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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EAltered intestinal microbiota in critically ill patients leads to increased pathogens and infections, which may be improved with synbiotic therapy. Stress, antibiotics, and parenteral therapy have been linked to gut dysbiosis. Fecal microbiota transplantation is a promising treatment for \u003Cem\u003EClostridium difficile\u003C\/em\u003E infection and may work by altering bile acid composition.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003Egut dysbiosis\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eparenteral therapy\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eenteral feeding\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Efecal microbiota transplantation\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003E\n               \u003Cem\u003EClostridium difficile\u003C\/em\u003E\n            \u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eshort-chain fatty acids\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Eepithelial barrier\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Einflammation\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Egut microbiota\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \n         \u003Cp id=\u0022p-2\u0022\u003EThe importance of the gut microbiota to health has been increasingly recognized as studies reveal the complex microbiota\u2013host interactions taking place in the gastrointestinal (GI) tract. Gail A. Cresci, PhD, Cleveland Clinic, Cleveland, Ohio, USA, discussed the role of gut dysbiosis and its consequences in critically ill patients.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EMany internal and external forces influence the gut microbiota. When a healthful diet including fermentable carbohydrate is ingested, gut bacteria produce short-chain fatty acids and other beneficial molecules. When crosstalk between the microbiota and the host breaks down, dysbiosis (microbial imbalance in the GI tract) and its clinical consequences can develop. Among factors that can alter the gut microbiota are host genetics, early colonization patterns, diet, stress, antibiotics, and other drugs.\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003ECritically ill patients in the intensive care unit are often treated with antibiotics, artificial nutrition, opioids, and other substances that alter the intestinal environment. In such circumstances, the gut microbiota must compete for limited resources and survive in harsh conditions. Antibiotic effects on the microbiota include reduced total bacteria, changes in microbial composition, depleted lactobacilli, and impaired immune defenses [Willing BP et al. \u003Cem\u003ENat Rev Microbiol\u003C\/em\u003E. 2011]. \u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E summarizes studies of gut microbiota alterations in critically ill patients, which demonstrate increased pathologic bacteria, virulence, and antibiotic resistance. These changes are associated with increased epithelial permeability, cell apoptosis, and altered mucus production, which are linked with multiple-organ dysfunction [Mittal R, Coopersmith CM. \u003Cem\u003ETrends Mol Med\u003C\/em\u003E. 2014].\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/16122\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/16122\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/16122\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-5\u0022 class=\u0022first-child\u0022\u003EStudies of Gut Microbiota Alterations in Critically Ill Patients\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EMultiple studies have demonstrated some benefit with therapies using probiotics, prebiotics, or synbiotics for treating gut dysbiosis in critically ill patients, particularly with respect to reducing the occurrence of ventilator-associated pneumonia and other infectious complications [Shimizu K et al. \u003Cem\u003EDig Dis Sci\u003C\/em\u003E. 2013]. However, the studies have used different strains, concentrations, and delivery methods. Large studies with stringent inclusion and exclusion criteria are needed to determine the optimal strains for targeting depleted gut bacteria.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EDaniel H. Teitelbaum, MD, University of Michigan, Ann Arbor, Michigan, USA, discussed the intestinal mucosal changes associated with parenteral nutrition (PN) that create an environment conducive to a shift in the gut microbiota and its translocation into the host. Dr Teitelbaum\u2019s laboratory has shown, using a mice model, that mice receiving PN have significantly increased bacterial translocation and sepsis rates associated with loss of mucosal barrier function, villus atrophy, and gut-associated lymphoid tissue aberrations (\u003Cem\u003EP\u003C\/em\u003E\u2009\u0026lt;\u2009.01) [Sun X et al. \u003Cem\u003EJPEN J Parenter Enteral Nutr\u003C\/em\u003E. 2006].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EAccording to Dr Teitelbaum, bacterial classification by pyrosequencing found decreased Firmicutes and expansion of Proteobacteria and Bacteroidetes in the colon and small bowel of a PN mouse model compared with control mice. At the genus level, expansion of \u003Cem\u003ESalmonella, Shigella, Proteus\u003C\/em\u003E, and several Gram-negative organisms has been observed, as well as reduction of potentially beneficial bacteria [Miyasaka EA et al. \u003Cem\u003EJ Immunol\u003C\/em\u003E. 2013]. The interface between the host and gut flora is critical and is mediated by toll-like receptors (TLRs) on epithelial cells and immunocytes [Fukata M, Abreu MT. \u003Cem\u003EBiochem Soc Trans\u003C\/em\u003E. 2007]. Marked upregulation of TLRs with PN activates a signaling pathway that leads to a marked upregulation of proinflammatory cytokines [Akira S, Takeda K. \u003Cem\u003ENat Rev Immunol\u003C\/em\u003E. 2004].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EDr Teitelbaum hypothesized that intestinal bacterial changes are a contributory factor to the mucosal inflammation observed in the small bowel with PN therapy. He tested this hypothesis in germ-free, enterally fed, and PN-fed mice and found decreased epithelial barrier function, increased inflammatory cytokines, and decreased T-regulatory cells in the PN mice versus the other groups. Based on these results, a study was conducted in clinical patients undergoing small bowel resection to determine if similar changes occur in humans [Ralls MW et al. \u003Cem\u003EJPEN J Parenter Enteral Nutr.