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Abstract Temperature increases due to climate change have affected the distribution and severity of diseases in natural systems, causing outbreaks that can destroy host populations. Host identity, diversity, and the associated microbiome can affect host responses to both infection and temperature, but little is known about how they could function as important mediators of disease in altered thermal environments. We conducted an 8‐week warming experiment to test the independent and interactive effects of warming, host genotypic identity, and host genotypic diversity on the prevalence and intensity of infections of seagrass (Zostera marina) by the wasting disease parasite (Labyrinthula zosterae). At elevated temperatures, we found that genotypically diverse host assemblages had reduced infection intensity, but not reduced prevalence, relative to less diverse assemblages. This dilution effect on parasite intensity was the result of both host composition effects as well as emergent properties of biodiversity. In contrast with the benefits of genotypic diversity under warming, diversity actually increased parasite intensity slightly in ambient temperatures. We found mixed support for the hypothesis that a growth–defense trade‐off contributed to elevated disease intensity under warming. Changes in the abundance (but not composition) of a few taxa in the host microbiome were correlated with genotype‐specific responses to wasting disease infections under warming, consistent with the emerging evidence linking changes in the host microbiome to the outcome of host–parasite interactions. This work emphasizes the context dependence of biodiversity–disease relationships and highlights the potential importance of interactions among biodiversity loss, climate change, and disease outbreaks in a key foundation species.
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This content will become publicly available on December 1, 2025
The effect of diversity on disease reverses from dilution to amplification in a 22-year biodiversity × N × CO2 experiment
Abstract Plant disease often increases with N, decreases with CO2, and increases as biodiversity is lost (i.e., the dilution effect). Additionally, all these factors can indirectly alter disease by changing host biomass and hence density-dependent disease transmission. Yet over long periods of time as communities undergo compositional changes, these biomass-mediated pathways might fade, intensify, or even reverse in direction. Using a field experiment that has manipulated N, CO2, and species richness for over 20 years, we compared severity of a specialist rust fungus (Puccinia andropogonis) on its grass host (Andropogon gerardii) shortly after the experiment began (1999) and twenty years later (2019). Between these two sampling periods, two decades apart, we found that disease severity consistently increased with N and decreased with CO2. However, the relationship between diversity and disease reversed from a dilution effect in 1999 (more severe disease in monocultures) to an amplification effect in 2019 (more severe disease in mixtures). The best explanation for this reversal centered on host density (i.e., aboveground biomass), which was initially highest in monoculture, but became highest in mixtures two decades later. Thus, the diversity-disease pattern reversed, but disease consistently increased with host biomass. These results highlight the consistency of N and CO2as drivers of plant disease in the Anthropocene and emphasize the critical role of host biomass—despite potentially variable effects of diversity—for relationships between biodiversity and disease.
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- PAR ID:
- 10554521
- Publisher / Repository:
- Nature Portfolio
- Date Published:
- Journal Name:
- Scientific Reports
- Volume:
- 14
- Issue:
- 1
- ISSN:
- 2045-2322
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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