Editorial commentary: Host-pathogen interactions in Clostridium difficile infection: it takes two to tango.
Editorial commentary: Host-pathogen interactions in Clostridium difficile infection: it takes two to tango.
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编辑评论：艰难梭菌感染中宿主与病原体的相互作用：需要两个人才能探戈。
DOI：
10.1093/cid/ciu141
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Aronoff,DavidM
中科院分区：
文献类型：
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作者：
Aronoff,DavidM
艰难梭菌感染（Clostridium difficile infection，CDI）是21世纪世纪的主要传染病。千禧年的第一个十年见证了CDI的出院诊断大约翻了一番，死亡率增加了近10倍[1]。这种感染对我们的健康和福利造成的负担是巨大的，最近估计，医院发病的CDI每年造成6000多人死亡，30万个额外的住院日，以及不少于8.5亿美元的额外住院费用[2]。2008年的数据显示，美国急性护理机构与CDI相关的额外费用近48亿美元[3]。这一流行病对老年人造成了不成比例的伤害。大约92%的CDI相关死亡发生在65岁或以上的患者中，使CDI成为该人群的第18大死亡原因[4]。此外，在美国，每100 000例≥ 85岁患者中的CDI相关住院年发生率超过所有其他年龄组的总和[5]。CDI作为医院和社区环境中的一个问题的巨大增长激发了人们对识别风险因素的极大兴趣，特别是可改变的风险因素，这些风险因素是传播，疾病严重程度和结果的重要驱动因素。difficile负责新的流行病[6，7]。该菌株将通过用于分型的方法而变得已知：限制性内切核酸酶分析（REA）BI型、北美脉冲场凝胶电泳（NAP）1型或聚合酶链反应（PCR）核糖体型027，以下称为NAP 1菌株。最近的研究完善了我们对疫情的理解，揭示了NAP1毒株的两种不同的流行谱系，而不是以前认为的一种，它们出现在北美并在全球传播[8]。对这种新出现的病原体进行了研究，确定了常见的地方性（历史性）C。艰难梭菌分离株：最显著的是氟喹诺酮耐药性和提示独特毒力特征的特征[6，9]。流行病的初步研究C。艰难梭菌NAP1分离株显示，这些菌株表达二元毒素，不存在于所有致病菌株中，并且在tcdC基因中具有遗传突变，编码2种主要的
Clostridium difficile infection (CDI) has reemerged as a major infectious disease in the 21st Century. The millennium’s first decade witnessed an approximate doubling of hospital discharge diagnoses for CDI and nearly a 10-fold increase in mortality [1]. The burden of this infection on our health and welfare has been significant, with recent estimates that hospital-onset CDI contributes annually to more than 6000 deaths, 300 000 excess hospital-days, and no fewer than $850 million in added hospital costs [2]. Data from 2008 revealed nearly $4.8 billion in added expenses associated with CDI in US acute-care facilities [3]. This epidemic has exacted a disproportionate toll on older adults. Approximately 92% of CDI--related deaths occur in patients aged 65 or older, making CDI the 18th leading cause of death in this population [4]. In addition, in the United States, the annual rate of CDI-related hospitalizations per 100 000 people in patients≥ 85 years of age was noted to exceed that of all other age groups combined [5]. The tremendous growth of CDI as a problem both within hospitals and community settings has motivated significant interest in identifying risk factors, particularly modifiable ones, which are important drivers of transmission, disease severity, and outcome.In the wake of the dramatic rise in the incidence and severity of CDI, investigators soon identified a novel strain of C. difficile responsible for the new epidemic [6, 7]. The strain would become known by the methods used to type it: restriction endonuclease analysis (REA) type BI, North American Pulsed-field Gel Electrophoresis (NAP) type 1, or polymerase chain reaction (PCR) ribotype 027, hereafter referred to as the NAP1 strain. More recent studies have refined our understanding of the outbreak, revealing 2 distinct epidemic lineages of NAP1 strain, not one as previously thought, which emerged in North America and spread globally [8]. Studies to characterize this emergent pathogen identified features absent from usual, endemic (historical) C. difficile isolates: most notably fluoroquinolone resistance and features suggesting unique virulence characteristics [6, 9]. Initial studies of the epidemic C. difficile NAP1 isolates revealed that these strains expressed a binary toxin, not present in all disease-causing strains, and harbored genetic mutations in the tcdC gene, encoding a putative negative regulator of expression of the 2 major