Rita Lynn Grunberg

The seasonal timing of pathogen development, i.e. its phenology, may be determined by host or environmental cues and shape pathogen communities. Yet, it is less clear to what degree seasonal patterns of pathogen community assembly vary over longer timescales and how strongly variation is determined by local environmental factors. This raises two general questions: how repeatable is seasonal pathogen community assembly across years? If community assembly is not repeatable, what role does environmental variation play in driving differing patterns of pathogen phenology? To address these questions, we tracked fungal pathogen prevalences in a field population of grass, tall fescue (Lolium arundinaceum) , over 3 years and used multivariate analyses to test for concordance between pathogen community assembly and seasonal environmental conditions. Ordination analyses showed that pathogen communities began at a similar community state each spring but diverged among years as the growing season progressed. To examine this, we tested for concordance between variation in the whole pathogen community structure and environmental conditions. Dissimilarity in pathogen community assembly was largely explained by interannual variation in environmental conditions, with precipitation and relative humidity being most important. Taken together, our results suggest linkages between interannual variation in environmental conditions and pathogen community assembly. This article is part of the theme issue ‘Wild plant pathosystems’.

Forecasting disease epidemics may require considering both abiotic and biotic conditions. Abiotic conditions can influence pathogen dispersal, survival, and infection, while prior infection by one pathogen species can alter host susceptibility to subsequent pathogens, creating historical contingencies. Yet, the relative importance of environmental conditions, within-host pathogen interactions, and their potential interplay in predicting seasonal disease dynamics remain underexplored. To better understand these interactions and improve ecological forecasts of disease risk, we analyzed more than 41,000 plant-level observations of three foliar fungal diseases on the grass species tall fescue in North Carolina, collected from 2017–2024. We built temporally explicit random forest models which for two of the three focal diseases accurately (>80%) predicted future disease dynamics from a complex abiotic and biotic predictor space. From these models, we identified key environmental thresholds that intensified annual epidemics. We then supplemented those machine-learning models with Bayesian hierarchical models and survival analyses, finding that pathogen-pathogen interactions can be as important as environmental conditions in predicting disease risk. Furthermore, for two of the three focal diseases, prior infection by a different pathogen facilitated the subsequent infection and the strength of this facilitation was modulated by environmental context. From this study we draw two major conclusions, one ecological and one methodological. First, knowledge of a host’s current disease state may be as important as local environmental conditions for predicting disease dynamics. Second, by integrating complementary modeling approaches, we can develop both predictive forecasts and mechanistic insight into the biotic and abiotic drivers of infectious disease. Open Research Statement: All data and code used to generate the results contained in this paper are available on GitHub ( https://github.com/cb-scott/WidenerLongTermAnalysis ). Upon publication the final version of all scripts and datafiles will be archived on Zenodo with a permanent DOI.

Phyllosphere microbial communities play important roles in plant health, yet the roles of plant defense hormones and coinfections in shaping these communities remain unclear. This study investigated how exogenous application of the plant defense hormone salicylic acid and fungal coinfection influenced microbial communities on leaves of tall fescue. In a factorial experiment, we treated leaves with salicylic acid (at 100 mg/L) or a control solution and inoculated them with one of four inoculation treatments: Rhizoctonia solani alone, mock inoculation, co-inoculation with both R. solani and Colletotrichum cereale , or mock co-inoculation. We characterized the fungal and bacterial communities using ITS and 16S rRNA gene sequencing, respectively. Salicylic acid application did not significantly alter the diversity, composition, or taxa abundances of either fungal or bacterial communities. In contrast, co-inoculation significantly shifted fungal community composition and increased fungal diversity compared to inoculation with R. solani alone. Bacterial communities were not significantly impacted by either inoculation treatment. These results suggest that in this system, coinfection has a stronger influence on phyllosphere fungal communities than exogenous salicylic acid application. Our findings highlight the potential for pathogen coinfections to shape plant-associated microbial communities, particularly fungi, and emphasize the need for further research on the effects of salicylic acid across different host species and experimental approaches.

