Prolonged delays in human microbiota transmission after a controlled antibiotic perturbation

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Humans constantly encounter new microbes, but few become long-term residents of the adult gut microbiome. Classical theories predict that colonization is determined by the availability of open niches, but it remains unclear whether other ecological barriers limit commensal colonization in natural settings. To disentangle these effects, we used a controlled perturbation with the antibiotic ciprofloxacin to investigate the dynamics of gut microbiome transmission in 22 households of healthy, cohabiting adults. Colonization was rare in three-quarters of antibiotic-taking subjects, whose resident strains rapidly recovered in the week after antibiotics ended. In contrast, the remaining antibiotic-taking subjects exhibited lasting responses, with extensive species losses and transient expansions of potential opportunistic pathogens. These subjects experienced elevated rates of commensal colonization, but only after long delays: many new colonizers underwent sudden, correlated expansions months after the antibiotic perturbation. Furthermore, strains that had previously transmitted between cohabiting partners rarely recolonized after antibiotic disruptions, showing that colonization displays substantial historical contingency. This work demonstrates that there remain substantial ecological barriers to colonization even after major microbiome disruptions, suggesting that dispersal interactions and priority effects limit the pace of community change.

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  1. tive abundance of ∼60% by day 64, which it maintained throughout the >1.5 years of follow-up sampling

    this is cool. Have you done any investigation of this specific strain's genome to see what makes it such a strong colonizer? Did this subject report any changes to their health following this shift?

  2. ese disrupted species exhibited much lower rates of recovery in subjects with lasting responses:

    Do you know if there are any strain level differences among the disrupted species in transient vs lasting that might explain this?

  3. net growth advantage for the colonizer of at least 0.5 doublings per day

    You could consider using tools like iRep to directly calculate the replication rate of different organisms in the community:

    Overall maybe that could help explain some of the transmission and engraftment differences - does a strain need to be actively replicating in the host in order to be transmitted? Are persister (non repelicating) strains more likely to to rebound in the antibiotic treated condition?

  4. pre- perturbation community diversity

    Even if there were not global differences in the amount of diversity, do you see any differences in common in the composition of the starting communities that might make them more sensitive to antibiotic perturbation? Fewer predicted antibiotic resistance genes?

  5. revious studies in mouse models have hypothesized that strain transmission from cohabiting individuals could contribute to these high levels of resident strain recovery

    I guess an important difference between humans and mice here is that mice are copraphagic, which probably wildly increases the rate of microbiome transfer. Is that worth pointing out here? Also, mice share genetic and food too which also probably helps community sharing.

  6. The total amount of strain sharing varied widely across households

    This variability is wild! Do you know if diet can help explain any of these differences? Do people who co-habitate but don't share strains have very different diets ?

  7. showing that subjects can have heterogeneous responses to the same antibiotic perturbation.

    Is looking at antibiotic resistance in these communities useful here? Either from CFU plating on cipro, or using tools like AMR finder? Perhaps that could explain some of the variation in response here.