All individuals transition through various life stages over the course of their development, and nearly all organisms must contend with infectious disease at some point in their lives. Yet the intersection of these two universal features of life – stage-structure and infectious disease – and their joint effects on population dynamics, are poorly understood. The aim of our work is to use models to provide theoretical insight into such effects. We explored a simple two-stage (juveniles and adults) differential equation population model in which density dependence slows juvenile maturation. As shown previously by Horst Thieme and André de Roos, such density dependence can be stabilizing or destabilizing (i.e., leading to persistent oscillations). The model is general enough to capture essential features of populations with overlapping generations and continual reproduction, and in which juveniles and adults consume different resources so that density dependence is stage-specific (e.g., many insect species, fish, amphibians). We examine how infectious disease alters the dynamical properties of such stage-structured populations, assuming density-dependent transmission of infection within a stage (using an SI model for that stage), where disease reduces rates of maturation, reproduction, or survival.
Results/Conclusions
Reducing maturation, reproduction, and survival rates in the disease-free model stabilizes population dynamics. We predicted that infectious disease lowering these same rates would stabilize as well. Indeed, for moderate transmission rates, infectious disease often stabilizes dynamics. In contrast, fast disease transmission is not generally stabilizing. However, introducing disease into populations that do not cycle when disease-free was not destabilizing, suggesting that infectious disease in our simple structured population model generally stabilizes dynamics. We also found that counterintuitive effects of disease on population size (called “hydra effects”) can arise when disease increases juvenile mortality or decreases adult fecundity (but do not occur when disease augments adult mortality or reduces maturation), resulting in increased population sizes as compared to the disease-free case. Our results show that infectious disease can sometimes stabilize otherwise unstable dynamics, and sometimes, surprisingly, boost population size. Future work is needed to empirically test these theoretical predictions about unexpected disease effects on stage-structured populations, and to examine impacts of infectious disease in more complex models of stage-structured populations.
