Integrating infection intensity and aggregation into the dynamics of pathogens with within‐host replication

Disease outcomes depend heavily on infection intensity which is often heterogeneous across and within host populations. Most individuals carry low pathogen loads and a few carry high loads, a pattern known as aggregation. Although well characterized in macroparasite systems, aggregation and infection intensity are rarely incorporated into microparasite models. This raises key questions: Do similar mechanisms underlie aggregation in macro- and microparasite systems? Moreover, how do aggregation and load-dependent effects shape outcomes such as host suppression and virulence-transmission trade-offs? To address these questions, we developed a series of differential equation models that allow the pathogen load distribution across hosts to evolve dynamically, shaped by both within- and between-host processes. We applied this framework to the amphibian chytrid fungus system caused by Batrachochytrium dendrobatidis (Bd), a fungal pathogen threatening amphibian populations worldwide. Our results show that both stronger load-dependent mortality and faster within-host replication reduce aggregation. Aggregation, in turn, weakens host suppression and flattens virulence-transmission trade-off, shifting peak transmission to higher replication rates. Overall, our models show that similar mechanisms of infection intensity and aggregation influence host-pathogen dynamics in microparasites as in macroparasites. This work offers a framework for advancing theoretical and data-driven understanding of how within-host processes scale to population-level disease dynamics, advocating for a unified approach to disease modelling that bridges the macro- and microparasites.