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The densities of highly competent plant hosts may shape pathogen community composition and disease severity, altering disease risk and impacts. Life history and evolutionary history influence host competence: longer-lived species tend to be better defended than shorter-lived species and pathogens adapt to infect species with which they have longer evolutionary histories. It is unclear, however, how the densities of species that differ in competence due to life and evolutionary histories affect plant pathogen community composition and disease severity.We examined foliar fungal pathogens on two host groups in a California grassland: native perennial and non-native annual grasses. We first characterized pathogen community composition and disease severity on the two host groups to approximate differences in competence. We then used observational and manipulated gradients of native perennial and non-native annual grass densities to assess the effects of each host group on pathogen community composition and disease severity in 1-m2 plots.Native perennial and non-native annual grasses hosted distinct pathogen communities but shared generalist pathogens. Native perennial grasses hosted pathogens with larger host ranges and experienced greater disease severity (75% higher proportions of leaves with lesions) than non-native annuals. While the relative abundances of three common pathogens tended to shift, and disease severity of native perennial grasses tended to increase with increasing densities of both host groups, these changes were not statistically significant.Synthesis. The life and evolutionary histories of grasses likely influence their competence for different pathogen species, leading to distinct pathogen communities and differences in disease severity. However, there was no evidence that the density of either host group significantly affected pathogen community composition or disease severity. Therefore, variation in competence for different pathogens likely shapes pathogen community composition and disease severity but may not interact with host density to alter disease risk and impacts at small scales.

Early detection and eradication of invasive plants are more cost-effective than managing well-established invasive plant populations and their impacts. However, there is high uncertainty around which taxa are likely to become invasive in a given area. Horizon scanning, which pairs rapid risk assessment with consensus building among experts, can help identify invasion threats. We performed a horizon scan of potential invasive plant threats to Florida, USA—a state with a high influx of introduced species, conditions that are favorable for plant establishment, and a history of negative impacts from invasive plants. We began with a list of 2128 non-native plant species and subspecies that are crop pests or invasive somewhere in the world and used publicly available data to prioritize 100 taxa for rapid risk assessment. We derived overall invasion risk scores by evaluating the likelihood and certainty of each of the 100 taxa arriving, establishing, and having an impact in Florida. Through the rapid risk assessments and a consensus-building discussion, we identified six plant taxa with high overall risk scores ranging from 75 to 100 out of a possible 125. The six taxa are globally distributed, easily transported to new areas, found in regions with climates similar to Florida’s, and can impact native plant communities, human health, or agriculture. We recommend more thorough risk assessments for each of these six species and, if appropriate, policy and management actions to limit invasive plant introduction and establishment in Florida.

Human activities alter elemental nutrient cycling, which can have profound impacts on agriculture, grasslands, lakes, and other systems. It is becoming increasingly clear that enhanced nitrogen and phosphorus levels can affect disease dynamics across a range of taxa. However, there are few mathematical models that explicitly incorporate nutrients into host-pathogen interactions. Using viral load and plant mass data from an experiment with cereal yellow dwarf virus and its host plant, Avena sativa, we propose and compare two models describing the overall infection dynamics. However, the first model considers nutrient-limited virus production while the other considers a nutrient-induced viral production delay. A virus reproduction number is derived for this nutrient model, which depends on environmental and physiological attributes. Results suggest that including nutrient mediated viral production mechanisms can give rise to robust models that can be used to untangle how nutrients impact pathogen dynamics.

Infectious diseases and invasive species can be strong drivers of biological systems that may interact to shift plant community composition. For example, disease can modify resource competition between invasive and native species. Invasive species tend to interact with a diversity of native species, and it is unclear how native species differ in response to disease-mediated competition with invasive species. Here, we quantified the biomass responses of three native North American grass species (Dichanthelium clandestinum, Elymus virginicus, and Eragrostis spectabilis) to disease-mediated competition with the non-native invasive grass Microstegium vimineum. The foliar fungal pathogen Bipolaris gigantea has recently emerged in Microstegium populations, causing a leaf spot disease that reduces Microstegium biomass and seed production. In a greenhouse experiment, we examined the effects of B. gigantea inoculation on two components of competitive ability for each native species: growth in the absence of competition and biomass responses to increasing densities of Microstegium. Bipolaris gigantea inoculation affected each of the three native species in unique ways, by increasing (Dichanthelium), decreasing (Elymus), or not changing (Eragrostis) their growth in the absence of competition relative to mock inoculation. Bipolaris gigantea inoculation did not, however, affect Microstegium biomass or mediate the effect of Microstegium density on native plant biomass. Thus, B. gigantea had species-specific effects on native plant competition with Microstegium through species-specific biomass responses to B. gigantea inoculation, but not through modified responses to Microstegium density. Our results suggest that disease may uniquely modify competitive interactions between invasive and native plants for different native plant species.

