Contrasting the consumptive and non-consumptive cascading effects of natural enemies on vector-borne pathogens

摘要

Predicting disease dynamics requires a community perspective, incorporating multi-species interactions involving hosts, pathogens, vectors, and consumers. In systems where pathogens are dependent on a vector for transmission from one host to another, predators can indirectly influence disease risk through direct effects on vectors. These effects may be consumptive if predators reduce vector abundance by capturing and killing vectors, or non-consumptive if predators induce anti-predator behavioral responses by vectors. Studies are accumulating that document cascading effects of predators on vector-borne disease risk, but the mechanisms underlying these effects are often uncertain. Using a previously developed epidemiological model as a framework, I outline several mechanistic pathways by which predators can have consumptive and non-consumptive effects on vectors, and present theoretical predictions about the cascading influence of these pathways on pathogen prevalence. I then review selected examples from the literature of vector-borne plant pathogen systems where particular mechanistic pathways have been implicated. Together, the model predictions and the literature review reveal that, depending on the particular mechanisms at work, predators may reduce, leave unaffected, or even increase pathogen prevalence. In general, the consumptive effects of predators on vectors result in consistent reductions in pathogen prevalence. However, the non-consumptive effects of predators that arise as a result of changes in pathogen transmission rates, vector birth rates, and non-predation vector mortality rates are more variable, with the potential for context-dependency and counter-intuitive outcomes. Interactions among pathways are also possible, such that the magnitude of consumptive effects can depend upon the strength of non-consumptive effects and vice versa. I conclude by highlighting the importance of teasing apart the various mechanistic pathways by which predators may indirectly influence pathogen prevalence, and clarifying the relationships among them, to accurately predict the consequences of predation for disease risk and the usefulness of biological control of vectors for suppression of plant pathogens.