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Gut microbial succession follows acute secretory diarrhea in humans.

David LA, Weil A, Ryan ET, Calderwood SB, Harris JB, Chowdhury F, Begum Y, Qadri F, LaRocque RC, Turnbaugh PJ - MBio (2015)

Bottom Line: Gut bacteria may affect this recovery, but it remains incompletely understood how resident microbes in the digestive tract respond to diarrheal illness.Genomic analyses associated the succession with bacterial dispersal in food, an altered microbial environment, and changing phage levels.Our findings suggest that it may one day be feasible to manage resident bacterial populations in the gut after infectious diarrhea.

View Article: PubMed Central - PubMed

Affiliation: Society of Fellows, Harvard University, Cambridge, Massachusetts, USA FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts, USA.

No MeSH data available.


Related in: MedlinePlus

Gut microbial succession in the weeks following V. cholerae infection. (A) Abundance of gut bacteria from the two cohorts over time. To simplify analysis, bacterial OTUs were collapsed at the genus level. Highly correlated genera were further grouped and named according to their dynamics. Cholera patients are shown at 0 dpp (cohort 2; labeled by subject ID) or from 1 dpp onwards (cohort 1; labeled by household ID). Microbiota from healthy household contacts in cohort 1 are shown in the healthy contacts group and distinguished by numbers following their household IDs; these samples were collected at the same time as patient 1-dpp samples. Absent samples are labeled with an X. The percentages of 16S rRNA reads associated with V. cholerae among subjects at 0 dpp are shown in boxes (median, 25%). (B) Median group abundances across subjects. Abundance values are also shown next to the bars. Significant differences relative to controls are labeled with an asterisk (P < 0.05; two-sided Mann-Whitney U test). (C) Microbial gene abundances, grouped using the COG hierarchy of functions (82). Gene levels are shown relative to median values in healthy subjects and are organized by subject (columns) and COG category (rows). Red boxes indicate gene functions enriched in subjects, relative to healthy controls, while blue boxes denote gene functions that are rarer. Categories labeled with asterisks to the right of a given recovery stage have significantly different abundances at that stage compared to controls (q < 0.05, Mann-Whitney U test). Rare COG categories (median fractional abundance, <0.0001 in healthy controls) are not shown here but are provided in Table S4 in the supplemental material, along with median COG abundances and full COG category names.
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fig2: Gut microbial succession in the weeks following V. cholerae infection. (A) Abundance of gut bacteria from the two cohorts over time. To simplify analysis, bacterial OTUs were collapsed at the genus level. Highly correlated genera were further grouped and named according to their dynamics. Cholera patients are shown at 0 dpp (cohort 2; labeled by subject ID) or from 1 dpp onwards (cohort 1; labeled by household ID). Microbiota from healthy household contacts in cohort 1 are shown in the healthy contacts group and distinguished by numbers following their household IDs; these samples were collected at the same time as patient 1-dpp samples. Absent samples are labeled with an X. The percentages of 16S rRNA reads associated with V. cholerae among subjects at 0 dpp are shown in boxes (median, 25%). (B) Median group abundances across subjects. Abundance values are also shown next to the bars. Significant differences relative to controls are labeled with an asterisk (P < 0.05; two-sided Mann-Whitney U test). (C) Microbial gene abundances, grouped using the COG hierarchy of functions (82). Gene levels are shown relative to median values in healthy subjects and are organized by subject (columns) and COG category (rows). Red boxes indicate gene functions enriched in subjects, relative to healthy controls, while blue boxes denote gene functions that are rarer. Categories labeled with asterisks to the right of a given recovery stage have significantly different abundances at that stage compared to controls (q < 0.05, Mann-Whitney U test). Rare COG categories (median fractional abundance, <0.0001 in healthy controls) are not shown here but are provided in Table S4 in the supplemental material, along with median COG abundances and full COG category names.

Mentions: To further visualize the dynamics of specific microbial taxa following cholera, we grouped bacteria at the genus level and then clustered genera exhibiting similar temporal patterns (see Materials and Methods). This technique reduced the number of variables to plot while still preserving taxonomic information (25). Our clustering yielded 5 major groups of bacteria (defined as accounting for more than 10% of subjects’ 16S rRNA reads for at least one sampling point [see Table S3 in the supplemental material]). These groups accounted for a median of 65.8% of 16S sequences from each sample (minimum, 19.7%; maximum, 97.1%). Groups exhibited unique temporal patterns, which we used to assign each group a name (Fig. 2A and B). The Infection-Stage group appeared only at 0 dpp; the Early-Stage group bloomed at 0 to 7 dpp but receded by the last time point; the Mid-Stage group appeared at only 7 dpp; the Late-Stage group dominated guts of healthy household contacts and the microbiota of recovering cholera patients at 30 dpp; and, the All-Swab group was only observed in rectal swab samples (i.e., absent from 0- and 1-dpp patient samples, which were whole stool samples). At 30 dpp, significant differences in group abundances relative to healthy household contacts were not observed.


Gut microbial succession follows acute secretory diarrhea in humans.

