Background: Latent tuberculosis infection (LTBI) treatment is an effective strategy to eliminate TB in low-incidence settings. Shorter LTBI regimens incorporating the antimicrobial class of rifamycins are designed to improve treatment completion rates. Recent evidence suggests that the rifamycins could induce irreversible gut microbiota changes that impact future anti-TB immunity. Methods: To document the immediate effect of the rifamycins on the gut microbiota, we followed six patients with LTBI initiating four months of monotherapy with rifampin (4R; n=4) or three months of rifapentine in combination with isoniazid (3HP; n=2) and tracked recovery to baseline two months posttreatment completion. We collected stool samples parallel to the LTBI group from healthy volunteers (N=6) unexposed to the rifamycins. We used a questionnaire to collect diet, antibiotics, and lifestyle changes during follow-up. We profiled the gut microbiota using 16S rRNA amplicon sequencing (V1-V2 region). Results: Rifamycin exposure resulted in a 4.24% decrease in alpha diversity, compared to a 3.27% decrease in the controls. While the change in alpha diversity was small and not statistically different from changes observed in controls, significant bacterial community dissimilarity correlated with treatment duration (R2 = 0.269, P=0.041) and dose (R2 =0.201, P = 0.001) were observed. This rifamycin-associated dysbiosis was characterized by a depletion of butyrate-producing taxa (Clostridium-XIVa and Roseburia) and expansion of potentially pathogenic taxa within the Firmicutes and Proteobacteria phyla. Recovery of the gut microbial composition was incomplete two months after treatment ended. Conclusion: TB prophylaxis with the rifamycins induced minimal changes in the overall gut microbiota diversity but a significant shift in gut microbial composition. A larger clinical study with a longer follow-up time is necessary to confirm the extent to which the gut microbiota can recover from this rifamycin-induced dysbiosis to inform strategies to mitigate potential LTBI treatment sequelae.
Objective We present 16s rRNA gene sequencing (V1-V2 region) and sample data from a pilot observational cohort study to describe the gut microbiota dynamics of subjects with latent tuberculosis infection (LTBI) treated with daily 600 mg rifampicin for four months (4R) or a weekly dose of 900 mg combination of rifapentine and isoniazid for three months (3HP). Our objectives were to (1) document changes to the gut microbiota immediately following exposure to the rifamycins and (2) document recovery to baseline two months after treatment completion. Data description We enrolled six subjects with subjects with LTBI and prospectively followed them for 5–6 months. Each subject provided stool samples before, during, and two months after treatment. Six healthy controls were sampled in parallel with the patients with LTBIs. We report amplicon sequence variants (ASVs) and taxonomic assignments for 60 stool samples. Additionally, we provide access to the raw amplicon sequences, and subject responses to questionnaires about their diet, medication, and lifestyle changes over the study follow-up period. Furthermore, we provide the concentration of the parent and partially active rifamycin metabolite concentrations measured validated LC-MS-MS assays of phosphate buffer washes of the stool samples collected from the LTBI participants. This comprehensive dataset is a valuable resource for future systematic reviews and meta-analyses of the impact of LTBI therapy on the gut microbiota.
Objective: We present 16s rRNA gene sequencing (V1-V2 region) and sample data from a pilot observational cohort study to describe the gut microbiota dynamics in patients with latent tuberculosis infection (LTBI) treated with a three to four-month course of a rifamycin-based regimen. Our objectives were to (1) document changes to the gut microbiota following exposure to the rifamycins and (2) document recovery to baseline two months after treatment completion. Data description: Six LTBI patients were followed for 5 – 6 months. Each patient provided stool samples before, during, and two months after treatment. Six healthy controls were sampled in parallel with the LTBI patients. We report amplicon sequence variants (ASVs) and taxonomic assignments for 60 stool samples. Also provided are the raw amplicon sequences, and data on diet, medication, and lifestyle changes over the follow-up period. Additionally, phosphate buffer washes of the stool samples from the LTBI participants were analyzed by validated LC-MS-MS assay to measure concentrations of the parent and partially active metabolite rifamycins. These data could be useful for future systematic reviews and meta-analyses on the impact of LTBI therapy on the gut microbiota.
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