Many disease epidemics recur seasonally, and such seasonal epidemics can be shaped by species interactions among parasites, pathogens, or other microbes. Field experiments are a classic approach for understanding species interactions but are rarely used to study seasonal epidemics. Our research objective was to help fill this gap by manipulating the seasonal timing of the establishment of infectious diseases while tracking epidemics and other ecological responses. To do this, we conducted a multiyear field experiment in an old field in the Piedmont of North Carolina, USA, dominated by the grass species tall fescue ( Lolium arundinaceum (Schreb). Darbysh). In the field, tall fescue experienced seasonal epidemics of multiple foliar fungal diseases: anthracnose in spring, brown patch in mid‐summer, and crown rust in late summer to fall. In a fully randomized design, we applied four fungicide treatments to replicate plots of intact vegetation in specific seasons to manipulate the timing of disease epidemics. One treatment was designed to delay the establishment of anthracnose until mid‐summer, and another to delay the establishment of both anthracnose and brown patch until fall. In a third treatment, fungicide was applied year‐round, and, in a fourth treatment, fungicide was never applied. The experiment comprised 64 plots, each 2 m × 2 m, surveyed from May 2017 to February 2020. Here, we report a dataset documenting responses in the community structure of both plants and foliar fungi. To track disease prevalence in the host population across seasons and years, this dataset includes monthly leaf‐level observations of the disease status of over 100,000 leaves. To quantify transmission and investigate within‐host pathogen interactions, we longitudinally surveyed disease status in host individuals of known age at least weekly over two growing seasons. Finally, the dataset includes annual data on infection prevalence of the systemic fungal endophyte Epichloë coenophiala , community‐level aboveground plant biomass, and plant community cover. These data can be used for meta‐analyses, comparisons, and syntheses across systems as ecologists seek to predict and mechanistically understand seasonal disease epidemics. There are no copyrights on the dataset, and we request that users of this dataset cite this paper in all publications resulting from its use.

A pathogen arriving on a host typically encounters a diverse community of microbes that can shape priority effects, other within-host interactions, and infection outcomes. In plants, environmental nutrients can drive tradeoffs between host growth and defense and can mediate interactions between coinfecting pathogens. Nutrients may thus alter the outcome of pathogen priority effects for the host, but this possibility has received little experimental investigation. To disentangle the relationship between nutrient availability and coinfection dynamics, we factorially manipulated nutrient availability and order of arrival of two foliar fungal pathogens ( Rhizoctonia solani and Colletotrichum cereale ) on the host grass tall fescue ( Festuca arundinacea ) and tracked disease outcomes. Overall, C. cereale infection facilitated infection by R. solani , increasing its infection rate regardless of their order of inoculation. Additionally, simultaneous and C. cereale -first inoculations decreased plant growth and – in plants that did not receive nutrient addition – increased leaf nitrogen concentrations compared to uninoculated plants. Nutrient addition did not influence infection rates, severity of infection, or plant biomass. These findings highlight the importance of understanding the intricate associations between the order of pathogen arrival, host nutrient availability, and host defense to better predict infection outcomes.

Disease may drive variation in host community structure by modifying the interplay of deterministic and stochastic processes that shape communities. For instance, deterministic processes like ecological selection can benefit species less impacted by disease. When communities have higher levels of disease and disease consistently selects for certain host species, this can reduce variation in host community composition. On the other hand, when host communities are less impacted by disease and selection is weaker, stochastic processes (e.g., drift, dispersal) may play a bigger role in host community structure, which can increase variation among communities. While effects of disease on host community structure have been quantified in field experiments, few have addressed the role of disease in modulating variation in structure among host communities. To address this, we conducted a field experiment spanning three years, using a tractable system: foliar fungal pathogens in an old-field grassland community dominated by the grassLolium arundinaceum, tall fescue. We reduced foliar fungal disease burden in replicate host communities (experimental plots in intact vegetation) in three fungicide regimens that varied in the seasonal duration of fungicide treatment and included a fungicide-free control. We measured host diversity, biomass, and variation in community structure among replicate communities. Disease reduction generally decreased plant richness and increased aboveground biomass relative to communities experiencing ambient levels of disease. These changes in richness and aboveground biomass were consistent across years despite changes in structure of the plant communities over the experiment’s three years. Importantly, disease reduction amplified host community variation, suggesting that disease diminished the degree to which host communities were structured by stochastic processes. These results of experimental disease reduction both highlight the potential importance of stochastic processes in plant communities and reveal the potential for disease to regulate variation in host community structure.

Parasite infections are ubiquitous and their effects on hosts could play a role in ecosystem processes. Ecological stoichiometry provides a framework to study linkages between consumers and their resource, such as parasites and their host, and ecosystem process; however, the stoichiometric traits of host-parasite associations are rarely quantified. Specifically, it is unclear whether parasites’ elemental ratios closely resemble those of their host or if infection is related to host stoichiometry, especially in vertebrate hosts. To answer such questions, we measured the elemental content (%C, %N, and %P) and molar ratios (C:N, C:P, and N:P) of parasitized and unparasitized Gasterosteus aculeatus (three-spined stickleback) and their cestode parasite, Schistocephalus solidus. Host and parasite elemental content were distinct from each other, and parasites were generally higher in %C and lower in %N and %P. Parasite infections were related to host C:N, with infected hosts being lower in C:N. Parasite elemental content was independent of their host, but parasite body mass and parasite density were important drivers of parasite stoichiometry. Overall, these potential effects of parasite infections on host stoichiometry along with parasites’ distinct elemental compositions suggest parasites may further contribute to differences in how individual hosts store and recycle nutrients.

