Within-host disease ecology in the sea fan Gorgonia ventalina: modeling the spatial immunodynamics of a coral-pathogen interaction.

We develop a spatially explicit model for the within-host interactions between a fungal pathogen and the immune response by its coral host. The model is parameterized for the recent epizootic of Aspergillus sydowii in the sea fan Gorgonia ventalina, but its structure is adaptable to many other diseases attacking corals worldwide, fungal infections in other invertebrates and plants, and opportunistic fungal infections in vertebrates. Model processes include pathogen growth and spread through consumption of host tissue, chemotactic attraction of undifferentiated host amoebocytes to infections, and amoebocyte differentiation into various cell types that attack the pathogen. Sensitivity analysis shows that the spread rate of a single localized infection is determined primarily by the pathogen's potential rate of host tissue consumption and by the host's ability to replenish the pool of undifferentiated amoebocytes and sustain a long-term response. The spatial localization of immune responses creates potentially strong indirect interactions between distant lesions, allowing new infections to grow rapidly while host resources are concentrated at older, larger infections. These findings provide possible mechanistic explanations for effects of environmental stressors (e.g., ocean warming, nutrient enrichment) on aspergillosis prevalence and severity and for the observed high spatial and between-host variability in disease impacts.