Search

Hosts rely on the availability of nutrients for growth, and for defense against pathogens. At the same time, changes in host nutrition can alter the dynamics of pathogens that rely on their host for reproduction. For primary producer hosts, enhanced nutrient loads may increase host biomass or pathogen reproduction, promoting faster density-dependent pathogen transmission. However, the effect of elevated nutrients may be reduced if hosts allocate a growth-limiting nutrient to pathogen defense. In canonical disease models, transmission is not a function of nutrient availability. Yet, including nutrient availability is necessary to mechanistically understand the response of infection to changes in the environment. Here, we explore the implications of nutrient-mediated pathogen infectivity and host immunity on infection outcomes. We developed a stoichiometric disease model that explicitly integrates the contrasting dependencies of pathogen infectivity and host immunity on nitrogen (N) and parameterized it for an algal-host system. Our findings reveal dynamic shifts in host biomass build-up, pathogen prevalence, and the force of infection along N supply gradients with N-mediated host infectivity and immunity, compared with a model in which the transmission rate was fixed. We show contrasting responses in pathogen performance with increasing N supply between N-mediated infectivity and N-mediated immunity, revealing an optimum for pathogen transmission at intermediate N supply. This was caused by N limitation of the pathogen at a low N supply and by pathogen suppression via enhanced host immunity at a high N supply. By integrating both nutrient-mediated pathogen infectivity and host immunity into a stoichiometric model, we provide a theoretical framework that is a first step in reconciling the contrasting role nutrients can have on host–pathogen dynamics.

Hosts rely on the availability of nutrients for growth, and for defense against pathogens. At the same time, changes in host nutrition can alter the dynamics of pathogens that rely on their host for reproduction. For primary producer hosts, enhanced nutrient loads may increase host biomass or pathogen reproduction, promoting faster density-dependent pathogen transmission. However, the effect of elevated nutrients may be reduced if hosts allocate a growth-limiting nutrient to pathogen defense. In canonical disease models, transmission is not a function of nutrient availability. Yet, including nutrient availability is necessary to mechanistically understand the response of infection to changes in the environment. Here, we explore the implications of nutrient-mediated pathogen infectivity and host immunity on infection outcomes. We developed a stoichiometric disease model that explicitly integrates the contrasting dependencies of pathogen infectivity and host immunity on nitrogen (N) and parameterized it for an algal-host system. Our findings reveal dynamic shifts in host biomass build-up, pathogen prevalence, and the force of infection along N supply gradients with N-mediated host infectivity and immunity, compared with a model in which the transmission rate was fixed. We show contrasting responses in pathogen performance with increasing N supply between N-mediated infectivity and N-mediated immunity, revealing an optimum for pathogen transmission at intermediate N supply. This was caused by N limitation of the pathogen at a low N supply and by pathogen suppression via enhanced host immunity at a high N supply. By integrating both nutrient-mediated pathogen infectivity and host immunity into a stoichiometric model, we provide a theoretical framework that is a first step in reconciling the contrasting role nutrients can have on host–pathogen dynamics.

Death is a common outcome of infection, but most disease models do not track hosts after death. Instead, these hosts disappear into a void. This assumption lacks critical realism, because dead hosts can alter host–pathogen dynamics. Here, we develop a theoretical framework of carbon-based models combining disease and ecosystem perspectives to investigate the consequences of feedbacks between living and dead hosts on disease dynamics and carbon cycling. Because autotrophs (i.e. plants and phytoplankton) are critical regulators of carbon cycling, we developed general model structures and parameter combinations to broadly reflect disease of autotrophic hosts across ecosystems. Analytical model solutions highlight the importance of disease–ecosystem coupling. For example, decomposition rates of dead hosts mediate pathogen spread, and carbon flux between live and dead biomass pools are sensitive to pathogen effects on host growth and death rates. Variation in dynamics arising from biologically realistic parameter combinations largely fell along a single gradient from slow to fast carbon turnover rates, and models predicted higher disease impacts in fast turnover systems (e.g. lakes and oceans) than slow turnover systems (e.g. boreal forests). Our results demonstrate that a unified framework, including the effects of pathogens on carbon cycling, provides novel hypotheses and insights at the nexus of disease and ecosystem ecology.

An overlooked effect of ecosystem eutrophication is the potential to alter disease dynamics in primary producers, inducing disease‐mediated feedbacks that alter net primary productivity and elemental recycling. Models in disease ecology rarely track organisms past death, yet death from infection can alter important ecosystem processes including elemental recycling rates and nutrient supply to living hosts. In contrast, models in ecosystem ecology rarely track disease dynamics, yet elemental nutrient pools (e.g. nitrogen, phosphorus) can regulate important disease processes including pathogen reproduction and transmission. Thus, both disease and ecosystem ecology stand to grow as fields by exploring questions that arise at their intersection. However, we currently lack a framework explicitly linking these disciplines. We developed a stoichiometric model using elemental currencies to track primary producer biomass (carbon) in vegetation and soil pools, and to track prevalence and the basic reproduction number (R0) of a directly transmitted pathogen. This model, parameterised for a deciduous forest, demonstrates that anthropogenic nutrient supply can interact with disease to qualitatively alter both ecosystem and disease dynamics. Using this element‐focused approach, we identify knowledge gaps and generate predictions about the impact of anthropogenic nutrient supply rates on infectious disease and feedbacks to ecosystem carbon and nutrient cycling.