Optimising gut colonisation resistance against Clostridium difficile infection

S. Yuille, W. G. Mackay, D. J. Morrison, Kate Tedford

Research output: Contribution to journalArticle

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.
Original languageEnglish
Pages (from-to)2161-2166
Number of pages6
JournalEuropean Journal of Clinical Microbiology & Infectious Diseases
Volume34
Issue number11
DOIs
Publication statusPublished - Nov 2015

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Clostridium Infections
Clostridium difficile
Pseudomembranous Enterocolitis
Metagenomics
Volatile Fatty Acids
Oxidation-Reduction
Inpatients
Economics
Anti-Bacterial Agents
Recurrence
Growth
Infection

Cite this

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title = "Optimising gut colonisation resistance against Clostridium difficile infection",
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.",
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Optimising gut colonisation resistance against Clostridium difficile infection. / Yuille, S.; Mackay, W. G.; Morrison, D. J.; Tedford, Kate.

In: European Journal of Clinical Microbiology & Infectious Diseases, Vol. 34, No. 11, 11.2015, p. 2161-2166.

Research output: Contribution to journalArticle

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AB - 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.

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