title: Environmental Enteric Dysfunction and the Fecal Microbiota in Malawian Children.
abstract: Environmental enteric dysfunction (EED) is often measured with a dual sugar absorption test and implicated as a causative factor in childhood stunting. Disturbances in the gut microbiota are hypothesized to be a mechanism by which EED is exacerbated, although this supposition lacks support. We performed 16S ribosomal RNA gene sequencing of fecal samples from 81 rural Malawian children with varying degrees of EED to determine which bacterial taxa were associated with EED. At the phyla level, Proteobacteria abundance is reduced with severe EED. Among bacterial genera,Megasphaera,Mitsuokella, andSutterellawere higher in EED andSuccinivibrio,Klebsiella, andClostridium_XIwere lower in EED. Bacterial diversity did not vary with the extent of EED. Though EED is a condition that is typically believed to affect the proximal small bowel, and our focus was on stool, our data do suggest that there are intraluminal microbial differences that reflect, or plausibly lead to, EED.
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: M Isabel
authors.initials: MI
authors.lastname: Ordiz
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: Kevin
authors.initials: K
authors.lastname: Stephenson
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: Sophia
authors.initials: S
authors.lastname: Agapova
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.|The McDonnell Genome Institute, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: Kristine M
authors.initials: KM
authors.lastname: Wylie
authors.affiliation: Department of Community Health, College of Medicine, University of Malawi, Malawi, Africa.
authors.forename: Ken
authors.initials: K
authors.lastname: Maleta
authors.affiliation: The McDonnell Genome Institute, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: John
authors.initials: J
authors.lastname: Martin
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.|College of Medicine, University of Malawi, Malawi, Africa.
authors.forename: Indi
authors.initials: I
authors.lastname: Trehan
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri.
authors.forename: Phillip I
authors.initials: PI
authors.lastname: Tarr
authors.affiliation: Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri. manary@kids.wustl.edu.|School of Public Health and Family Medicine, University of Malawi, Blantyre, Malawi.|United States Department of Agriculture/Agricultural Research Service Childrens Nutrition Research Center, Houston, Texas.
authors.forename: Mark J
authors.initials: MJ
authors.lastname: Manary
mesh_terms: D002657:Child Development; D002675:Child, Preschool; D004781:Environmental Exposure; D005243:Feces / Q000382:microbiology*; D005260:Female; D000069196:Gastrointestinal Microbiome / Q000235:genetics*; D006130:Growth Disorders / Q000175:diagnosis* / Q000382:microbiology* / Q000503:physiopathology; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008295:Malawi; D008297:Male; D020560:Proteobacteria / Q000235:genetics* / Q000302:isolation & purification*; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012424:Rural Population
chemical_list: D012336:RNA, Ribosomal, 16S