ORCID Profile
0000-0003-1684-5983
Current Organisation
University of Trento
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Springer Science and Business Media LLC
Date: 09-08-2022
DOI: 10.1186/S42523-022-00198-5
Abstract: Parasitic infections disturb gut microbial communities beyond their natural range of variation, possibly leading to dysbiosis. Yet it remains underappreciated that most infections are accompanied by one or more co-infections and their collective impact is largely unexplored. Here we developed a framework illustrating changes to the host gut microbiome following single infections, and build on it by describing the neutral, synergistic or antagonistic impacts on microbial α- and ß- ersity expected from co-infections. We tested the framework on microbiome data from a non-human primate population co-infected with helminths and Adenovirus, and matched patterns reported in published studies to the introduced framework. In this case study, α- ersity of co-infected Malagasy mouse lemurs ( Microcebus griseorufus ) did not differ in comparison with that of singly infected or uninfected in iduals, even though community composition captured with ß- ersity metrices changed significantly. Explicitly, we record stochastic changes in dispersion, a sign of dysbiosis, following the Anna-Karenina principle rather than deterministic shifts in the microbial gut community. From the literature review and our case study, neutral and synergistic impacts emerged as common outcomes from co-infections, wherein both shifts and dispersion of microbial communities following co-infections were often more severe than after a single infection alone, but microbial α- ersity was not universally altered. Important functions of the microbiome may also suffer from such heavily altered, though no less species-rich microbial community. Lastly, we pose the hypothesis that the reshuffling of host-associated microbial communities due to the impact of various, often coinciding parasitic infections may become a source of novel or zoonotic diseases.
Publisher: Wiley
Date: 12-09-2022
Abstract: Human habitat disturbance affects both species ersity and intraspecific genetic ersity, leading to correlations between these two components of bio ersity (termed species–genetic ersity correlation, SGDC). However, whether SGDC predictions extend to host‐associated communities, such as the intestinal parasite and gut microbial ersity, remains largely unexplored. Additionally, the role of dominant generalist species is often neglected despite their importance in shaping the environment experienced by other members of the ecological community, and their role as source, reservoir and vector of zoonotic diseases. New analytical approaches (e.g. structural equation modelling, SEM) can be used to assess SGDC relationships and distinguish among direct and indirect effects of habitat characteristics and disturbance on the various components of bio ersity. With six concrete and biologically sound models in mind, we collected habitat characteristics of 22 study sites from four distinct landscapes located in central Panama. Each landscape differed in the degree of human disturbance and fragmentation measured by several quantitative variables, such as canopy cover, canopy height and understorey density. In terms of bio ersity, we estimated on the one hand, (a) small mammal species ersity, and, on the other hand, (b) genome‐wide ersity, (c) intestinal parasite ersity and (d) gut microbial heterogeneity of the most dominant generalist species (Tome's spiny rat, Proechimys semispinosus ). We used SEMs to assess the links between habitat characteristics and biological ersity measures. The best supported SEM suggested that habitat characteristics directly and positively affect the richness of small mammals, the genetic ersity of P. semispinosus and its gut microbial heterogeneity. Habitat characteristics did not, however, directly impact intestinal parasite ersity. We also detected indirect, positive effects of habitat characteristics on both host‐associated assemblages via small mammal richness. For microbes, this is likely linked to cross species transmission, particularly in shared and/or anthropogenically altered habitats, whereas host ersity mitigates parasite infections. The SEM revealed an additional indirect but negative effect on intestinal parasite ersity via host genetic ersity. Our study showcases that habitat alterations not only affect species ersity and host genetic ersity in parallel, but also species ersity of host‐associated assemblages. The impacts from human disturbance are therefore expected to ripple through entire ecosystems with far reaching effects felt even by generalist species.
No related grants have been discovered for Gloria Fackelmann.