\u003C\/em\u003E 2014]. Samples were obtained from the mid\u2013small bowel to the terminal ileum. Samples were considered unfed if the patient was without oral nutrition for \u0026gt;\u200914 days. Bacterial pyrosequencing revealed a difference in bacterial composition between the fed and unfed groups. Transepithelial resistance on samples from fed and unfed infants and adolescents found a significant decline in epithelial barrier function in the unfed patients (\u003Cem\u003EP\u003C\/em\u003E\u2009\u0026lt;\u2009.05; \u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Ralls MW et al. \u003Cem\u003ESurgery.\u003C\/em\u003E 2015].\u003C\/p\u003E\n         \u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/3\/16\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Transepithelial Resistance: Decreased Epithelial Barrier Function in Unfed Patients*P\u0026#x2009;\u0026amp;lt;\u0026#x2009;.05 by t test.Unfed, no oral nutrition for \u0026amp;gt;\u0026#x2009;14 d.Adapted from Surgery, Ralls MW et al. Enteral nutrient deprivation in patient leads to a loss of intestinal epithelial barrier function, Copyright 2015, with permission from Elsevier.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-2096964182\u0022 data-figure-caption=\u0022\u0026amp;lt;div xmlns=\u0026amp;quot;http:\/\/www.w3.org\/1999\/xhtml\u0026amp;quot;\u0026amp;gt;Transepithelial Resistance: Decreased Epithelial Barrier Function in Unfed Patients*\u0026amp;lt;em\u0026amp;gt;P\u0026amp;lt;\/em\u0026amp;gt;\u0026#x2009;\u0026amp;amp;lt;\u0026#x2009;.05 by t test.Unfed, no oral nutrition for \u0026amp;amp;gt;\u0026#x2009;14 d.Adapted from \u0026amp;lt;em\u0026amp;gt;Surgery\u0026amp;lt;\/em\u0026amp;gt;, Ralls MW et al. Enteral nutrient deprivation in patient leads to a loss of intestinal epithelial barrier function, Copyright 2015, with permission from Elsevier.\u0026amp;lt;\/div\u0026amp;gt;\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/3\/16\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/3\/16\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/15\/3\/16\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/16121\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-11\u0022 class=\u0022first-child\u0022\u003ETransepithelial Resistance: Decreased Epithelial Barrier Function in Unfed Patients\u003C\/p\u003E\n               \u003Cp id=\u0022p-12\u0022\u003E*\u003Cem\u003EP\u003C\/em\u003E\u2009\u0026lt;\u2009.05 by t test.\u003C\/p\u003E\n               \u003Cp id=\u0022p-13\u0022\u003EUnfed, no oral nutrition for \u0026gt;\u200914 d.\u003C\/p\u003E\n               \u003Cp id=\u0022p-14\u0022\u003EAdapted from \u003Cem\u003ESurgery\u003C\/em\u003E, Ralls MW et al. Enteral nutrient deprivation in patient leads to a loss of intestinal epithelial barrier function, Copyright 2015, with permission from Elsevier.\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EDr Teitelbaum concluded that the same changes in bacterial composition, epithelial barrier function, and inflammation that were observed in mice also occur in humans. These studies show that the microbiome plays an important role in the adverse effects of PN.\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003ETreatment with antibiotics, which alters gut microbiota, is a major risk factor for \u003Cem\u003EClostridium difficile\u003C\/em\u003E infection (CDI), a severe, fulminant, and often recurrent disease that is an important cause of infectious disease death in the United States. Michael J. Sadowsky, PhD, University of Minnesota, St Paul, Minnesota, USA, described fecal microbiota transplantation (FMT) for recurrent CDI.\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EIn the past, fresh fecal slurries were used for FMT [Hamilton MJ et al. \u003Cem\u003EGut Microbes\u003C\/em\u003E. 2013]. Current methods use purified, standardized, frozen fecal microbiota preparations made by selective sieving, filtration, and differential centrifugation to obtain a highly pure microbe preparation. According to Dr Sadowsky, the University of Minnesota has established an FMT program with a rigorously screened donor volunteer program and frozen fecal microbe banking. High-throughput 16S amplicon sequencing has demonstrated that before FMT, CDI patient samples are dominated by Proteobacteria [Hamilton MJ et al. \u003Cem\u003EGut Microbes\u003C\/em\u003E. 2013]. Donor samples and patient samples taken after engraftment are dominated by Bacteroidetes and Firmicutes.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EThe success rate for CDI cure is 91% with the first FMT engraftment and 98% with 2 FMTs [Brandt L et al. \u003Cem\u003EAm J Gastroenterol.\u003C\/em\u003E 2012]. A direct correlation between engraftment and the presence of secondary bile acids has been observed. Whereas primary bile acids promote \u003Cem\u003EC. difficile\u003C\/em\u003E spore germination, secondary bile acids, which are produced by gut bacteria, inhibit spore germination and growth. A study to determine fecal bile acid composition before and after FMT in patients (n\u2009=\u200912) with recurrent CDI sequenced bacterial 16S rRNA genes and measured fecal bile acids [Weingarden AR et al. \u003Cem\u003EAm J Physiol Gastrointest Liver Physiol\u003C\/em\u003E. 2014]. Eleven of the patients recovered fully after 1 FMT. Fecal primary bile acids decreased and secondary bile acids increased after FMT.\u003C\/p\u003E\n         \u003Cp id=\u0022p-19\u0022\u003EThese investigations show that FMT is an alternative option to colectomy for some severe CDI cases. Two FMT procedures are recommended for severe CDI: one to stabilize the patient and one to ensure engraftment. Engraftment results in patient recovery and changes in bile acids. The changes in fecal bile acid composition may be a mechanism of FMT. Formal clinical trials of FMT are planned for the future.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2015 SAGE Publications\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/15\/3\/16.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzlrhe\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzlrhe\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzlrhe\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}