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Updated: Feb 18, 2026

Guided Protocol for Fecal Microbial Characterization by 16S rRNA-Amplicon Sequencing
Published on: March 19, 2018
Intestinal Microbiota Composition in Sudden Infant Death Syndrome and Age-Matched Controls
Lex E X Leong1, Steven L Taylor1, Aravind Shivasami1
1South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia; South Australian Health and Medical Research Institute, Microbiome Research Laboratory, School of Medicine, Flinders University, Adelaide, South Australia, Australia.
Objective:
To assess whether features of the infant intestinal microbiome, including the carriage of toxigenic bacteria, are associated with sudden infant death syndrome (SIDS).
Study Design:
We undertook a case-controlled analysis of fecal microbiology in SIDS. Fecal material was obtained from 44 cases and 44 aged-matched controls. Microbiota composition was determined by 16S ribosomal RNA gene amplicon sequencing and comparisons between cases and controls made based on both bacterial alpha diversity measures and unconstrained ordination. Specific quantitative polymerase chain reaction assays were used to determine intestinal carriage of Staphylococcus aureus, toxigenic Clostridium difficile, and pathogenic and nonpathogenic Escherichia coli.
Results:
The microbial composition for the study population as a whole was consistent with previous studies of infants <12 months of age, with a correlation between alpha diversity and age (r2 = 0.08; P = .007). However, no difference was observed in alpha diversity between SIDS cases and controls (P > .4). Nonmetric multidimensional scaling also revealed no evidence of differences in microbiota dispersal between SIDS cases and controls (P = .4, permutational multivariate ANOVA test; Pseudo-F = 0.9), nor was a difference observed in microbiota dispersion (P = .19, PERMDISP test; F = 1.9). There were no significant intergroup differences in the carriage of S aureus, toxigenic C difficile, total E coli, or pathogenic E coli.
Conclusions:
We found no evidence of an association between altered intestinal microbiology and SIDS, or to support the development of strategies to reduce the incidence of SIDS that target intestinal microbiology.
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