Studies of host-pathogen systems indicate that host species’ diversity can regulate pathogen establishment. Studies of natural populations have examined correlations between the spatial distribution of disease and environmental variables, particularly those that may contribute to a population’s immunologic susceptibility. However, there may be tradeoffs between species diversity and environmental conditions of particular importance for invasive species, or species pioneering new range. The interaction of environmental conditions influencing the host or pathogen may operate at scales different than those of species diversity, generating asymmetric effects on pathogen transmission. These effects may also differ for pathogens with a narrow versus broad host range. To date, studies investigating relationships between pathogen persistence, environmental factors, and species diversity for pathogens with narrow and wide host ranges are still relatively limited.
We use a hierarchical Bayesian model accounting for imperfect detection to investigate the influence of species diversity on the infection probability in wild pigs for pathogens with broad (swine brucellosis) and narrow (Pseudorabies virus) host ranges. We investigate if amplification or dilution effects caused by species diversity might contribute to pathogen prevalence, and if environmental conditions that commonly cause host stress increase or dampen the effect of species diversity.
Results/Conclusions
We found support for species richness dilution effects for both pathogens after controlling for environmental gradients influencing host survival, host density, and pathogen detection errors. Results for Pseudorabies align well with proposed theory that increased diversity of non-competent hosts reduces pathogen prevalence. Environmental gradients had a negative effect on pathogen prevalence that may be associated with reduced host survival. We did not observe the expected effect for swine brucellosis. Current species-diversity disease theory predicted amplification of swine brucellosis as competent host species increased. Contrary to the amplification hypothesis, we observed a negative relationship between host species-diversity and swine brucellosis prevalence. We also observed large differences in detection errors that could not be explained by reported diagnostic test sensitivity and specificity.
Our study fills a gap in the current knowledge related to the drivers of macro-scale disease occurrence for an important North American invasive species. Our results and approach have several implications for studies investigating pathogen prevalence and species-diversity. Relationships may be obscured for multi-host pathogens if the range of host competency is not adequately represented. Studies that do not account for detection errors might under estimate pathogen prevalence influencing estimated effect sizes. Our method addresses these and can improve insights into these relationships.