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优化肠道定植抗力以抵御艰难梭菌感染。

Optimising gut colonisation resistance against Clostridium difficile infection.

作者信息

Yuille S, Mackay W G, Morrison D J, Tedford M C

机构信息

School of Science, University of the West of Scotland, Hamilton Campus, Almada Street, Hamilton, ML3 0JB, UK.

School of Science, University of the West of Scotland, Paisley Campus, Paisley, PA1 2BE, UK.

出版信息

Eur J Clin Microbiol Infect Dis. 2015 Nov;34(11):2161-6. doi: 10.1007/s10096-015-2479-6. Epub 2015 Sep 9.

Abstract

Clostridium difficile is the dominant cause of pseudomembranous colitis in nosocomial environments. C. difficile infection (CDI) generally affects elderly (≥65 years of age) hospital inpatients who have received broad-spectrum antimicrobial treatment. CDI has a 30 % risk of re-infection and a subsequent 60 % risk of relapse thereafter, leading to a high economic burden of over 7 billion pounds sterling and over 900,000 cases in the USA and Europe per annum. With the long-term consequences of faecal transplantation currently unknown, and limited spectrum of effective antibiotics, there is an urgent requirement for alternative means of preventing and treating CDI in high-risk individuals. Metagenomics has recently improved our understanding of the colonisation resistance barrier and how this could be optimised. pH, oxidation-reduction potentials and short-chain fatty acids have been suggested to inhibit C. difficile growth and toxin production in in vitro and in vivo studies. This review aims to pull together the evidence in support of a colonisation resistance barrier against CDI.

摘要

艰难梭菌是医院环境中伪膜性结肠炎的主要病因。艰难梭菌感染(CDI)通常影响接受过广谱抗菌治疗的老年(≥65岁)住院患者。CDI有30%的再感染风险,此后还有60%的复发风险,导致每年在美国和欧洲造成超过70亿英镑的高额经济负担以及超过90万例病例。由于粪便移植的长期后果目前尚不清楚,且有效抗生素的范围有限,因此迫切需要有其他方法来预防和治疗高危个体的CDI。宏基因组学最近增进了我们对定植抗性屏障以及如何对其进行优化的理解。在体外和体内研究中,已表明pH值、氧化还原电位和短链脂肪酸可抑制艰难梭菌的生长和毒素产生。本综述旨在汇总支持针对CDI的定植抗性屏障的证据。

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