Infectious diseases and invasive species are strong drivers of biological systems that may interact to shift plant community composition. Disease and invasion can each directly suppress native populations, but variation in responses among native species to disease, invasion, and their combined effects are not well characterized. Here, we quantified the responses of three native North American grass species to experimental inoculation with the fungal pathogen Bipolaris gigantea, which has recently emerged in populations of the invasive grass Microstegium vimineum, causing leaf spot disease. In a greenhouse experiment, we examined the direct effects of disease on the native species and the indirect effects of disease on the native species through altered competition with M. vimineum, which was planted at a range of densities. Pathogen inoculation directly affected each of the three native species in unique ways, by increasing, decreasing, or not changing their biomass relative to mock inoculation. Higher M. vimineum densities, however, reduced the biomass of all three native species, regardless of inoculation treatment, suggesting that disease had no indirect effects through altered competition. In addition, competition with M. vimineum suppressed native plant biomass to a greater extent than disease. The differential impacts of B. gigantea and the consistent impacts of M. vimineum on native species biomass suggest that disease may modify native plant community composition while plant invasion may suppress multiple native plant species in systems where these drivers co-occur.

Non-native invasive plants can establish in natural areas, where they can be ecologically damaging and costly to manage. Like cultivated plants, invasive plants can experience a relatively disease-free period upon introduction and accumulate pathogens over time. Diseases of invasive plant populations are infrequently studied compared to diseases of agriculture, forestry, and even native plant populations. We evaluated similarities and differences in the processes that are likely to affect pathogen accumulation and disease in invasive plants compared to cultivated plants, which are the dominant focus of the field of plant pathology. Invasive plants experience more genetic, biotic, and abiotic variation across space and over time than cultivated plants, which is expected to stabilize the ecological and evolutionary dynamics of interactions with pathogens and possibly weaken the efficacy of infectious disease in their control. Although disease is expected to be context dependent, the widespread distribution of invasive plants makes them important pathogen reservoirs. Research on invasive plant diseases can both protect crops and help manage invasive plant populations.

Ecological theory that predicts the effects of resource availability on species interactions has been explored across a range of systems. Yet, application of this theory to communities of host-associated pathogens has been limited. Host resources and diet can impact disease severity and prevalence, and these resource effects on disease may be mediated by pathogen-pathogen interactions within hosts infected with multiple pathogens. As with free-living organisms, pathogen species can alter each other’s population growth rates, population densities, and transmission to new hosts through facilitative or antagonistic processes. We used a model grass-virus system (Barley and Cereal Yellow Dwarf Viruses) to test the hypothesis that host nutrition can constrain virus-virus interactions by simultaneously determining both within-host density and transmission to new hosts. Hosts (oats) were grown in growth chambers with different concentrations of soil nitrogen (N) and phosphorus (P) and infected with one or both viruses (i.e., coinfection). We quantified the impacts of nutrient addition on virus-virus interactions through within-host density (i.e., the concentration of viruses in a plant) and transmission to new hosts. Nutrients promoted facilitation of one virus (CYDV-RPV) through increased density (elevated N) and increased transmission (elevated N and P) with coinfection relative to single infection. The other virus (BYDV-PAV) experienced facilitation through increased density when nutrients were limited, but nutrient addition led to antagonistic effects of coinfection on density (elevated N and P) and transmission (elevated N). Our results highlight opportunities for novel insights from testing predictions of community ecology in disease systems, including nutrient-dependent facilitation and nutrient-mediated interactions during transmission that were not predicted by within-host dynamics. This study contributes to the growing literature on ecological interactions among coinfecting pathogens by demonstrating that resource availability can mediate pathogen-pathogen interactions both within hosts and during transmission.

International audience; Disease and community ecology share conceptual and theoretical lineages, and there has been a resurgence of interest in strengthening links between these fields. Building on recent syntheses focused on the effects of host community composition on single pathogen systems, we examine pathogen (microparasite) communities using a stochastic metacommunity model as a starting point to bridge community and disease ecology perspectives. Such models incorporate the effects of core community processes, such as ecological drift, selection and dispersal, but have not been extended to incorporate host-pathogen interactions, such as immunosuppression or synergistic mortality, that are central to disease ecology. We use a two-pathogen susceptible-infected (SI) model to fill these gaps in the metacommunity approach; however, SI models can be intractable for examining species-diverse, spatially structured systems. By placing disease into a framework developed for community ecology, our synthesis highlights areas ripe for progress, including a theoretical framework that incorporates host dynamics, spatial structuring and evolutionary processes, as well as the data needed to test the predictions of such a model. Our synthesis points the way for this framework and demonstrates that a deeper understanding of pathogen community dynamics will emerge from approaches working at the interface of disease and community ecology.