How do toxicants affect epidemiological dynamics?

Populations are formed of their constituent interacting individuals, each with their own respective within-host biological processes. Infection not only spreads within the host organism but also spreads between individuals. Here we propose and study a multilevel model which links the within-host statuses of immunity and parasite density to population epidemiology under sublethal and lethal toxicant exposure. We analyse this nested model in order to better understand how toxicants impact the spread of disease within populations. We demonstrate that outbreak of infection within a population is completely determined by the level of toxicant exposure, and that it is maximised by intermediate toxicant dosage. We classify the population epidemiology into five phases of increasing toxicant exposure and calculate the conditions under which disease will spread, showing that there exists a threshold toxicant level under which epidemics will not occur. In general, higher toxicant load results in either extinction of the population or outbreak of infection. The within-host statuses of the individual host also determine the outcome of the epidemic at the population level. We discuss applications of our model in the context of environmental epidemiology, predicting that increased exposure to toxicants could result in greater risk of epidemics within ecological systems. We predict that reducing sublethal toxicant exposure below our predicted safe threshold could contribute to controlling population level disease and infection

Stress-Mediated Allee Effects Can Cause the Sudden Collapse of Honey Bee Colonies.

The recent rapid decline in global honey bee populations could have significant implications for ecological systems, economics and food security. No single cause of honey bee collapse has yet to be identified, although pesticides, mites and other pathogens have all been shown to have a sublethal effect. We present a model of a functioning bee hive and introduce external stress to investigate the impact on the regulatory processes of recruitment to the forager class, social inhibition and the laying rate of the queen. The model predicts that constant density-dependent stress acting through an Allee effect on the hive can result in sudden catastrophic switches in dynamical behaviour and the eventual collapse of the hive. The model proposes that around a critical point the hive undergoes a saddle-node bifurcation, and that a small increase in model parameters can have irreversible consequences for the entire hive. We predict that increased stress levels can be counteracted by a higher laying rate of the queen, lower levels of forager recruitment or lower levels of natural mortality of foragers, and that increasing social inhibition can not maintain the colony under high levels of stress. We lay the theoretical foundation for sudden honey bee collapse in order to facilitate further experimental and theoretical consideration