The context of host competence: a role for plasticity in host-parasite dynamics

Abstract

Even apparently similar hosts can respond differently to the same parasites. Some individuals or specific groups of individuals disproportionately affect disease dynamics. Understanding the sources of among-host heterogeneity in the ability to transmit parasites would improve disease management. A major source of host variation might be phenotypic plasticity - the tendency for phenotypes to change across different environments. Plasticity might be as important as, or even more important than, genetic change, especially in light of human modifications of the environment, because it can occur on a more rapid timescale than evolution. We argue that variation in phenotypic plasticity among and within species strongly contributes to epidemiological dynamics when parasites are shared among multiple hosts, which is often the case.

Keywords: competence; disease; global change; host heterogeneity; phenotypic plasticity.

Figure I

Heterogeneity in host competence.

Figure 1

Plasticity in host competence and its potential effects on disease dynamics. Disease risk is a product of a hierarchy of host traits arising via fixed and plastic genetic differences at the level of the individual but extending to a multi-host community of species. The figure illustrates how the risk of parasite transmission (denoted as the transmission coefficient, β, shown on the y axis) for a hypothetical population (A), species (B), or community (C) varies as host competence changes along an environmental gradient (x axis). Importantly, variation in transmission risk is fundamentally derived from processes at the individual level. In (A) the solid black line shows the average contribution to transmission of individuals (e.g., mice) of genotypes 1–4 (G1–G4) across an environmental gradient (i.e., a single reaction norm for the population), but the dashed lines emphasize the extent of variation in reaction norms for host competence among individual genotypes, such that the contributions of individuals to transmission through variation in competence might be very distinct. At the species level (B) the range of genotypes present in the population determines the mean and variance in transmission potential. S1–S3 denote three example species (e.g., a deer, a mouse, and a squirrel). Broken lines depict variation in β in three species across environments. Despite variation in shape, all reaction norms for all three species have the same mean β. However, average β and variation in β differ among species depending on their position along the environmental gradient. At the community level (C) both species composition (i.e., host identity) and plasticities within species differ across the environment and shape the community value of β. Broken lines indicate species absence, unbroken lines indicate species presence, and dashed boxes encompass particular environment types. Black boxes denote the mean ± SD community-level β.

Figure I

How plasticity in host competence can affect parasite dynamics: a simple model.