|Publication Type||Journal Article|
|Year of Publication||2015|
|Authors||Taft, DH, Ambalavanan, N, Schibler, KR, Yu, Z, Newburg, DS, Deshmukh, H, Ward, DV, Morrow, AL|
|Keywords||Feces, Female, Gastrointestinal Microbiome, Humans, Infant, Infant, Newborn, Infant, Premature, Infant, Premature, Diseases, Male, Sepsis|
OBJECTIVE: Late onset sepsis (LOS) contributes to mortality and morbidity in preterm infants. We tested the hypotheses that microbes causing LOS originate from the gut, and that distortions in the gut microbial community increases subsequent risk of LOS.
STUDY DESIGN: We examined the gut microbial community in prospectively collected stool samples from preterm infants with LOS and an equal number of age-matched controls at two sites (Cincinnati, OH and Birmingham, AL), by sequencing the bacterial 16S rDNA. We confirmed our findings in a subset of infants by whole genome shotgun sequencing, and analyzed the data using R and LEfSe.
RESULTS: Infants with LOS in Cincinnati, as compared to controls, had less abundant Actinobacteria in the first samples after birth (median 18 days before sepsis onset), and less abundant Pseudomonadales in the last samples collected prior to LOS (median 8 days before sepsis onset). Infants with LOS in Birmingham, as compared to controls, had no differences identified in the first sample microbial communities, but Lactobacillales was less abundant in the last samples prior to LOS (median 4 days before sepsis onset). Sequencing identified detectable levels of the sepsis-causative organism in stool samples prior to disease onset for 82% of LOS cases.
CONCLUSIONS: Translocation of gut microbes may account for the majority of LOS cases. Distortions in the fecal microbiota occur prior to LOS, but the form of distortion depends on timing and site. The microbial composition of fecal samples does not predict LOS onset in a generalizable fashion.
|Alternate Journal||PLoS ONE|
|PubMed Central ID||PMC4482142|
|Grant List||U54HG004969 / HG / NHGRI NIH HHS / United States |
HHSN272200900018C / AI / NIAID NIH HHS / United States
R01HD059140 / HD / NICHD NIH HHS / United States
HD27853 / HD / NICHD NIH HHS / United States
T32 ES 10957-11 / ES / NIEHS NIH HHS / United States
P01 HD013021 / HD / NICHD NIH HHS / United States
P30 DK078392 / DK / NIDDK NIH HHS / United States
UG1 HD027853 / HD / NICHD NIH HHS / United States
5UL1RR026314-03 / RR / NCRR NIH HHS / United States
HG005969 / HG / NHGRI NIH HHS / United States
U10 HD027853 / HD / NICHD NIH HHS / United States
K08 HD084686 / HD / NICHD NIH HHS / United States
P01HD13021 / HD / NICHD NIH HHS / United States
HHSN272200900018C / / PHS HHS / United States
R01 HG005969 / HG / NHGRI NIH HHS / United States
U54 HG004969 / HG / NHGRI NIH HHS / United States
R01 HD059140 / HD / NICHD NIH HHS / United States
T32 ES010957 / ES / NIEHS NIH HHS / United States
UL1 RR026314 / RR / NCRR NIH HHS / United States