Host physiological traits mediate interspecific and plastic variation in reservoir competence

Background/Question/Methods

The likelihood of acquiring and transmitting pathogen infection varies both within and among hosts. This individual-level variation in reservoir competence scales up to create observed differences in pathogen transmission across host populations and communities. Estimates of reservoir competence are needed to forecast the epidemic consequences of host community response to environmental change. Often, these estimates are necessarily observational and system-specific. While effective on a case-by-case basis, this approach quantifies variation in reservoir competence but doesn’t explain it. Understanding why hosts vary in their ability to harbor disease could lend generality to our models and increase our ability to respond rapidly when new outbreaks occur. In an experimentally tractable system, we asked whether broad patterns of covariation in the physiological traits of hosts underlie differences in reservoir competence. Using several grass hosts of a generalist, vector-borne virus, we manipulated host physiology by varying host identity and resource supply in two greenhouse experiments. On each host, we measured several physiological traits that could influence host-pathogen and host-vector interactions. By manipulating exposure to infected vectors or vector feeding on infected hosts, we quantified the likelihood of pathogen infection and transmission. We tested whether these components of reservoir competence varied with host physiological traits.  

Results/Conclusions

In 23 hosts of an aphid-borne Barley Yellow Dwarf Virus, species differences and plastic responses to a nitrogen supply treatment created substantial variation in a covarying set of physiological traits. Host susceptibility (the likelihood of acquiring infection) and host infectiousness (the probability of vector infection) both varied significantly with host physiological traits. Fast-growing hosts with high photosynthetic rates and high tissue nutrient concentrations were more susceptible and more infectious, whereas slow-growing hosts with the opposite traits were less susceptible and infectious. Thus, competent hosts that become infected often and readily transmit infection share a common set of physiological traits, and hosts with these traits will likely amplify pathogen transmission. These same traits have long been used to understand and predict plant adaptation and acclimation to resource environments. In working towards a general theory of pathogen response to environmental change, this result offers a means of integrating disease ecology with trait-based models of host community assembly and response to shifting abiotic conditions.