Both within-host and between-host processes concurrently operate to structure pathogen community composition. However, some processes may be more important than others in regulating pathogen communities, and novel tools are needed to formally quantify how each of these mechanisms contribute to pathogen coexistence or competitive exclusion. Here, we modify and extend recent advances in modern coexistence theory (MCT) to study infectious disease systems. Applying MCT to pathogen communities allows us to decompose the strength of pathogen coexistence - defined as each pathogen's growth rate when rare - into its mechanistic constituents, thereby allowing us to evaluate how concurrently operating within- and between-host processes promote pathogen coexistence or competitive exclusion.
We demonstrate our approach by constructing a two pathogen, multi-scale model in which 1) host immunity is either strain-specific or non-specific, and 2) pathogens are either neutral or exhibit a competition/colonization trade-off (i.e. one pathogen is superior within-hosts and the other is superior between-hosts). Using MCT, we conduct a mechanistic decomposition to evaluate how spatial variation in pathogen fitness and pathogen density contribute to coexistence under these different competition and host immunity regimes.
Results/Conclusions
We found that assumptions regarding coexistence among free-living organisms do not necessarily hold in disease systems. In particular, we show that stable coexistence of neutral pathogens is possible due to host immune memory, whereas neutral, free-living species follow a random walk to extinction. For pathogens exhibiting a competition/colonization tradeoff and facing non-specific immune responses, spatial variability is necessary for both pathogens to coexist in the system, mirroring results from free-living organisms. Without spatial variability, the superior within-host competitor will competitively exclude the superior between-host colonizer in the host population. However, for pathogens exhibiting competitive trade-offs but facing strain-specific immunity, both pathogens coexist due to the compartmentalization of immune responses to each pathogen, with spatial variability playing a minimal role.
Our study highlights novel insights gained by applying MCT to disease and other non free-living systems, while providing a powerful tool with which disease ecologists and epidemiologists can study the mechanisms regulating pathogen community structure. We show how mechanistic decompositions can be performed in disease systems, assess how ecological processes at different spatial scales might regulate pathogen coexistence, and show that key signatures of coexistence in pathogen metacommunities differ from general metacommunity models of free-living species.