David LA, Weil A, Ryan ET, Calderwood SB, Harris JB, Chowdhury F, Begum Y, Qadri F, LaRocque RC, Turnbaugh PJ - MBio (2015)

Gut microbial succession in the weeks following V. cholerae infection. (A) Abundance of gut bacteria from the two cohorts over time. To simplify analysis, bacterial OTUs were collapsed at the genus level. Highly correlated genera were further grouped and named according to their dynamics. Cholera patients are shown at 0 dpp (cohort 2; labeled by subject ID) or from 1 dpp onwards (cohort 1; labeled by household ID). Microbiota from healthy household contacts in cohort 1 are shown in the healthy contacts group and distinguished by numbers following their household IDs; these samples were collected at the same time as patient 1-dpp samples. Absent samples are labeled with an X. The percentages of 16S rRNA reads associated with V. cholerae among subjects at 0 dpp are shown in boxes (median, 25%). (B) Median group abundances across subjects. Abundance values are also shown next to the bars. Significant differences relative to controls are labeled with an asterisk (P < 0.05; two-sided Mann-Whitney U test). (C) Microbial gene abundances, grouped using the COG hierarchy of functions (82). Gene levels are shown relative to median values in healthy subjects and are organized by subject (columns) and COG category (rows). Red boxes indicate gene functions enriched in subjects, relative to healthy controls, while blue boxes denote gene functions that are rarer. Categories labeled with asterisks to the right of a given recovery stage have significantly different abundances at that stage compared to controls (q < 0.05, Mann-Whitney U test). Rare COG categories (median fractional abundance, <0.0001 in healthy controls) are not shown here but are provided in Table S4 in the supplemental material, along with median COG abundances and full COG category names.
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Related In: Results  -  Collection

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fig2: Gut microbial succession in the weeks following V. cholerae infection. (A) Abundance of gut bacteria from the two cohorts over time. To simplify analysis, bacterial OTUs were collapsed at the genus level. Highly correlated genera were further grouped and named according to their dynamics. Cholera patients are shown at 0 dpp (cohort 2; labeled by subject ID) or from 1 dpp onwards (cohort 1; labeled by household ID). Microbiota from healthy household contacts in cohort 1 are shown in the healthy contacts group and distinguished by numbers following their household IDs; these samples were collected at the same time as patient 1-dpp samples. Absent samples are labeled with an X. The percentages of 16S rRNA reads associated with V. cholerae among subjects at 0 dpp are shown in boxes (median, 25%). (B) Median group abundances across subjects. Abundance values are also shown next to the bars. Significant differences relative to controls are labeled with an asterisk (P < 0.05; two-sided Mann-Whitney U test). (C) Microbial gene abundances, grouped using the COG hierarchy of functions (82). Gene levels are shown relative to median values in healthy subjects and are organized by subject (columns) and COG category (rows). Red boxes indicate gene functions enriched in subjects, relative to healthy controls, while blue boxes denote gene functions that are rarer. Categories labeled with asterisks to the right of a given recovery stage have significantly different abundances at that stage compared to controls (q < 0.05, Mann-Whitney U test). Rare COG categories (median fractional abundance, <0.0001 in healthy controls) are not shown here but are provided in Table S4 in the supplemental material, along with median COG abundances and full COG category names.
Mentions: To further visualize the dynamics of specific microbial taxa following cholera, we grouped bacteria at the genus level and then clustered genera exhibiting similar temporal patterns (see Materials and Methods). This technique reduced the number of variables to plot while still preserving taxonomic information (25). Our clustering yielded 5 major groups of bacteria (defined as accounting for more than 10% of subjects’ 16S rRNA reads for at least one sampling point [see Table S3 in the supplemental material]). These groups accounted for a median of 65.8% of 16S sequences from each sample (minimum, 19.7%; maximum, 97.1%). Groups exhibited unique temporal patterns, which we used to assign each group a name (Fig. 2A and B). The Infection-Stage group appeared only at 0 dpp; the Early-Stage group bloomed at 0 to 7 dpp but receded by the last time point; the Mid-Stage group appeared at only 7 dpp; the Late-Stage group dominated guts of healthy household contacts and the microbiota of recovering cholera patients at 30 dpp; and, the All-Swab group was only observed in rectal swab samples (i.e., absent from 0- and 1-dpp patient samples, which were whole stool samples). At 30 dpp, significant differences in group abundances relative to healthy household contacts were not observed.

Bottom Line: Gut bacteria may affect this recovery, but it remains incompletely understood how resident microbes in the digestive tract respond to diarrheal illness.Genomic analyses associated the succession with bacterial dispersal in food, an altered microbial environment, and changing phage levels.Our findings suggest that it may one day be feasible to manage resident bacterial populations in the gut after infectious diarrhea.

View Article: PubMed Central - PubMed

Affiliation: Society of Fellows, Harvard University, Cambridge, Massachusetts, USA FAS Center for Systems Biology, Harvard University, Cambridge, Massachusetts, USA.

No MeSH data available.


Related in: MedlinePlus