has traditionally been the most prevalent MRSA strain; infections with USA100 largely affect individuals with significant comorbidities and prior healthcare exposures [11]. However, the epidemiology of MRSA has changed with the emergence of CA-MRSA. In addition to widespread reports from community settings [3], USA300 has been reported as a cause of nosocomial infections in the United States [12]. Although the most common clinical manifestation of USA300 MRSA is skin and soft-tissue infection [13], severe infections such as necrotizing pneumonia [14], necrotizing fasciitis [6], and overwhelming sepsis [7] have also been seen. These severe USA300 MRSA infections, which often occur in populations distinct from those affected by traditional hospital-acquired MRSA strains, led to research into whether USA300 MRSA strains have added virulence factors. While one study observed that cases of invasive community-onset pneumonia due to the USA300 strain type were more likely to have early onset complications [15], several studies have demonstrated that the USA300 strain type is not associated with a higher mortality rate than non-USA300 strains [16]. It remains unclear why certain individuals develop overwhelming infection due to MRSA and which host or microbial factors may be responsible. A recent study by Calderwood et al [17] used genome sequencing to identify staphylococcal factors that predicted the development of bloodstream infection in individuals who were colonized with MRSA. After controlling for various host factors in their analysis, the authors observed that MRSA colonization with a strain carrying the staphylococcal enterotoxin P (sep) gene was significantly associated with development of a subsequent MRSA infection. The authors [17] and an accompanying editorial [18] noted the importance of incorporating host factors into an analysis of virulence factors and suggested that future work in this field should look at the combined effects of these factors to optimize prediction models for who will develop the most severe disease.