Abstract: Species interactions can increase or decrease the severity of disease outbreaks. We know, for instance, that competition can reduce disease – a ‘dilution effect’. However, the circumstances under which dilution occurs are not well-understood. Under what conditions should a system in which dilution is possible assemble? Additionally, dilution is generally attributed to two mechanisms: host regulation and encounter reduction. Despite this, the contributions of each mechanism to dilution are not clear. This study aims to address these outstanding questions by examining a simple model of dilution. We construct a linear system of Ordinary Differential Equations to examine a minimal model of dilution. Using this system of equations, we can address two goals. We can evaluate what is required for a competing diluter to invade a disease system. We can also assess which mechanism(s) are important for the outcomes of dilution – namely, reduced disease prevalence and infected density.
Here, we find that competitor invasion (and thus, dilution) has two requirements. First, the disease must be sufficiently virulent to allow a competitor to invade. Second, the competitor must be sufficiently competitive to make use of the space the virulence ‘opens’ for it. When the host, competitor, and disease all coexist we can see dilution at work. Host regulation drives down prevalence, density of infectious propagules, and the densities of the focal host. Dilution, then, comes at the cost of focal host density, at least when it is driven by host regulation. Encounter reduction, on the other hand, reduces how many competitors are needed to achieve lowered virulence. This means that encounter reduction can mitigate the cost of dilution in terms of lowered host density. Interestingly, encounter reduction does not impact prevalence of infection or spore density. When individual spore yield is a function of resource density, encounter reduction is more beneficial. Additionally, we find that competitors can cause the system to oscillate in parameter-spaces wherein the focal disease system exists stably, alone. Likewise, however, the addition of competitors can stabilize regions the focal disease system would normally oscillate in. We conclude that simple models can show us when to expect dilution, and what mechanisms drive the dynamics of dilution systems. The traits of hosts, competitors, and parasites shape when we expect to see dilution by competition. Host regulation predominantly drives dilution in this model, but encounter reduction can play a role in outcomes.