Host individuals are commonly coinfected with multiple parasite species that may interact to shape within-host parasite community structure. In addition to within-host species interactions, parasite communities may also be structured by other processes like dispersal and ecological drift. The timing of dispersal (in particular, the temporal sequence in which parasite species infect a host individual) can alter within-host species interactions, setting the stage for historical contingency by priority effects, but how persistently such effects drive the trajectory of parasite community assembly is unclear, particularly under continued dispersal and ecological drift. We tested the role of species interactions under continued dispersal and ecological drift by simultaneously inoculating individual plants of tall fescue with a factorial combination of three symbionts (two foliar fungal parasites and a mutualistic endophyte), then deploying the plants in the field and tracking parasite communities as they assembled within host individuals. In the field, hosts were exposed to continued dispersal from a common pool of parasites, which should promote convergence in the structure of within-host parasite communities. Yet, analysis of parasite community trajectories found no signal of convergence. Instead, parasite community trajectories generally diverged from each other, and the magnitude of divergence depended on the initial composition of symbionts within each host, indicating historical contingency. Early in assembly, parasite communities also showed evidence of drift, revealing another source of among-host divergence in parasite community structure. Overall, these results show that both historical contingency and ecological drift contributed to divergence in parasite community assembly within hosts.

Disease may modulate variation in host community structure by modifying the interplay of deterministic and stochastic processes. For instance, deterministic processes like ecological selection can benefit species less impacted by disease. When disease consistently selects for certain host species, this can reduce variation in host community composition. On the other hand, when host communities are less impacted by disease and selection is weaker, stochastic processes (e.g., drift, dispersal) may play a bigger role in host community structure, which can increase variation in structure among communities. While effects of disease on host community structure have been quantified in field experiments, few have addressed the role of disease in modulating variation in structure among host communities. To address this, we conducted a field experiment spanning three years, using a tractable system: foliar fungal pathogens in an old-field grassland community dominated by the grass Lolium arundinaceum , tall fescue. We reduced foliar fungal disease burden in replicate host communities (experimental plots in intact vegetation) in three fungicide regimens that varied in the duration of fungicide exposure and included a fungicide-free control. We measured host diversity, biomass, and variation in community structure among replicate communities. Disease reduction generally decreased plant richness and increased aboveground biomass relative to communities experiencing ambient levels of disease. Despite changes in structure of the plant communities over the experiment’s three years, the effects of disease reduction on plant richness and biomass were consistent across years. However, disease reduction did not reduce variation in host community structure, providing little evidence for ecological selection by competition or other deterministic processes. Instead, disease reduction tended to amplify variation in host community structure among replicate communities (i.e., within fungicide treatment groups), suggesting that disease diminished the degree to which host communities were structured by stochastic processes. These results of experimental disease reduction both highlight the potential importance of stochastic processes in plant communities and reveal the potential for disease to regulate variation in host community structure.

Historical contingency has long figured prominently in the conceptual frameworks of evolutionary biology and community ecology. Evolutionary biologists typically consider the effects of chance mutation and historical contingency in driving divergence and convergence of traits in populations, whereas ecologists instead are often interested in the role of historical contingency in community assembly and succession. Although genetic differences among individuals in populations can influence community interactions, variability among populations of the same species has received relatively little attention for its potential role in community assembly and succession. We used a community‐level study of experimental evolution in two compositionally different assemblages of protists and rotifers to explore whether initial differences in species abundances among communities attributed to differences in evolutionary history, persisted as species that continued to evolve over time. In each assemblage, we observed significant convergence between two invaded treatments initially differing in evolutionary history over an observation period equal to ~40–80 generations for most species. Nonetheless, community structure failed to converge completely across all invaded treatments within an assemblage to a single structure. This suggests that whereas the species in the assemblage represent a common selective regime, differences in populations reflecting their evolutionary history can produce long‐lasting transient alternative community states. In one assemblage, we also observed increasing within‐treatment variability among replicate communities over time, suggesting that ecological drift may be another factor contributing to community change. Although subtle, these transient alternative states, in which communities differed in the abundance of interacting species, could nonetheless have important functional consequences, suggesting that the role of evolution in driving these states deserves greater attention.