Disease dynamics during ecosystem restoration and faunal reassembly

Biodiversity recovery is increasingly promoted as a strategy for restoring ecosystem services, including the regulation of infectious diseases. However, it remains unclear how the potential for pathogen transmission interacts with the timing of biodiversity recovery and the life history of the recovering species to shape the disease dynamics during restoration. Here, we developed a stochastic multi-host metacommunity epidemic model to investigate how the timing of the establishment of slow life history species, pathogen transmissibility, and host-community succession jointly influence disease outcomes in recovering ecosystems. Pathogen transmissibility (R_0) was the dominant predictor of epidemic intensity, whereas the delayed timing of establishment of slow life history species during restoration emerged as a major ecological determinant of pathogen persistence. Delayed establishment of slow life-history hosts consistently increased disease prevalence and persistence by prolonging the dominance of highly competent fast life-history hosts. Generalized additive models revealed a strong interaction between delayed timing of slow life-history species establishment and pathogen transmissibility, explaining more than 90% of the variation in pathogen persistence. The influence of timing of establishment of slow life history species was weak for pathogens with low transmission potential but increased markedly as R_0 increased. Sensitivity analyses further showed that, once pathogen transmissibility was controlled, timing of establishment became the strongest predictor of persistence, whereas among-host spillover transmission primarily influenced the speed of epidemic spread. In contrast, maximum species richness had comparatively little influence on disease outcomes, indicating that the functional composition and assembly timing of recovering communities may be more important than richness alone for predicting disease dynamics. Together, these results demonstrate that disease regulation during ecosystem restoration depends not only on pathogen transmissibility, but also on the life history traits and the timing of establishment of species within recovering communities. Our findings identify life history traits and the timing of when functional communities are restored as a key ecological lever influencing long-term pathogen maintenance in restored ecosystems.

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Publication Details

Journal
bioRxiv (Cold Spring Harbor Laboratory)
Published
2026-11-09
DOI
https://doi.org/10.64898/2026.11.05.764583
Primary Topic
Mathematical and Theoretical Epidemiology and Ecology Models
Type
preprint
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preprint

Disease dynamics during ecosystem restoration and faunal reassembly

Alfan A. Rija, Herwig Leirs, Diana Erazo, Christina L. Faust et al.
bioRxiv (Cold Spring Harbor Laboratory)
Mathematical and Theoretical Epidemiology and Ecology Models
preprint

Disease dynamics during ecosystem restoration and faunal reassembly

Alfan A. Rija, Herwig Leirs, Diana Erazo, Christina L. Faust, Vincent Sluydts, Joachim Mariën, Nils Bunnefeld, Marina Voinson, Luisa Páez-Triana, Lucinda Kirkpatrick
preprint en

Abstract

Biodiversity recovery is increasingly promoted as a strategy for restoring ecosystem services, including the regulation of infectious diseases. However, it remains unclear how the potential for pathogen transmission interacts with the timing of biodiversity recovery and the life history of the recovering species to shape the disease dynamics during restoration. Here, we developed a stochastic multi-host metacommunity epidemic model to investigate how the timing of the establishment of slow life history species, pathogen transmissibility, and host-community succession jointly influence disease outcomes in recovering ecosystems. Pathogen transmissibility (R_0) was the dominant predictor of epidemic intensity, whereas the delayed timing of establishment of slow life history species during restoration emerged as a major ecological determinant of pathogen persistence. Delayed establishment of slow life-history hosts consistently increased disease prevalence and persistence by prolonging the dominance of highly competent fast life-history hosts. Generalized additive models revealed a strong interaction between delayed timing of slow life-history species establishment and pathogen transmissibility, explaining more than 90% of the variation in pathogen persistence. The influence of timing of establishment of slow life history species was weak for pathogens with low transmission potential but increased markedly as R_0 increased. Sensitivity analyses further showed that, once pathogen transmissibility was controlled, timing of establishment became the strongest predictor of persistence, whereas among-host spillover transmission primarily influenced the speed of epidemic spread. In contrast, maximum species richness had comparatively little influence on disease outcomes, indicating that the functional composition and assembly timing of recovering communities may be more important than richness alone for predicting disease dynamics. Together, these results demonstrate that disease regulation during ecosystem restoration depends not only on pathogen transmissibility, but also on the life history traits and the timing of establishment of species within recovering communities. Our findings identify life history traits and the timing of when functional communities are restored as a key ecological lever influencing long-term pathogen maintenance in restored ecosystems.

bioRxiv (Cold Spring Harbor Laboratory)
University of Stirling (GB), University of Antwerp (BE), Bangor University (GB), Instituut voor Tropische Geneeskunde (BE), University of Glasgow (GB), Sokoine University of Agriculture (TZ)
Mathematical and Theoretical Epidemiology and Ecology Models
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